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https://api.wikimedia.org/core/v1/wikipedia/en/page/Mosquito_net/html

Mosquito net

A mosquito net is a type of meshed curtain that is circumferentially draped over a bed or a sleeping area, to offer the sleeper barrier protection against bites and stings from mosquitos , flies , and other pest insects , and thus against the diseases they may carry. Examples of such preventable insect-borne diseases include malaria , dengue fever , yellow fever , zika virus , Chagas disease and various forms of encephalitis , including the West Nile virus . To be effective, the mesh of a mosquito net must be fine enough to exclude such insects without obscuring visibility or ventilation to unacceptable levels. It is possible to increase the effectiveness of a mosquito net greatly by pretreating it with an appropriate insecticide or insect repellent . Research has shown mosquito nets to be an extremely effective method of malaria prevention, averting approximately 663 million cases of malaria over the period 2000–2015. Mosquito netting is mainly used for the protection against the malaria transmitting vector, Anopheles gambiae . The first record of malaria-like symptoms occurred as early as 2700 BCE from China . The vector for this disease was not identified until 1880 when Sir Ronald Ross identified mosquitoes as a vector for malaria. Conopeum or Conopium ( Ancient Greek : κωνώπιον or κωνόπιον or κωνωπεῖον ) was a mosquito-curtain. It was made to keep away mosquitos and other flying insects. It took its name from κώνωψ, which means mosquito in Greek, and is the origin of the English word canopy. These curtains were especially used in Egypt because of the mosquitoes which infest the Nile. The Scholiast on Juvenal mention that at Rome they were called cubiculare . They are still used in Greece and other countries surrounding the Mediterranean. Mosquito netting has a long history. Though use of the term dates from the mid-18th century, Indian literature from the late medieval period has references to the usage of mosquito nets in ritual Hindu worship. Poetry composed by Annamayya , the earliest known Telugu musician and poet, references domatera , which means "mosquito net" in Telugu . Use of mosquito nets has been dated to prehistoric times. It is said that Cleopatra , the last active pharaoh of Ancient Egypt , also slept under a mosquito net. Mosquito nets were used during the malaria-plagued construction of the Suez Canal . Mosquito netting can be made from cotton , polyethylene , polyester , polypropylene , or nylon . A mesh size of 1.2 millimetres (0.047 in) stops mosquitoes, and smaller, such as 0.6 millimetres (0.024 in) , stops other biting insects such as biting midges/no-see-ums . A mosquito bar is an alternate form of a mosquito net. It is constructed of a fine see-through mesh fabric mounted on and draped over a box-shaped frame. It is designed to fit over an area or item such as a sleeping bag to provide protection from insects. A mosquito bar could be used to protect oneself from mosquitoes and other insects while sleeping in jungle areas. The mesh is woven tightly enough to stop insects from entering but loosely enough to not interfere with ventilation. The frame is usually self-supporting or freestanding although it can be designed to be attached from the top to an alternative support such as tree limbs. Mosquito nets are often used where malaria or other insect-borne diseases are common, especially as a tent-like covering over a bed. For effectiveness, it is important that the netting not have holes or gaps large enough to allow insects to enter. It is also important to 'seal' the net properly because mosquitoes are able to 'squeeze' through improperly secured nets. Because an insect can bite a person through the net, the net must not rest directly on the skin. Mosquito netting can be hung over beds from the ceiling or a frame, built into tents , or installed in windows and doors. When hung over beds, rectangular nets provide more room for sleeping without the danger of netting contacting skin, at which point mosquitoes may bite through untreated netting. Some newer mosquito nets are designed to be both easy to deploy and foldable after use. Where mosquito nets are freely or cheaply distributed, local residents sometimes opportunistically use them inappropriately, for example as fishing nets . When used for fishing, mosquito nets have harmful ecological consequences because the fine mesh of a mosquito net retains almost all fish, including bycatch such as immature or small fish and fish species that are not suitable for consumption. In addition, insecticides with which the mesh has been treated, such as permethrin , may be harmful to the fish and other aquatic fauna . Mosquito nets treated with insecticides—known as insecticide-treated nets (ITNs) or bednets—were developed and tested in the 1980s for malaria prevention by P. Carnevale and his team in Bobo-Dioulasso, Burkina Faso . ITNs are estimated to be twice as effective as untreated nets, and offer greater than 70% protection compared with no net. These nets are dip-treated using a synthetic pyrethroid insecticide such as deltamethrin or permethrin which will double the protection over a non-treated net by killing and repelling mosquitoes. For maximum effectiveness, ITNs should be re-impregnated with insecticide every six months. This process poses a significant logistical problem in rural areas. Newer, long-lasting insecticidal nets (LLINs) have now replaced ITNs in most countries. The distribution of mosquito nets or bednets treated with insecticides such as permethrin or deltamethrin has been shown to be an extremely effective method of malaria prevention. According to a 2015 Nature study, mosquito nets averted 68% of an estimated 663 million averted cases of malaria infection since 2000. It is also one of the most cost-effective methods of prevention. These nets can often be obtained for around $2.50–$3.50 (2–3 euros) from the United Nations , the World Health Organization (WHO), and others. ITNs have been shown to be the most cost-effective prevention method against malaria and are part of WHO's Millennium Development Goals (MDGs). Generally LLINs are purchased by donor groups and delivered through in-country distribution networks. ITNs protect people sleeping under them and simultaneously kill mosquitoes that contact the nets. Some protection is provided to others by this method, including people sleeping in the same room but not under the net. However, mathematical modeling has suggested that disease transmission may be exacerbated after bed nets have lost their insecticidal properties under certain circumstances. Although ITN users are still protected by the physical barrier of the netting, non-users could experience an increased bite rate as mosquitoes are deflected away from the non-lethal bed net users. The modeling suggests that this could increase transmission when the human population density is high or at lower human densities when mosquitoes are more adept at locating their blood meals. In December 2019 it was reported that West African populations of Anopheles gambiae include mutants with higher levels of sensory appendage protein 2 (a type of chemosensory protein in the legs), which binds to pyrethroids, sequestering them and so preventing them from functioning, thus making the mosquitoes with this mutation more likely to survive contact with bednets. While some experts argue that international organizations should distribute ITNs and LLINs to people for free to maximize coverage (since such a policy would reduce price barriers), others insist that cost-sharing between the international organization and recipients would lead to greater use of the net (arguing that people will value a good more if they pay for it). Additionally, proponents of cost-sharing argue that such a policy ensures that nets are efficiently allocated to the people who most need them (or are most vulnerable to infection). Through a "selection effect", they argue, the people who most need the bed nets will choose to purchase them, while those less in need will opt out. However, a randomized controlled trial study of ITNs uptake among pregnant women in Kenya , conducted by economists Pascaline Dupas and Jessica Cohen, found that cost-sharing does not necessarily increase the usage intensity of ITNs nor does it induce uptake by those most vulnerable to infection, as compared to a policy of free distribution. In some cases, cost-sharing can decrease demand for mosquito nets by erecting a price barrier. Dupas and Cohen's findings support the argument that free distribution of ITNs can be more effective than cost-sharing in increasing coverage and saving lives. In a cost-effectiveness analysis, Dupas and Cohen note that "cost-sharing is at best marginally more cost-effective than free distribution, but free distribution leads to many more lives saved." The researchers base their conclusions about the cost-effectiveness of free distribution on the proven spillover benefits of increased ITN usage. ITNs protect the individuals or households that use them, and they protect people in the surrounding community in one of two ways. When a large number of nets are distributed in one residential area, their chemical additives help reduce the number of mosquitoes in the environment. With fewer mosquitoes, the chances of malaria infection for recipients and non-recipients are significantly reduced. (In other words, the importance of the physical barrier effect of ITNs decreases relative to the positive externality effect [ clarification needed ] of the nets in creating a mosquito-free environment when ITNs are highly concentrated in one residential cluster or community.) Standard ITNs must be replaced or re-treated with insecticide after six washes and, therefore, are not seen as a convenient, effective long-term solution to the malaria problem. As a result, the mosquito netting and pesticide industries developed so-called long-lasting insecticidal mosquito nets, which also use pyrethroid insecticides. There are three types of LLINs — polyester netting which has insecticide bound to the external surface of the netting fibre using a resin; polyethylene which has insecticide incorporated into the fibre and polypropylene which has insecticide incorporated into the fibre. All types can be washed at least 20 times, but physical durability will vary. A survey carried out in Tanzania concluded that effective life of polyester nets was 2 to 3 years; with polyethylene LLINs there are data to support over 5 years of life with trials in showing nets which were still effective after 7 years. A review of 22 randomized controlled trials of ITNs found (for Plasmodium falciparum malaria) that ITNs can reduce deaths in children by one fifth and episodes of malaria by half. More specifically, in areas of stable malaria "ITNs reduced the incidence of uncomplicated malarial episodes by 50% compared to no nets, and 39% compared to untreated nets" and in areas of unstable malaria "by 62% compared to no nets and 43% compared to untreated nets". As such the review calculated that for every 1000 children protected by ITNs, 5.5 lives would be saved each year. Through the years 1999 and 2010 the abundance of female anopheles gambiae densities in houses throughout western Kenya were recorded. This data set was paired with the spatial data of bed net usage in order to determine correlation. Results showed that from 2008 to 2010 the relative population density of the female anopheles gambiae decreased from 90.6% to 60.7%. The conclusion of this study showed that as the number of houses which used insecticide treated bed nets increased the population density of female anopheles gambiae decreased. This result did however vary from region to region based on the local environment. A 2019 study in PLoS ONE found that a campaign to distribute mosquito bednets in the Democratic Republic of Congo led to a 41% decline mortality for children under five who lived in areas with a high malaria risk. While some experts argue that international organizations should distribute ITNs and LLINs to people for free to maximize coverage (since such a policy would reduce price barriers), others insist that cost-sharing between the international organization and recipients would lead to greater use of the net (arguing that people will value a good more if they pay for it). Additionally, proponents of cost-sharing argue that such a policy ensures that nets are efficiently allocated to the people who most need them (or are most vulnerable to infection). Through a "selection effect", they argue, the people who most need the bed nets will choose to purchase them, while those less in need will opt out. However, a randomized controlled trial study of ITNs uptake among pregnant women in Kenya , conducted by economists Pascaline Dupas and Jessica Cohen, found that cost-sharing does not necessarily increase the usage intensity of ITNs nor does it induce uptake by those most vulnerable to infection, as compared to a policy of free distribution. In some cases, cost-sharing can decrease demand for mosquito nets by erecting a price barrier. Dupas and Cohen's findings support the argument that free distribution of ITNs can be more effective than cost-sharing in increasing coverage and saving lives. In a cost-effectiveness analysis, Dupas and Cohen note that "cost-sharing is at best marginally more cost-effective than free distribution, but free distribution leads to many more lives saved." The researchers base their conclusions about the cost-effectiveness of free distribution on the proven spillover benefits of increased ITN usage. ITNs protect the individuals or households that use them, and they protect people in the surrounding community in one of two ways. When a large number of nets are distributed in one residential area, their chemical additives help reduce the number of mosquitoes in the environment. With fewer mosquitoes, the chances of malaria infection for recipients and non-recipients are significantly reduced. (In other words, the importance of the physical barrier effect of ITNs decreases relative to the positive externality effect [ clarification needed ] of the nets in creating a mosquito-free environment when ITNs are highly concentrated in one residential cluster or community.) Standard ITNs must be replaced or re-treated with insecticide after six washes and, therefore, are not seen as a convenient, effective long-term solution to the malaria problem. As a result, the mosquito netting and pesticide industries developed so-called long-lasting insecticidal mosquito nets, which also use pyrethroid insecticides. There are three types of LLINs — polyester netting which has insecticide bound to the external surface of the netting fibre using a resin; polyethylene which has insecticide incorporated into the fibre and polypropylene which has insecticide incorporated into the fibre. All types can be washed at least 20 times, but physical durability will vary. A survey carried out in Tanzania concluded that effective life of polyester nets was 2 to 3 years; with polyethylene LLINs there are data to support over 5 years of life with trials in showing nets which were still effective after 7 years. A review of 22 randomized controlled trials of ITNs found (for Plasmodium falciparum malaria) that ITNs can reduce deaths in children by one fifth and episodes of malaria by half. More specifically, in areas of stable malaria "ITNs reduced the incidence of uncomplicated malarial episodes by 50% compared to no nets, and 39% compared to untreated nets" and in areas of unstable malaria "by 62% compared to no nets and 43% compared to untreated nets". As such the review calculated that for every 1000 children protected by ITNs, 5.5 lives would be saved each year. Through the years 1999 and 2010 the abundance of female anopheles gambiae densities in houses throughout western Kenya were recorded. This data set was paired with the spatial data of bed net usage in order to determine correlation. Results showed that from 2008 to 2010 the relative population density of the female anopheles gambiae decreased from 90.6% to 60.7%. The conclusion of this study showed that as the number of houses which used insecticide treated bed nets increased the population density of female anopheles gambiae decreased. This result did however vary from region to region based on the local environment. A 2019 study in PLoS ONE found that a campaign to distribute mosquito bednets in the Democratic Republic of Congo led to a 41% decline mortality for children under five who lived in areas with a high malaria risk. Malaria and other arboviruses are known to contribute to economic disparity within that country and vice versa. This opens the stage for corruption associated to the distribution of self-protection aides. The least wealthy members of society are both more likely to be in closer proximity to the vectors' prime habitat and less likely to be protected from the vectors. This increase in probability of being infected increases the demand for self-protection which therefore allows for higher pricing and uneven distribution of self-protection means. A decrease in per capita income exaggerates a high demand for resources such as water and food resulting in civil unrest among communities. Protecting resources as well as attempting to obtain resources are both a cause for conflict. Mosquito nets have been observed to be used in fisheries across the world, where their strength, light weight and free or cheap accessibility make them an attractive tool for fishing. People who use them for fishing catch vast numbers of juvenile fish. Mosquito nets do reduce air flow to an extent and sleeping under a net is hotter than sleeping without one, which can be uncomfortable in tropical areas without air-conditioning . Some alternatives are:

Wiki

West Nile

https://api.wikimedia.org/core/v1/wikipedia/en/page/Brown-headed_cowbird/html

Brown-headed cowbird

The brown-headed cowbird ( Molothrus ater ) is a small, obligate brood parasitic icterid native to temperate and subtropical North America. It is a permanent resident in the southern parts of its range; northern birds migrate to the southern United States and Mexico in winter, returning to their summer habitat around March or April. The brown-headed cowbird was described by the French polymath Georges-Louis Leclerc, Comte de Buffon in 1775 in his Histoire Naturelle des Oiseaux from a specimen collected in the Carolinas . The bird was also illustrated in a hand-colored plate engraved by François-Nicolas Martinet in the Planches Enluminées D'Histoire Naturelle , which was produced under the supervision of Edme-Louis Daubenton to accompany Buffon's text. Neither the plate caption nor Buffon's description included a scientific name, but in 1783, Dutch naturalist Pieter Boddaert coined the binomial name Oriolus ater in his catalogue of the Planches Enluminées . The brown-headed cowbird is now placed in the genus Molothrus that was introduced by English naturalist William John Swainson in 1832 with the brown-headed cowbird as the type species . The genus name combines the Ancient Greek mōlos meaning "struggle" or "battle" with thrōskō meaning "to sire" or "to impregnate". The specific name ater is Latin for "dull black". The English name "cowbird", first recorded in 1839, refers to this species often being seen near cattle. Three subspecies are recognised: The brown-headed cowbird is typical for an icterid in general shape, but is distinguished by its finch -like head and beak and smaller size. The adult male is iridescent black in color with a brown head. The adult female is slightly smaller and is dull grey with a pale throat and very fine streaking on the underparts. Their total length is 16–22 cm (6.3–8.7 in) and the average wingspan is 36 cm (14 in) . Body mass can range from 30–60 g (1.1–2.1 oz) , with females averaging 38.8 g (1.37 oz) against the males' average of 49 g (1.7 oz) . The species lives in open or semiopen country, and often travels in flocks, sometimes mixed with red-winged blackbirds (particularly in spring) and bobolinks (particularly in fall), as well as common grackles or European starlings . These birds forage on the ground, often following grazing animals such as horses and cattle to catch insects stirred up by the larger animals. They mainly eat seeds , insects and rarely, berries. [ citation needed ] Before European settlement, brown-headed cowbirds followed bison herds across the prairies . Their population expanded with the clearing of forested areas and the introduction of new grazing animals by settlers across North America. They are now commonly seen at suburban birdfeeders. In 2012, brown-headed cowbirds in northwest Riverside County , CA tested positive for West Nile Virus . The brown-headed cowbird is an obligate brood parasite; it lays its eggs in the nests of other small passerines (perching birds), particularly those that build cup-like nests. The brown-headed cowbird eggs have been documented in nests of at least 220 host species, including hummingbirds and raptors . More than 140 different species of birds are known to have raised young cowbirds. The young cowbird is fed by the host parents at the expense of their own young. Brown-headed cowbird females can lay up to 40 eggs in a season. Some host species, such as the house finch , feed their young a vegetarian diet. This is unsuitable for young brown-headed cowbirds, meaning few survive to fledge. Accepting a cowbird egg and rearing a cowbird chick can be costly to a host species. In the American redstart , nests parasitized by cowbirds were found to have a higher rate of predation, likely due in part to the loud begging calls by the cowbird nestling, but also partly explained by the fact that nests likely to be parasitized are also more likely to be preyed upon. : 199 Unlike the common cuckoo , the brown-headed cowbird is not divided into gentes whose eggs imitate those of a particular host . Host species sometimes notice the cowbird egg, with different hosts reacting to the egg in different ways. Some, like the blue-grey gnatcatcher , abandon their nest, losing their own eggs as well. Others, like the American yellow warbler , bury the foreign egg under nest material, where it perishes. The brown thrasher physically ejects the egg from the nest. Experiments with grey catbirds , a known cowbird host, have shown that this species rejects cowbird eggs more than 95% of the time. For this species, the cost of accepting cowbird eggs (i.e. the loss of their own eggs or nestlings through starvation or the actions of the nestling cowbird) was far higher than the cost of rejecting those eggs (i.e. where the host might conceivably eject its own egg accidentally). Brown-headed cowbird nestlings are also sometimes expelled from the nest. Nestlings of host species can also alter their behavior in response to the presence of a cowbird nestling. Song sparrow nestlings in parasitized nests alter their vocalizations in frequency and amplitude so that they resemble the cowbird nestling, and these nestlings tend to be fed equally often as nestlings in unparasitized nests. Brown-headed cowbirds seem to periodically check on their eggs and young after they have deposited them. Removal of the parasitic egg may trigger a retaliatory reaction termed " mafia behavior". According to one study the cowbird returned to ransack the nests of a range of host species 56% of the time when their egg was removed. In addition, the cowbird also destroyed nests in a type of "farming behavior" to force the hosts to build new ones. The cowbirds then laid their eggs in the new nests 85% of the time. Young cowbirds are not exposed to species-typical visual and auditory information like other birds. Despite this, they are able to develop species-typical singing, social, and breeding behaviors. Cowbird brains are wired to respond to the vocalizations of other cowbirds, allowing young to find and join flocks of their own species. These vocalizations are consistent across all cowbird populations, and serve as a sort of species-recognition password. If a young cowbird is not exposed to these "password" vocalizations by a certain age, it will mistakenly imprint on the host species. Social behaviors of cowbird males include aggressive, competitive singing bouts with other males and pair bonding and monogamy with females. By manipulating demographics so juveniles only had access to females, juvenile males developed atypical social behavior; they did not engage in the typical social singing bouts with other males, did not pair bond with females, and were promiscuous. This demonstrates that great flexibility occurs in the behavior of cowbirds, and that the social environment is extremely important in structuring their behavior. Adult males housed with juvenile males were shown to have greater reproductive success compared to adult males housed with other adult males. Being housed with juvenile males honed the reproductive skills of the adult males by providing them with a more complex social environment. This finding was further studied by comparing the behaviors and reproductive success of males exposed to a dynamic flock, consisting of changing individuals, with males exposed to a static group of individuals. The individuals that stayed with the same group (i.e., static flock) had a stable, predictable relationship between social behavior and reproductive success; the males that sang frequently to females experienced the greatest reproductive success. The adult males that were exposed to a rotating roster of new individuals (i.e., dynamic flock) had an unpredictable relationship between social variables and reproductive success; these males were able to copulate using a much greater variety of social strategies. The males that lived in static flocks had high levels of consistency in their behaviors and reproductive success across multiple years, whereas the males in dynamic flocks experienced varying levels of dominance with other males, differing levels of singing to females, and differing levels of reproductive success. The brown-headed cowbird is an obligate brood parasite; it lays its eggs in the nests of other small passerines (perching birds), particularly those that build cup-like nests. The brown-headed cowbird eggs have been documented in nests of at least 220 host species, including hummingbirds and raptors . More than 140 different species of birds are known to have raised young cowbirds. The young cowbird is fed by the host parents at the expense of their own young. Brown-headed cowbird females can lay up to 40 eggs in a season. Some host species, such as the house finch , feed their young a vegetarian diet. This is unsuitable for young brown-headed cowbirds, meaning few survive to fledge. Accepting a cowbird egg and rearing a cowbird chick can be costly to a host species. In the American redstart , nests parasitized by cowbirds were found to have a higher rate of predation, likely due in part to the loud begging calls by the cowbird nestling, but also partly explained by the fact that nests likely to be parasitized are also more likely to be preyed upon. : 199 Unlike the common cuckoo , the brown-headed cowbird is not divided into gentes whose eggs imitate those of a particular host . Host species sometimes notice the cowbird egg, with different hosts reacting to the egg in different ways. Some, like the blue-grey gnatcatcher , abandon their nest, losing their own eggs as well. Others, like the American yellow warbler , bury the foreign egg under nest material, where it perishes. The brown thrasher physically ejects the egg from the nest. Experiments with grey catbirds , a known cowbird host, have shown that this species rejects cowbird eggs more than 95% of the time. For this species, the cost of accepting cowbird eggs (i.e. the loss of their own eggs or nestlings through starvation or the actions of the nestling cowbird) was far higher than the cost of rejecting those eggs (i.e. where the host might conceivably eject its own egg accidentally). Brown-headed cowbird nestlings are also sometimes expelled from the nest. Nestlings of host species can also alter their behavior in response to the presence of a cowbird nestling. Song sparrow nestlings in parasitized nests alter their vocalizations in frequency and amplitude so that they resemble the cowbird nestling, and these nestlings tend to be fed equally often as nestlings in unparasitized nests. Brown-headed cowbirds seem to periodically check on their eggs and young after they have deposited them. Removal of the parasitic egg may trigger a retaliatory reaction termed " mafia behavior". According to one study the cowbird returned to ransack the nests of a range of host species 56% of the time when their egg was removed. In addition, the cowbird also destroyed nests in a type of "farming behavior" to force the hosts to build new ones. The cowbirds then laid their eggs in the new nests 85% of the time. Young cowbirds are not exposed to species-typical visual and auditory information like other birds. Despite this, they are able to develop species-typical singing, social, and breeding behaviors. Cowbird brains are wired to respond to the vocalizations of other cowbirds, allowing young to find and join flocks of their own species. These vocalizations are consistent across all cowbird populations, and serve as a sort of species-recognition password. If a young cowbird is not exposed to these "password" vocalizations by a certain age, it will mistakenly imprint on the host species. Some host species, such as the house finch , feed their young a vegetarian diet. This is unsuitable for young brown-headed cowbirds, meaning few survive to fledge. Accepting a cowbird egg and rearing a cowbird chick can be costly to a host species. In the American redstart , nests parasitized by cowbirds were found to have a higher rate of predation, likely due in part to the loud begging calls by the cowbird nestling, but also partly explained by the fact that nests likely to be parasitized are also more likely to be preyed upon. : 199 Unlike the common cuckoo , the brown-headed cowbird is not divided into gentes whose eggs imitate those of a particular host . Host species sometimes notice the cowbird egg, with different hosts reacting to the egg in different ways. Some, like the blue-grey gnatcatcher , abandon their nest, losing their own eggs as well. Others, like the American yellow warbler , bury the foreign egg under nest material, where it perishes. The brown thrasher physically ejects the egg from the nest. Experiments with grey catbirds , a known cowbird host, have shown that this species rejects cowbird eggs more than 95% of the time. For this species, the cost of accepting cowbird eggs (i.e. the loss of their own eggs or nestlings through starvation or the actions of the nestling cowbird) was far higher than the cost of rejecting those eggs (i.e. where the host might conceivably eject its own egg accidentally). Brown-headed cowbird nestlings are also sometimes expelled from the nest. Nestlings of host species can also alter their behavior in response to the presence of a cowbird nestling.Song sparrow nestlings in parasitized nests alter their vocalizations in frequency and amplitude so that they resemble the cowbird nestling, and these nestlings tend to be fed equally often as nestlings in unparasitized nests. Brown-headed cowbirds seem to periodically check on their eggs and young after they have deposited them. Removal of the parasitic egg may trigger a retaliatory reaction termed " mafia behavior". According to one study the cowbird returned to ransack the nests of a range of host species 56% of the time when their egg was removed. In addition, the cowbird also destroyed nests in a type of "farming behavior" to force the hosts to build new ones. The cowbirds then laid their eggs in the new nests 85% of the time. Young cowbirds are not exposed to species-typical visual and auditory information like other birds. Despite this, they are able to develop species-typical singing, social, and breeding behaviors. Cowbird brains are wired to respond to the vocalizations of other cowbirds, allowing young to find and join flocks of their own species. These vocalizations are consistent across all cowbird populations, and serve as a sort of species-recognition password. If a young cowbird is not exposed to these "password" vocalizations by a certain age, it will mistakenly imprint on the host species. Social behaviors of cowbird males include aggressive, competitive singing bouts with other males and pair bonding and monogamy with females. By manipulating demographics so juveniles only had access to females, juvenile males developed atypical social behavior; they did not engage in the typical social singing bouts with other males, did not pair bond with females, and were promiscuous. This demonstrates that great flexibility occurs in the behavior of cowbirds, and that the social environment is extremely important in structuring their behavior. Adult males housed with juvenile males were shown to have greater reproductive success compared to adult males housed with other adult males. Being housed with juvenile males honed the reproductive skills of the adult males by providing them with a more complex social environment. This finding was further studied by comparing the behaviors and reproductive success of males exposed to a dynamic flock, consisting of changing individuals, with males exposed to a static group of individuals. The individuals that stayed with the same group (i.e., static flock) had a stable, predictable relationship between social behavior and reproductive success; the males that sang frequently to females experienced the greatest reproductive success. The adult males that were exposed to a rotating roster of new individuals (i.e., dynamic flock) had an unpredictable relationship between social variables and reproductive success; these males were able to copulate using a much greater variety of social strategies. The males that lived in static flocks had high levels of consistency in their behaviors and reproductive success across multiple years, whereas the males in dynamic flocks experienced varying levels of dominance with other males, differing levels of singing to females, and differing levels of reproductive success. With the expansion of its range and its parasitic behavior, the brown-headed cowbird is often regarded as a pest. People sometimes engage in cowbird control programs, with the intention of protecting species negatively impacted by the cowbirds' brood parasitism. A study of nests of Bell's vireo highlighted a potential limitation of these control programs, demonstrating that removal of cowbirds from a site may create an unintended consequence of increasing cowbird productivity on that site, because with fewer cowbirds, fewer parasitized nests are deserted, resulting in greater nest success for cowbirds.

Wiki

West Nile

https://api.wikimedia.org/core/v1/wikipedia/en/page/Zoonosis/html

Zoonosis

A zoonosis ( / z oʊ ˈ ɒ n ə s ɪ s , ˌ z oʊ ə ˈ n oʊ s ɪ s / ; plural zoonoses ) or zoonotic disease is an infectious disease of humans caused by a pathogen (an infectious agent, such as a bacterium , virus , parasite , or prion ) that can jump from a non-human (usually a vertebrate ) to a human and vice versa. Major modern diseases such as Ebola and salmonellosis are zoonoses. HIV was a zoonotic disease transmitted to humans in the early part of the 20th century, though it has now evolved into a separate human-only disease. Human infection with animal influenza viruses is rare, as they do not transmit easily to or among humans. However, avian and swine influenza viruses in particular possess high zoonotic potential, and these occasionally recombine with human strains of the flu and can cause pandemics such as the 2009 swine flu . Taenia solium infection is one of the neglected tropical diseases with public health and veterinary concern in endemic regions. Zoonoses can be caused by a range of disease pathogens such as emergent viruses , bacteria, fungi and parasites; of 1,415 pathogens known to infect humans, 61% were zoonotic. Most human diseases originated in non-humans; however, only diseases that routinely involve non-human to human transmission, such as rabies , are considered direct zoonoses. Zoonoses have different modes of transmission. In direct zoonosis the disease is directly transmitted from non-humans to humans through media such as air (influenza) or bites and saliva (rabies). In contrast, transmission can also occur via an intermediate species (referred to as a vector ), which carry the disease pathogen without getting sick. When humans infect non-humans, it is called reverse zoonosis or anthroponosis. The term is from Greek : ζῷον zoon "animal" and νόσος nosos "sickness". Host genetics plays an important role in determining which non-human viruses will be able to make copies of themselves in the human body. Dangerous non-human viruses are those that require few mutations to begin replicating themselves in human cells. These viruses are dangerous since the required combinations of mutations might randomly arise in the natural reservoir . The emergence of zoonotic diseases originated with the domestication of animals. Zoonotic transmission can occur in any context in which there is contact with or consumption of animals, animal products, or animal derivatives. This can occur in a companionistic (pets), economic (farming, trade, butchering, etc.), predatory (hunting, butchering, or consuming wild game), or research context. Recently, there has been a rise in frequency of appearance of new zoonotic diseases. "Approximately 1.67 million undescribed viruses are thought to exist in mammals and birds, up to half of which are estimated to have the potential to spill over into humans", says a study led by researchers at the University of California, Davis . According to a report from the United Nations Environment Programme and International Livestock Research Institute a large part of the causes are environmental like climate change , unsustainable agriculture, exploitation of wildlife, and land use change . Others are linked to changes in human society such as an increase in mobility. The organizations propose a set of measures to stop the rise. The most significant zoonotic pathogens causing foodborne diseases are Escherichia coli O157:H7 , Campylobacter , Caliciviridae , and Salmonella . In 2006 a conference held in Berlin focused on the issue of zoonotic pathogen effects on food safety , urging government intervention and public vigilance against the risks of catching food-borne diseases from farm-to-table dining. Many food-borne outbreaks can be linked to zoonotic pathogens. Many different types of food that have an animal origin can become contaminated. Some common food items linked to zoonotic contaminations include eggs, seafood, meat, dairy, and even some vegetables. Outbreaks involving contaminated food should be handled in preparedness plans to prevent widespread outbreaks and to efficiently and effectively contain outbreaks. Contact with farm animals can lead to disease in farmers or others that come into contact with infected farm animals. Glanders primarily affects those who work closely with horses and donkeys. Close contact with cattle can lead to cutaneous anthrax infection, whereas inhalation anthrax infection is more common for workers in slaughterhouses , tanneries , and wool mills . Close contact with sheep who have recently given birth can lead to infection with the bacterium Chlamydia psittaci , causing chlamydiosis (and enzootic abortion in pregnant women), as well as increase the risk of Q fever , toxoplasmosis , and listeriosis , in the pregnant or otherwise immunocompromised . Echinococcosis is caused by a tapeworm, which can spread from infected sheep by food or water contaminated by feces or wool. Avian influenza is common in chickens, and, while it is rare in humans, the main public health worry is that a strain of avian influenza will recombine with a human influenza virus and cause a pandemic like the 1918 Spanish flu . [ citation needed ] In 2017, free-range chickens in the UK were temporarily ordered to remain inside due to the threat of avian influenza. Cattle are an important reservoir of cryptosporidiosis , which mainly affects the immunocompromised. Reports have shown mink can also become infected. In Western countries, hepatitis E burden is largely dependent on exposure to animal products, and pork is a significant source of infection, in this respect. Veterinarians are exposed to unique occupational hazards when it comes to zoonotic disease. In the US, studies have highlighted an increased risk of injuries and lack of veterinary awareness of these hazards. Research has proved the importance for continued clinical veterinarian education on occupational risks associated with musculoskeletal injuries, animal bites, needle-sticks, and cuts. A July 2020 report by the United Nations Environment Programme stated that the increase in zoonotic pandemics is directly attributable to anthropogenic destruction of nature and the increased global demand for meat and that the industrial farming of pigs and chickens in particular will be a primary risk factor for the spillover of zoonotic diseases in the future. Habitat loss of viral reservoir species has been identified as a significant source in at least one spillover event . The wildlife trade may increase spillover risk because it directly increases the number of interactions across animal species, sometimes in small spaces. The origin of the ongoing COVID-19 pandemic is traced to the wet markets in China . Zoonotic disease emergence is demonstrably linked to the consumption of wildlife meat, exacerbated by human encroachment into natural habitats and amplified by the unsanitary conditions of wildlife markets. These markets, where diverse species converge, facilitate the mixing and transmission of pathogens, including those responsible for outbreaks of HIV-1, Ebola, and mpox , and potentially even the COVID-19 pandemic. Notably, small mammals often harbor a vast array of zoonotic bacteria and viruses, yet endemic bacterial transmission among wildlife remains largely unexplored. Therefore, accurately determining the pathogenic landscape of traded wildlife is crucial for guiding effective measures to combat zoonotic diseases and documenting the societal and environmental costs associated with this practice. Pets can transmit a number of diseases. Dogs and cats are routinely vaccinated against rabies . Pets can also transmit ringworm and Giardia , which are endemic in both animal and human populations. Toxoplasmosis is a common infection of cats; in humans it is a mild disease although it can be dangerous to pregnant women. Dirofilariasis is caused by Dirofilaria immitis through mosquitoes infected by mammals like dogs and cats. Cat-scratch disease is caused by Bartonella henselae and Bartonella quintana , which are transmitted by fleas that are endemic to cats. Toxocariasis is the infection of humans by any of species of roundworm , including species specific to dogs ( Toxocara canis ) or cats ( Toxocara cati ). Cryptosporidiosis can be spread to humans from pet lizards, such as the leopard gecko . Encephalitozoon cuniculi is a microsporidial parasite carried by many mammals, including rabbits, and is an important opportunistic pathogen in people immunocompromised by HIV/AIDS , organ transplantation , or CD4+ T-lymphocyte deficiency. Pets may also serve as a reservoir of viral disease and contribute to the chronic presence of certain viral diseases in the human population. For instance, approximately 20% of domestic dogs, cats, and horses carry anti-hepatitis E virus antibodies and thus these animals probably contribute to human hepatitis E burden as well. For non-vulnerable populations (e.g., people who are not immunocompromised) the associated disease burden is, however, small. [ citation needed ] Furthermore, the trade of non domestic animals such as wild animals as pets can also increase the risk of zoonosis spread. Outbreaks of zoonoses have been traced to human interaction with, and exposure to, other animals at fairs , live animal markets , petting zoos , and other settings. In 2005, the Centers for Disease Control and Prevention (CDC) issued an updated list of recommendations for preventing zoonosis transmission in public settings. The recommendations, developed in conjunction with the National Association of State Public Health Veterinarians , include educational responsibilities of venue operators, limiting public animal contact, and animal care and management. Hunting involves humans tracking, chasing, and capturing wild animals, primarily for food or materials like fur. However, other reasons like pest control or managing wildlife populations can also exist. Transmission of zoonotic diseases, those leaping from animals to humans, can occur through various routes: direct physical contact, airborne droplets or particles, bites or vector transport by insects, oral ingestion, or even contact with contaminated environments. Wildlife activities like hunting and trade bring humans closer to dangerous zoonotic pathogens, threatening global health. According to the Center for Diseases Control and Prevention (CDC) hunting and consuming wild animal meat ("bushmeat") in regions like Africa can expose people to infectious diseases due to the types of animals involved, like bats and primates. Unfortunately, common preservation methods like smoking or drying aren't enough to eliminate these risks. Although bushmeat provides protein and income for many, the practice is intricately linked to numerous emerging infectious diseases like Ebola, HIV, and SARS , raising critical public health concerns. A review published in 2022 found evidence that zoonotic spillover linked to wildmeat consumption has been reported across all continents. Kate Jones , Chair of Ecology and Biodiversity at University College London , says zoonotic diseases are increasingly linked to environmental change and human behavior. The disruption of pristine forests driven by logging, mining, road building through remote places, rapid urbanization, and population growth is bringing people into closer contact with animal species they may never have been near before. The resulting transmission of disease from wildlife to humans, she says, is now "a hidden cost of human economic development". In a guest article, published by IPBES , President of the EcoHealth Alliance and zoologist Peter Daszak , along with three co-chairs of the 2019 Global Assessment Report on Biodiversity and Ecosystem Services , Josef Settele, Sandra Díaz , and Eduardo Brondizio, wrote that "rampant deforestation, uncontrolled expansion of agriculture, intensive farming , mining and infrastructure development, as well as the exploitation of wild species have created a 'perfect storm' for the spillover of diseases from wildlife to people." Joshua Moon, Clare Wenham, and Sophie Harman said that there is evidence that decreased biodiversity has an effect on the diversity of hosts and frequency of human-animal interactions with potential for pathogenic spillover. An April 2020 study, published in the Proceedings of the Royal Society ' s Part B journal, found that increased virus spillover events from animals to humans can be linked to biodiversity loss and environmental degradation , as humans further encroach on wildlands to engage in agriculture, hunting, and resource extraction they become exposed to pathogens which normally would remain in these areas. Such spillover events have been tripling every decade since 1980. An August 2020 study, published in Nature , concludes that the anthropogenic destruction of ecosystems for the purpose of expanding agriculture and human settlements reduces biodiversity and allows for smaller animals such as bats and rats, which are more adaptable to human pressures and also carry the most zoonotic diseases, to proliferate. This in turn can result in more pandemics. In October 2020, the Intergovernmental Science-Policy Platform on Biodiversity and Ecosystem Services published its report on the 'era of pandemics' by 22 experts in a variety of fields and concluded that anthropogenic destruction of biodiversity is paving the way to the pandemic era and could result in as many as 850,000 viruses being transmitted from animals – in particular birds and mammals – to humans. The increased pressure on ecosystems is being driven by the "exponential rise" in consumption and trade of commodities such as meat, palm oil , and metals, largely facilitated by developed nations, and by a growing human population . According to Peter Daszak, the chair of the group who produced the report, "there is no great mystery about the cause of the Covid-19 pandemic, or of any modern pandemic. The same human activities that drive climate change and biodiversity loss also drive pandemic risk through their impacts on our environment." According to a report from the United Nations Environment Programme and International Livestock Research Institute , entitled "Preventing the next pandemic – Zoonotic diseases and how to break the chain of transmission", climate change is one of the 7 human-related causes of the increase in the number of zoonotic diseases. The University of Sydney issued a study, in March 2021, that examines factors increasing the likelihood of epidemics and pandemics like the COVID-19 pandemic. The researchers found that "pressure on ecosystems, climate change and economic development are key factors" in doing so. More zoonotic diseases were found in high-income countries . A 2022 study dedicated to the link between climate change and zoonosis found a strong link between climate change and the epidemic emergence in the last 15 years, as it caused a massive migration of species to new areas, and consequently contact between species which do not normally come in contact with one another. Even in a scenario with weak climatic changes, there will be 15,000 spillover of viruses to new hosts in the next decades. The areas with the most possibilities for spillover are the mountainous tropical regions of Africa and southeast Asia. Southeast Asia is especially vulnerable as it has a large number of bat species that generally do not mix, but could easily if climate change forced them to begin migrating. A 2021 study found possible links between climate change and transmission of COVID-19 through bats. The authors suggest that climate-driven changes in the distribution and robustness of bat species harboring coronaviruses may have occurred in eastern Asian hotspots (southern China, Myanmar, and Laos), constituting a driver behind the evolution and spread of the virus. The most significant zoonotic pathogens causing foodborne diseases are Escherichia coli O157:H7 , Campylobacter , Caliciviridae , and Salmonella . In 2006 a conference held in Berlin focused on the issue of zoonotic pathogen effects on food safety , urging government intervention and public vigilance against the risks of catching food-borne diseases from farm-to-table dining. Many food-borne outbreaks can be linked to zoonotic pathogens. Many different types of food that have an animal origin can become contaminated. Some common food items linked to zoonotic contaminations include eggs, seafood, meat, dairy, and even some vegetables. Outbreaks involving contaminated food should be handled in preparedness plans to prevent widespread outbreaks and to efficiently and effectively contain outbreaks. Contact with farm animals can lead to disease in farmers or others that come into contact with infected farm animals. Glanders primarily affects those who work closely with horses and donkeys. Close contact with cattle can lead to cutaneous anthrax infection, whereas inhalation anthrax infection is more common for workers in slaughterhouses , tanneries , and wool mills . Close contact with sheep who have recently given birth can lead to infection with the bacterium Chlamydia psittaci , causing chlamydiosis (and enzootic abortion in pregnant women), as well as increase the risk of Q fever , toxoplasmosis , and listeriosis , in the pregnant or otherwise immunocompromised . Echinococcosis is caused by a tapeworm, which can spread from infected sheep by food or water contaminated by feces or wool. Avian influenza is common in chickens, and, while it is rare in humans, the main public health worry is that a strain of avian influenza will recombine with a human influenza virus and cause a pandemic like the 1918 Spanish flu . [ citation needed ] In 2017, free-range chickens in the UK were temporarily ordered to remain inside due to the threat of avian influenza. Cattle are an important reservoir of cryptosporidiosis , which mainly affects the immunocompromised. Reports have shown mink can also become infected. In Western countries, hepatitis E burden is largely dependent on exposure to animal products, and pork is a significant source of infection, in this respect. Veterinarians are exposed to unique occupational hazards when it comes to zoonotic disease. In the US, studies have highlighted an increased risk of injuries and lack of veterinary awareness of these hazards. Research has proved the importance for continued clinical veterinarian education on occupational risks associated with musculoskeletal injuries, animal bites, needle-sticks, and cuts. A July 2020 report by the United Nations Environment Programme stated that the increase in zoonotic pandemics is directly attributable to anthropogenic destruction of nature and the increased global demand for meat and that the industrial farming of pigs and chickens in particular will be a primary risk factor for the spillover of zoonotic diseases in the future. Habitat loss of viral reservoir species has been identified as a significant source in at least one spillover event . The wildlife trade may increase spillover risk because it directly increases the number of interactions across animal species, sometimes in small spaces. The origin of the ongoing COVID-19 pandemic is traced to the wet markets in China . Zoonotic disease emergence is demonstrably linked to the consumption of wildlife meat, exacerbated by human encroachment into natural habitats and amplified by the unsanitary conditions of wildlife markets. These markets, where diverse species converge, facilitate the mixing and transmission of pathogens, including those responsible for outbreaks of HIV-1, Ebola, and mpox , and potentially even the COVID-19 pandemic. Notably, small mammals often harbor a vast array of zoonotic bacteria and viruses, yet endemic bacterial transmission among wildlife remains largely unexplored. Therefore, accurately determining the pathogenic landscape of traded wildlife is crucial for guiding effective measures to combat zoonotic diseases and documenting the societal and environmental costs associated with this practice.Pets can transmit a number of diseases. Dogs and cats are routinely vaccinated against rabies . Pets can also transmit ringworm and Giardia , which are endemic in both animal and human populations. Toxoplasmosis is a common infection of cats; in humans it is a mild disease although it can be dangerous to pregnant women. Dirofilariasis is caused by Dirofilaria immitis through mosquitoes infected by mammals like dogs and cats. Cat-scratch disease is caused by Bartonella henselae and Bartonella quintana , which are transmitted by fleas that are endemic to cats. Toxocariasis is the infection of humans by any of species of roundworm , including species specific to dogs ( Toxocara canis ) or cats ( Toxocara cati ). Cryptosporidiosis can be spread to humans from pet lizards, such as the leopard gecko . Encephalitozoon cuniculi is a microsporidial parasite carried by many mammals, including rabbits, and is an important opportunistic pathogen in people immunocompromised by HIV/AIDS , organ transplantation , or CD4+ T-lymphocyte deficiency. Pets may also serve as a reservoir of viral disease and contribute to the chronic presence of certain viral diseases in the human population. For instance, approximately 20% of domestic dogs, cats, and horses carry anti-hepatitis E virus antibodies and thus these animals probably contribute to human hepatitis E burden as well. For non-vulnerable populations (e.g., people who are not immunocompromised) the associated disease burden is, however, small. [ citation needed ] Furthermore, the trade of non domestic animals such as wild animals as pets can also increase the risk of zoonosis spread. Outbreaks of zoonoses have been traced to human interaction with, and exposure to, other animals at fairs , live animal markets , petting zoos , and other settings. In 2005, the Centers for Disease Control and Prevention (CDC) issued an updated list of recommendations for preventing zoonosis transmission in public settings. The recommendations, developed in conjunction with the National Association of State Public Health Veterinarians , include educational responsibilities of venue operators, limiting public animal contact, and animal care and management.Hunting involves humans tracking, chasing, and capturing wild animals, primarily for food or materials like fur. However, other reasons like pest control or managing wildlife populations can also exist. Transmission of zoonotic diseases, those leaping from animals to humans, can occur through various routes: direct physical contact, airborne droplets or particles, bites or vector transport by insects, oral ingestion, or even contact with contaminated environments. Wildlife activities like hunting and trade bring humans closer to dangerous zoonotic pathogens, threatening global health. According to the Center for Diseases Control and Prevention (CDC) hunting and consuming wild animal meat ("bushmeat") in regions like Africa can expose people to infectious diseases due to the types of animals involved, like bats and primates. Unfortunately, common preservation methods like smoking or drying aren't enough to eliminate these risks. Although bushmeat provides protein and income for many, the practice is intricately linked to numerous emerging infectious diseases like Ebola, HIV, and SARS , raising critical public health concerns. A review published in 2022 found evidence that zoonotic spillover linked to wildmeat consumption has been reported across all continents. Kate Jones , Chair of Ecology and Biodiversity at University College London , says zoonotic diseases are increasingly linked to environmental change and human behavior. The disruption of pristine forests driven by logging, mining, road building through remote places, rapid urbanization, and population growth is bringing people into closer contact with animal species they may never have been near before. The resulting transmission of disease from wildlife to humans, she says, is now "a hidden cost of human economic development". In a guest article, published by IPBES , President of the EcoHealth Alliance and zoologist Peter Daszak , along with three co-chairs of the 2019 Global Assessment Report on Biodiversity and Ecosystem Services , Josef Settele, Sandra Díaz , and Eduardo Brondizio, wrote that "rampant deforestation, uncontrolled expansion of agriculture, intensive farming , mining and infrastructure development, as well as the exploitation of wild species have created a 'perfect storm' for the spillover of diseases from wildlife to people." Joshua Moon, Clare Wenham, and Sophie Harman said that there is evidence that decreased biodiversity has an effect on the diversity of hosts and frequency of human-animal interactions with potential for pathogenic spillover. An April 2020 study, published in the Proceedings of the Royal Society ' s Part B journal, found that increased virus spillover events from animals to humans can be linked to biodiversity loss and environmental degradation , as humans further encroach on wildlands to engage in agriculture, hunting, and resource extraction they become exposed to pathogens which normally would remain in these areas. Such spillover events have been tripling every decade since 1980. An August 2020 study, published in Nature , concludes that the anthropogenic destruction of ecosystems for the purpose of expanding agriculture and human settlements reduces biodiversity and allows for smaller animals such as bats and rats, which are more adaptable to human pressures and also carry the most zoonotic diseases, to proliferate. This in turn can result in more pandemics. In October 2020, the Intergovernmental Science-Policy Platform on Biodiversity and Ecosystem Services published its report on the 'era of pandemics' by 22 experts in a variety of fields and concluded that anthropogenic destruction of biodiversity is paving the way to the pandemic era and could result in as many as 850,000 viruses being transmitted from animals – in particular birds and mammals – to humans. The increased pressure on ecosystems is being driven by the "exponential rise" in consumption and trade of commodities such as meat, palm oil , and metals, largely facilitated by developed nations, and by a growing human population . According to Peter Daszak, the chair of the group who produced the report, "there is no great mystery about the cause of the Covid-19 pandemic, or of any modern pandemic. The same human activities that drive climate change and biodiversity loss also drive pandemic risk through their impacts on our environment." According to a report from the United Nations Environment Programme and International Livestock Research Institute , entitled "Preventing the next pandemic – Zoonotic diseases and how to break the chain of transmission", climate change is one of the 7 human-related causes of the increase in the number of zoonotic diseases. The University of Sydney issued a study, in March 2021, that examines factors increasing the likelihood of epidemics and pandemics like the COVID-19 pandemic. The researchers found that "pressure on ecosystems, climate change and economic development are key factors" in doing so. More zoonotic diseases were found in high-income countries . A 2022 study dedicated to the link between climate change and zoonosis found a strong link between climate change and the epidemic emergence in the last 15 years, as it caused a massive migration of species to new areas, and consequently contact between species which do not normally come in contact with one another. Even in a scenario with weak climatic changes, there will be 15,000 spillover of viruses to new hosts in the next decades. The areas with the most possibilities for spillover are the mountainous tropical regions of Africa and southeast Asia. Southeast Asia is especially vulnerable as it has a large number of bat species that generally do not mix, but could easily if climate change forced them to begin migrating. A 2021 study found possible links between climate change and transmission of COVID-19 through bats. The authors suggest that climate-driven changes in the distribution and robustness of bat species harboring coronaviruses may have occurred in eastern Asian hotspots (southern China, Myanmar, and Laos), constituting a driver behind the evolution and spread of the virus. During most of human prehistory groups of hunter-gatherers were probably very small. Such groups probably made contact with other such bands only rarely. Such isolation would have caused epidemic diseases to be restricted to any given local population, because propagation and expansion of epidemics depend on frequent contact with other individuals who have not yet developed an adequate immune response . To persist in such a population, a pathogen either had to be a chronic infection, staying present and potentially infectious in the infected host for long periods, or it had to have other additional species as reservoir where it can maintain itself until further susceptible hosts are contacted and infected. In fact, for many "human" diseases, the human is actually better viewed as an accidental or incidental victim and a dead-end host . Examples include rabies, anthrax, tularemia, and West Nile fever. Thus, much of human exposure to infectious disease has been zoonotic. Many diseases, even epidemic ones, have zoonotic origin and measles , smallpox , influenza , HIV, and diphtheria are particular examples. Various forms of the common cold and tuberculosis also are adaptations of strains originating in other species. [ citation needed ] Some experts have suggested that all human viral infections were originally zoonotic. Zoonoses are of interest because they are often previously unrecognized diseases or have increased virulence in populations lacking immunity. The West Nile virus first appeared in the United States in 1999 , in the New York City area. Bubonic plague is a zoonotic disease, as are salmonellosis , Rocky Mountain spotted fever , and Lyme disease . A major factor contributing to the appearance of new zoonotic pathogens in human populations is increased contact between humans and wildlife. This can be caused either by encroachment of human activity into wilderness areas or by movement of wild animals into areas of human activity. An example of this is the outbreak of Nipah virus in peninsular Malaysia, in 1999, when intensive pig farming began within the habitat of infected fruit bats. The unidentified infection of these pigs amplified the force of infection, transmitting the virus to farmers, and eventually causing 105 human deaths. Similarly, in recent times avian influenza and West Nile virus have spilled over into human populations probably due to interactions between the carrier host and domestic animals. [ citation needed ] Highly mobile animals, such as bats and birds, may present a greater risk of zoonotic transmission than other animals due to the ease with which they can move into areas of human habitation. Because they depend on the human host for part of their life-cycle, diseases such as African schistosomiasis , river blindness , and elephantiasis are not defined as zoonotic, even though they may depend on transmission by insects or other vectors . The first vaccine against smallpox by Edward Jenner in 1800 was by infection of a zoonotic bovine virus which caused a disease called cowpox . Jenner had noticed that milkmaids were resistant to smallpox. Milkmaids contracted a milder version of the disease from infected cows that conferred cross immunity to the human disease. Jenner abstracted an infectious preparation of 'cowpox' and subsequently used it to inoculate persons against smallpox. As a result of vaccination, smallpox has been eradicated globally, and mass inoculation against this disease ceased in 1981. There are a variety of vaccine types, including traditional inactivated pathogen vaccines, subunit vaccines , live attenuated vaccines . There are also new vaccine technologies such as viral vector vaccines and DNA/RNA vaccines , which include many of the COVID-19 vaccines .

Wiki

West Nile

https://api.wikimedia.org/core/v1/wikipedia/en/page/Flaccid_paralysis/html

Flaccid paralysis

Flaccid paralysis is a neurological condition characterized by weakness or paralysis and reduced muscle tone without other obvious cause (e.g., trauma ). This abnormal condition may be caused by disease or by trauma affecting the nerves associated with the involved muscles. For example, if the somatic nerves to a skeletal muscle are severed, then the muscle will exhibit flaccid paralysis. When muscles enter this state, they become limp and cannot contract . This condition can become fatal if it affects the respiratory muscles , posing the threat of suffocation . It also occurs in the spinal shock stage in complete transection of the spinal cord occurring in injuries such as gunshot wounds. The term acute flaccid paralysis (AFP) is often used to describe an instance with a sudden onset, as might be found with polio. AFP is the most common sign of acute polio , and used for surveillance during polio outbreaks. AFP is also associated with a number of other pathogenic agents including enteroviruses other than polio, echoviruses , West Nile virus , and adenoviruses , among others. The Clostridium botulinum bacteria are the cause of botulism . Vegetative cells of C. botulinum may be ingested. Introduction of the bacteria may also occur via endospores in a wound. When the bacteria are in vivo , they induce flaccid paralysis. This happens because C. botulinum produces a toxin that blocks the release of acetylcholine . Botulism toxin blocks the exocytosis of presynaptic vesicles containing acetylcholine (ACh). When this occurs, the muscles are unable to contract. Other symptoms associated with infection from this neurotoxin include double vision, blurred vision, drooping eyelids, slurred speech, difficulty swallowing, dry mouth, and muscle weakness. Botulism prevents muscle contraction by blocking the release of acetylcholine, thereby halting postsynaptic activity of the neuromuscular junction. If its effects reach the respiratory muscles, then it can lead to respiratory failure, leading to death. Curare is a plant poison derived from – among other species – Chondrodendron tomentosum and various species belonging to the genus Strychnos , which are native to the rainforests of South America. Certain peoples indigenous to the region – notably the Macushi – crush and cook the roots and stems of these and certain other plants and then mix the resulting decoction with various other plant poisons and animal venoms to create a syrupy liquid in which to dip their arrow heads and the tips of their blowgun darts. Curare has also been used medicinally by South Americans to treat madness, dropsy, edema, fever, kidney stones, and bruises. Curare acts as a neuromuscular blocking agent that induces flaccid paralysis. This poison binds to the acetylcholine (ACh) receptors on the muscle, blocking them from binding to ACh. As a result, ACh accumulates within the neuromuscular junction, but since ACh cannot bind to the receptors on the muscle, the muscle cannot be stimulated. This poison must enter the bloodstream for it to work. If curare affects the respiratory muscles, then its effects can become life-threatening, placing the victim at risk for suffocation. Flaccid paralysis can be associated with a lower motor neuron lesion . This is in contrast to an upper motor neuron lesion , which often presents with spasticity , although early on this may present with flaccid paralysis. Included in AFP's list are poliomyelitis (polio), transverse myelitis, Guillain–Barré syndrome , enteroviral encephalopathy, traumatic neuritis, Reye's syndrome , etc. An AFP surveillance programme is conducted to increase case yield of poliomyelitis. This includes collection of two stool samples within fourteen days of onset of paralysis and identification of virus, and control of the outbreak and strengthening immunization in that area. [ citation needed ] Historical records from the 1950s, modern CDC reports, and recent analysis of patterns in India suggest that flaccid paralysis may be caused in some cases by oral polio vaccinations. Venomous snakes that contain neurotoxic venom such as kraits , mambas , and cobras can also cause complete flaccid paralysis. Some chemical warfare nerve agents such as VX can also cause complete flaccid paralysis. In some situations, prominently in those of oriental descent hyperthyroidism can affect the consumption and restoration equilibrium of potassium ions in neurons resulting in hypokalaemic paralysis.The term acute flaccid paralysis (AFP) is often used to describe an instance with a sudden onset, as might be found with polio. AFP is the most common sign of acute polio , and used for surveillance during polio outbreaks. AFP is also associated with a number of other pathogenic agents including enteroviruses other than polio, echoviruses , West Nile virus , and adenoviruses , among others. The Clostridium botulinum bacteria are the cause of botulism . Vegetative cells of C. botulinum may be ingested. Introduction of the bacteria may also occur via endospores in a wound. When the bacteria are in vivo , they induce flaccid paralysis. This happens because C. botulinum produces a toxin that blocks the release of acetylcholine . Botulism toxin blocks the exocytosis of presynaptic vesicles containing acetylcholine (ACh). When this occurs, the muscles are unable to contract. Other symptoms associated with infection from this neurotoxin include double vision, blurred vision, drooping eyelids, slurred speech, difficulty swallowing, dry mouth, and muscle weakness. Botulism prevents muscle contraction by blocking the release of acetylcholine, thereby halting postsynaptic activity of the neuromuscular junction. If its effects reach the respiratory muscles, then it can lead to respiratory failure, leading to death. Curare is a plant poison derived from – among other species – Chondrodendron tomentosum and various species belonging to the genus Strychnos , which are native to the rainforests of South America. Certain peoples indigenous to the region – notably the Macushi – crush and cook the roots and stems of these and certain other plants and then mix the resulting decoction with various other plant poisons and animal venoms to create a syrupy liquid in which to dip their arrow heads and the tips of their blowgun darts. Curare has also been used medicinally by South Americans to treat madness, dropsy, edema, fever, kidney stones, and bruises. Curare acts as a neuromuscular blocking agent that induces flaccid paralysis. This poison binds to the acetylcholine (ACh) receptors on the muscle, blocking them from binding to ACh. As a result, ACh accumulates within the neuromuscular junction, but since ACh cannot bind to the receptors on the muscle, the muscle cannot be stimulated. This poison must enter the bloodstream for it to work. If curare affects the respiratory muscles, then its effects can become life-threatening, placing the victim at risk for suffocation. Flaccid paralysis can be associated with a lower motor neuron lesion . This is in contrast to an upper motor neuron lesion , which often presents with spasticity , although early on this may present with flaccid paralysis. Included in AFP's list are poliomyelitis (polio), transverse myelitis, Guillain–Barré syndrome , enteroviral encephalopathy, traumatic neuritis, Reye's syndrome , etc. An AFP surveillance programme is conducted to increase case yield of poliomyelitis. This includes collection of two stool samples within fourteen days of onset of paralysis and identification of virus, and control of the outbreak and strengthening immunization in that area. [ citation needed ] Historical records from the 1950s, modern CDC reports, and recent analysis of patterns in India suggest that flaccid paralysis may be caused in some cases by oral polio vaccinations. Venomous snakes that contain neurotoxic venom such as kraits , mambas , and cobras can also cause complete flaccid paralysis. Some chemical warfare nerve agents such as VX can also cause complete flaccid paralysis. In some situations, prominently in those of oriental descent hyperthyroidism can affect the consumption and restoration equilibrium of potassium ions in neurons resulting in hypokalaemic paralysis.

Wiki

West Nile

https://api.wikimedia.org/core/v1/wikipedia/en/page/W._Ian_Lipkin/html

W. Ian Lipkin

Chronic Disease Infectious Disease Pathogen Discovery Epidemiology Walter Ian Lipkin (born November 18, 1952) is the John Snow Professor of Epidemiology at the Mailman School of Public Health at Columbia University and a professor of Neurology and Pathology at the College of Physicians and Surgeons at Columbia University. He is also director of the Center for Infection and Immunity, an academic laboratory for microbe hunting in acute and chronic diseases. Lipkin is internationally recognized for his work with West Nile virus , SARS and COVID-19 .Lipkin was born in Chicago, Illinois, where he attended the University of Chicago Laboratory School and was president of the student board in 1969. He relocated to New York and earned his BA from Sarah Lawrence College in 1974. At Sarah Lawrence, he "felt that if I went straight into cultural anthropology after college I'd be a parasite. I'd go someplace, take information about myths and ritual, and have nothing to offer. So I decided to become a medical anthropologist and try to bring back traditional medicines. Suddenly I found myself in medical school." Returning to his hometown Chicago, Lipkin earned his MD from Rush Medical College , in 1978. He then became a clinical clerk at the UCL Institute of Neurology in Queen Square, London, on a fellowship, and an intern in Medicine at University of Pittsburgh (1978–1979). He completed a residency in Medicine at University of Washington (1979–1981), and completed a residency in Neurology at University of California, San Francisco (1981–1984). He conducted postdoctoral research in microbiology and neuroscience at The Scripps Research Institute , from 1984 to 1990, under the mentorship of Michael Oldstone and Floyd Bloom . In his six years at Scripps, Lipkin became a senior research associate upon completing his postdoctoral work, and was president of the Scripps' Society of Fellows in 1987.Lipkin has earned the reputation of a "master virus hunter" due to his speed and innovative methods of identifying new viruses, and has been lauded by National Institute of Allergy and Infectious Diseases director Dr. Anthony S. Fauci . As director of the Center for Infection and Immunity at the Mailman School of Public Health; Lipkin, from the onset of the COVID-19 pandemic , has led CII researchers collaborating with researchers at Sun Yat-sen University in China. Dr. Lipkin had also advised the Chinese government and the World Health Organization (WHO) during the 2002–2004 SARS outbreak . Dr. Lipkin described his own infection with the SARS-CoV-2 virus, beginning mid-March 2020, which resulted in a case of COVID-19 and necessitated his recovering from the illness at home, on the podcast This Week in Virology . Lipkin was the Louise Turner Arnold Chair in the Neurosciences at the University of California, Irvine from 1990 to 2001 and was recruited shortly thereafter by Columbia University. He began his current tenure at Columbia as the founding director of the Jerome L. and Dawn Greene Infectious Disease Laboratory from 2002 to 2007, which transitioned to the John Snow Professorship he holds at present. A physician-scientist, Lipkin is internationally recognized for his work with West Nile virus and SARS , as well as advancing pathogen discovery techniques by developing a staged strategy using techniques pioneered in his lab. These molecular biological methods, including MassTag-PCR , the GreeneChip diagnostic, and High Throughput Sequencing, are a major step towards identifying and studying new viral pathogens that emerge locally throughout the globe. A major node in a global network of investigators working to address the challenges of pathogen surveillance and discovery, Dr. Lipkin has trained over 30 internationally based scientists in these state-of-the art diagnostic techniques. Lipkin is the director for the Center for Research in Diagnostics and Discovery, under the National Institutes of Health Centers of Excellence for Translational Research program. The Center for Research brings together leading investigators in microbial and human genetics, engineering, microbial ecology and public health to develop insights into mechanisms of disease and methods for detecting infectious agents, characterizing microflora and identifying biomarkers that can be used to guide clinical management. Lipkin was previously the Director of the Northeast Biodefense Center, the Regional Center of Excellence in Biodefense and Emerging Infectious Diseases which comprised 28 private and public academic and public health institutions in New York, New Jersey and Connecticut. Within this consortium, his research focused on pathogen discovery, using unexplained hemorrhagic fever, febrile illness, encephalitis, and meningoencephalitis as targets. He is the Principal Investigator of the Autism Birth Cohort, a unique international program that investigates the epidemiology and basis of neurodevelopmental disorders through analyses of a prospective birth cohort of 100,000 children and their parents. The ABC is examining gene-environment-timing interactions, biomarkers and the trajectory of normal development and disease. Lipkin also directs the World Health Organization Collaborating Centre for Diagnostics in Zoonotic and Emerging Infectious Diseases, the only academic center, and one of two in the US (the other is CDC), that participates in outbreak investigation for the WHO . Lipkin was co-chair of CDC Steering Committee of the National Biosurveillance Advisory Subcommittee (NBAS). The NBAS was established in response to Homeland Security Presidential Directive 21 (HSPD-21), "Public Health and Medical Preparedness." He is Honorary Director of the Beijing Infectious Disease Center, Chair of the Scientific Advisory Board of the Institut Pasteur de Shanghai and serves on boards of the Australian Biosecurity Cooperative Research Centre for Emerging Infectious Disease, the Guangzhou Institute for Biomedicine and Health, the EcoHealth Alliance , Tetragenetics, and 454 Life Sciences Corporation. Lipkin served as a science consultant for the film Contagion . The film has been praised for its scientific accuracy . While not quite a medical anthropologist, Lipkin specializes in infectious diseases and their neurological impact. His first professional publication came in 1979 during the time of his fellowship in London as a letter to the Editor at the Archives of Internal Medicine (now JAMA Internal Medicine ), where he poses a potential correlation between eosinopenia and bacteremia in diagnostic evaluations for a bacteremic patient. While at UCL, he worked with John Newsom-Davis , who was utilizing plasmapheresis to better understand myasthenia gravis , a neuromuscular disease . In 1981, Lipkin began his neurology residency and worked in a local San Francisco clinic, which was about the time AIDS began to affect the local city population. Because of the social view of homosexual people at the time, very few clinicians would see patients with these symptoms. He "was watching many patients fall ill with AIDS. It took years for scientists to discover the virus responsible for the disease... 'I saw all of this, and I said, 'We have to find new and better ways to do this.'" It was during this epidemic that Lipkin took the approach of looking for a virus' genes instead of looking for antibodies in infected people as a way to speed up the diagnosis process. By the mid-1980s, Lipkin had published two papers specifically about AIDS research and transitioned into utilizing a more pathological approach to virus identification. He identified AIDS-associated immunological abnormalities and inflammatory neuropathy, which he showed could be treated with plasmapheresis and demonstrated early life exposure to viral infections affects neurotransmitter function. In 1989, Lipkin was the first to identify a microbe using purely molecular tools. During his time as Chair at UC Irvine, Lipkin published several papers throughout the decade dissecting and interpreting bornavirus . Once it was apparent the viral infections could selectively alter behavior and steady state brain levels of neurotransmitter mRNAs , the next step was to look for infectious agents which could be used as probes to map anatomic and functional domains in the central nervous system (CNS). By the mid-1990s, it was asserted that "Borna disease is a neurotropic negative-strand RNA virus that infects a wide range of vertebrate hosts," causing "an immune-mediated syndrome resulting in disturbances in movement and behavior." This led to several groups across the globe working to determine if there was a link between Borna disease virus (BDV) or a related agent and human neuropsychiatric disease. The group was formally called Microbiology and Immunology of Neuropsychiatric Disorders (MIND) and the multicenter, multi-national group focused on using standardized methods for clinical diagnosis and blinded laboratory assessment of BDV infection. After nearly two decades of inquiry, the first blinded case-controlled study of the link between BDV and psychiatric illness was completed by the researchers at Columbia University's Center for Infection and Immunity in a joint effort that concluded there is no association between the two. Lipkin noted that "it was concern over the potential role of BDV in mental illness and the inability to identify it using classical techniques that led us to develop molecular methods for pathogen discovery. Ultimately these new techniques enabled us to refute a role for BDV in human disease. But the fact remains that we gained strategies for the discovery of hundreds of other pathogens that have important implications for medicine, agriculture, and environmental health." In 1999, West Nile virus was reported in two patients in Flushing Hospital Medical Center in Queens, New York. Lipkin led the team identifying West Nile virus in brain tissue of encephalitis victims in New York State. It was determined potential routes for the spread of West Nile virus throughout New York (and the Eastern United States) originated from predominantly mosquitoes, but also possible from infected birds or human beings. There is a high likelihood the two international airports nearby the initial reported cases were also the initial points of entry into the United States. During the five years after the first reported case, Lipkin worked on a study with the National Institutes of Health (NIH) and the Wadsworth Center at the New York State Department of Health to determine how a vaccine could be developed. While they had some success with the immunization of mice with particles resembling the structural protein prME of West Nile Virus, as of 2018, there is still no human vaccine for West Nile Virus. Chinese scientists first discovered the severe acute respiratory syndrome (SARS) coronavirus in February 2003, but due to initial misinterpretation of the data, the information of the correct agent associated with SARS was suppressed and the outbreak investigation had a delayed start. Advanced hospital facilities were at the greatest risk as they were most susceptible to virus transmission, so it was the "classical gumshoe epidemiology" of "contact tracing and isolation" that brought swift action against the epidemic . Lipkin was requested to assist with the investigation by Chen Zhou, vice president of the Chinese Academy of Sciences and Xu Guanhua, minister of the Ministry of Science and Technology in China to "assess the state of the epidemic, identify the gaps in science, and develop a strategy for containing the virus and reducing morbidity and mortality." This brought the development of real-time polymerase chain reaction technology, which essentially allowed for the detection of infection at earlier time points as the process, in this instance, targets the N gene sequence and amplify the analysis in a closed system. This markedly reduces the risk of contamination during processing. Test kits were developed with this PCR-based assay analysis and 10,000 were hand-delivered to Beijing during the height of the outbreak by Lipkin, whereupon he trained local clinical microbiologists on the proper usage. He became ill upon his return to the U.S. and was quarantined. Lipkin was asked to join the Defense Science Board Task Force on SARS Quarantine Guidance during the height of the SARS outbreak between 2003 and 2004, to advise the U.S. Department of Defense on steps to domestically manage the epidemic. As part of the EcoHealth Alliance, Lipkin's center worked in conjunction with an NIH / NIAID grant assessing bats as the reservoir for the SARS virus. 47 publications resulted from this grant, which also included assessment on Nipah , Hendra , Ebola , and Marburg viruses. This proved to be significant research on the overall study of viral reservoirs as it was determined that bats carry coronaviruses and either directly infect humans with an exchange of bodily fluid (such as a bite) or indirectly by infecting an intermediate host, such as swine. Lipkin addressed a health forum in Guangzhou in January 2004 where China Daily reported him as saying: "SARS virus is probably rooted and spread by rats." In 2016, the Chinese government awarded him the International Science and Technology Cooperation Award, the nation's top science honor for foreign scientists, and in January 2020, it awarded him a medal marking the People's Republic of China's 70th Anniversary, both awards for his work during the 2002–2004 SARS outbreak and in strengthening China's public health system. Middle East respiratory syndrome (MERS) was first reported in Saudi Arabia during June 2012 when a local man was initially diagnosed with acute pneumonia and later died of kidney failure . The early reports of the disease were similar to SARS as the symptoms are similar, but it was quickly determined these cases were caused by a new strain called MERS coronavirus (MERS-CoV). Given Lipkin's expertise with the SARS outbreak in China nearly ten years prior, the Saudi Arabian Ministry of Health granted Lipkin and his lab local access to animal samples related to the initial reported cases. With the rare opportunity, Lipkin's team created a mobile lab able to fit in six pieces of personal luggage and was transported from New York to Saudi Arabia via commercial flight to complete the analysis of samples. It seemed unlikely that bats were directly infecting humans, as the direct physical interaction between the two is limited at best. A study was completed in more local proximity, examining the diverse bat populations in southeastern Mexico and determining how diverse the viruses they carry could be. However, it became apparent that dromedary camels were the intermediary in the transmission between bats and humans, since camel milk and meat are dietary staples in the Saudi Arabian region. The instances of human-to-human transmission appeared to be isolated to case-patients and anyone in close direct contact with them, as opposed to a broad open-air transmission. By 2017, it was determined that bats are most likely the evolutionary original source for MERS-CoV along with several other coronaviruses, though not all of those types of zoonotic viruses are direct threats to humans like MERS-CoV and "[c]ollectively, these examples demonstrate that the MERS-related coronaviruses are high associated with bats and are geographically widespread." Myalgic encephalomyelitis/chronic fatigue syndrome ( ME/CFS ) is a chronic condition characterized by extreme fatigue after exertion that is not relieved by rest and includes other symptoms, such as muscle and joint pain and cognitive dysfunction. In September 2017, the NIH awarded a $9.6 million grant to Columbia University for the "CfS for ME/CFS" intended for the pursuit of basic research and the development of tools to help both physicians and patients effectively monitor the course of the illness. This collaboration effort led by Lipkin includes other institutions, such as the Bateman Horne Center (Lucinda Bateman), Harvard University ( Anthony L. Komaroff ), Stanford University (Kegan Moneghetti), Sierra Internal Medicine ( Daniel Peterson ), University of California, Davis (Oliver Fiehn), and Albert Einstein College of Medicine (John Greally), along with private clinicians in New York City. The team of researchers and clinicians initially collaborated to de-link xenotropic murine leukemia virus-related virus (XMRV) to ME/CFS after the NIH requested research into the conflicting reports between XMRV and ME/CFS. The group "consolidated its vision with support from the Hutchins Family Foundation Chronic Fatigue Initiative and a crowd-funding organization, The Microbe Discovery Project, to explore the role of infection and immunity in disease and identify biomarkers for diagnosis through functional genomic , proteomic , and metabolomic discovery." The project will collect a large clinical database and sample repository representing oral, fecal, and blood samples from well-characterized ME/CFS subjects and frequency-matched controls collected nationwide over a period of several years. Additionally, researchers are working with ME/CFS community and advocacy groups as the project progresses. Acute flaccid myelitis (AFM) is a serious condition of the spinal cord with symptoms including rapid onset of arm or leg weakness, decreased reflexes, difficulty moving the eyes, speaking, or swallowing may also occur. Occasionally numbness or pain may be present and complications can include trouble breathing. In August 2019, Lipkin and Dr. Nischay Mishra published a collaborative study with the CDC in analyzing serological data for serum and cerebrospinal fluid (CSF) samples of AFM patients. The Lipkin team utilized high-density peptide arrays (also known as Serochips) to identify antibodies to EV-D68 in those samples. The technology was featured on the Dr. Oz Show in mid-September, illustrating how the enterovirus affects the CSF and the actual Serochip used to do the analysis. In October, the University of California, San Francisco published a separate collaborative study with the CDC that confirmed the presence of antibodies to enterovirus in AFM patient CSF samples using phage display (VirScan). "It's always good to see reproducibility. It gives more confidence in the findings for sure," commented Lipkin in an October 2019 CNN article. "This gives us more support of what we found." According to the Financial Times , Lipkin first learnt of COVID-19 from contacts in China, where it first emerged, in mid-December. In early January he repeatedly urged his Chinese counterparts to publish the virus's genetic sequencing to aid research, and visited senior Chinese officials, including Premier Li Keqiang , to discuss the disease. Lipkin described his engagement with the early COVID-19 investigations during an April 2023 interview with the U.S. House of Representatives Select Committee on the Coronavirus Pandemic . On January 29, 2020, Lipkin flew into Guangzhou , China to learn about the outbreak of SARS-CoV-2 . Lipkin met with the epidemiologist and pulmonologist Zhong Nanshan , the lead advisor to the Chinese government during the outbreak. Lipkin also worked with the China CDC to access blood samples from across the country for further study into the origin and spread of the virus. Lipkin did not travel to Wuhan , the epicenter of the outbreak, due to fears that this would prevent him from returning to the United States. On returning to the United States, Lipkin self-quarantined for 14 days. Lipkin later contracted SARS-CoV-2 in New York City, refusing to go to hospital and treating himself with hydroxychloroquine at home. Lipkin criticized what he considered a xenophobic response that blames China for the virus, specifically the words of US president Donald Trump calling it the "China virus" and his decision to suspend funding to the World Health Organization for being "China-centric", calling for "global problems" to be addressed by "global solutions". He said that a series of government missteps helped spread the virus around the world very rapidly, and criticized the US and UK's responses, calling them slow, and blamed insufficient and inadequate testing and tracing for rising fatality numbers. In the US, he singled out as an issue what he saw as an inconsistency in advice, including by president Trump, and highlighted the need for national leadership, while acknowledging states had the ability to make decisions in certain areas. He praised his NIAID superior Anthony Fauci for his integrity. He also warned about the danger of future emergence of new deadly viruses. After his trip to China, Lipkin maintained links with Lu Jiahai, his research partner at Sun Yat-sen University in Guangzhou , and Zhong Nanshan, to try to establish the origins of the virus. Their efforts, aimed at finding out whether the virus emerged in other parts of China and circulated before it was first discovered in Wuhan in December, include antibody tests of nationwide blood bank samples from pneumonia patients which predate the pandemic, which led to a collaboration with the Chinese Centers for Disease Control and Prevention. According to Lipkin, this research began in early February. The international research team also began studying blood samples from different wild animals which it deemed potential origins of the virus, in order to understand animal-to-human transmission. Lipkin thinks the virus could have originated in the wild animal trade and undergone "repeated jumps" from animal to human in the weeks before the first cases were logged, such a stream of events having recent precedents in the emergence of MERS-CoV, which jumped from dromedary camels to humans in 2012, and SARS-CoV, from civet cats to humans in 2003. Lipkin co-authored a paper on "The proximal origin of SARS-CoV-2", which was published in Nature Medicine in March 2020. The conclusion of the genomic analyses was that COVID-19 was not a case of lab leak or human-made infection. In 2023, the paper was alleged by the US Republicans as a coverup based on certain misconducts to eliminate the lab leak theory . The paper and the controversy became known as the " Proximal Origin ". While not quite a medical anthropologist, Lipkin specializes in infectious diseases and their neurological impact. His first professional publication came in 1979 during the time of his fellowship in London as a letter to the Editor at the Archives of Internal Medicine (now JAMA Internal Medicine ), where he poses a potential correlation between eosinopenia and bacteremia in diagnostic evaluations for a bacteremic patient. While at UCL, he worked with John Newsom-Davis , who was utilizing plasmapheresis to better understand myasthenia gravis , a neuromuscular disease . In 1981, Lipkin began his neurology residency and worked in a local San Francisco clinic, which was about the time AIDS began to affect the local city population. Because of the social view of homosexual people at the time, very few clinicians would see patients with these symptoms. He "was watching many patients fall ill with AIDS. It took years for scientists to discover the virus responsible for the disease... 'I saw all of this, and I said, 'We have to find new and better ways to do this.'" It was during this epidemic that Lipkin took the approach of looking for a virus' genes instead of looking for antibodies in infected people as a way to speed up the diagnosis process. By the mid-1980s, Lipkin had published two papers specifically about AIDS research and transitioned into utilizing a more pathological approach to virus identification. He identified AIDS-associated immunological abnormalities and inflammatory neuropathy, which he showed could be treated with plasmapheresis and demonstrated early life exposure to viral infections affects neurotransmitter function.In 1989, Lipkin was the first to identify a microbe using purely molecular tools. During his time as Chair at UC Irvine, Lipkin published several papers throughout the decade dissecting and interpreting bornavirus . Once it was apparent the viral infections could selectively alter behavior and steady state brain levels of neurotransmitter mRNAs , the next step was to look for infectious agents which could be used as probes to map anatomic and functional domains in the central nervous system (CNS). By the mid-1990s, it was asserted that "Borna disease is a neurotropic negative-strand RNA virus that infects a wide range of vertebrate hosts," causing "an immune-mediated syndrome resulting in disturbances in movement and behavior." This led to several groups across the globe working to determine if there was a link between Borna disease virus (BDV) or a related agent and human neuropsychiatric disease. The group was formally called Microbiology and Immunology of Neuropsychiatric Disorders (MIND) and the multicenter, multi-national group focused on using standardized methods for clinical diagnosis and blinded laboratory assessment of BDV infection. After nearly two decades of inquiry, the first blinded case-controlled study of the link between BDV and psychiatric illness was completed by the researchers at Columbia University's Center for Infection and Immunity in a joint effort that concluded there is no association between the two. Lipkin noted that "it was concern over the potential role of BDV in mental illness and the inability to identify it using classical techniques that led us to develop molecular methods for pathogen discovery. Ultimately these new techniques enabled us to refute a role for BDV in human disease. But the fact remains that we gained strategies for the discovery of hundreds of other pathogens that have important implications for medicine, agriculture, and environmental health." In 1999, West Nile virus was reported in two patients in Flushing Hospital Medical Center in Queens, New York. Lipkin led the team identifying West Nile virus in brain tissue of encephalitis victims in New York State. It was determined potential routes for the spread of West Nile virus throughout New York (and the Eastern United States) originated from predominantly mosquitoes, but also possible from infected birds or human beings. There is a high likelihood the two international airports nearby the initial reported cases were also the initial points of entry into the United States. During the five years after the first reported case, Lipkin worked on a study with the National Institutes of Health (NIH) and the Wadsworth Center at the New York State Department of Health to determine how a vaccine could be developed. While they had some success with the immunization of mice with particles resembling the structural protein prME of West Nile Virus, as of 2018, there is still no human vaccine for West Nile Virus. Chinese scientists first discovered the severe acute respiratory syndrome (SARS) coronavirus in February 2003, but due to initial misinterpretation of the data, the information of the correct agent associated with SARS was suppressed and the outbreak investigation had a delayed start. Advanced hospital facilities were at the greatest risk as they were most susceptible to virus transmission, so it was the "classical gumshoe epidemiology" of "contact tracing and isolation" that brought swift action against the epidemic . Lipkin was requested to assist with the investigation by Chen Zhou, vice president of the Chinese Academy of Sciences and Xu Guanhua, minister of the Ministry of Science and Technology in China to "assess the state of the epidemic, identify the gaps in science, and develop a strategy for containing the virus and reducing morbidity and mortality." This brought the development of real-time polymerase chain reaction technology, which essentially allowed for the detection of infection at earlier time points as the process, in this instance, targets the N gene sequence and amplify the analysis in a closed system. This markedly reduces the risk of contamination during processing. Test kits were developed with this PCR-based assay analysis and 10,000 were hand-delivered to Beijing during the height of the outbreak by Lipkin, whereupon he trained local clinical microbiologists on the proper usage. He became ill upon his return to the U.S. and was quarantined. Lipkin was asked to join the Defense Science Board Task Force on SARS Quarantine Guidance during the height of the SARS outbreak between 2003 and 2004, to advise the U.S. Department of Defense on steps to domestically manage the epidemic. As part of the EcoHealth Alliance, Lipkin's center worked in conjunction with an NIH / NIAID grant assessing bats as the reservoir for the SARS virus. 47 publications resulted from this grant, which also included assessment on Nipah , Hendra , Ebola , and Marburg viruses. This proved to be significant research on the overall study of viral reservoirs as it was determined that bats carry coronaviruses and either directly infect humans with an exchange of bodily fluid (such as a bite) or indirectly by infecting an intermediate host, such as swine. Lipkin addressed a health forum in Guangzhou in January 2004 where China Daily reported him as saying: "SARS virus is probably rooted and spread by rats." In 2016, the Chinese government awarded him the International Science and Technology Cooperation Award, the nation's top science honor for foreign scientists, and in January 2020, it awarded him a medal marking the People's Republic of China's 70th Anniversary, both awards for his work during the 2002–2004 SARS outbreak and in strengthening China's public health system. Middle East respiratory syndrome (MERS) was first reported in Saudi Arabia during June 2012 when a local man was initially diagnosed with acute pneumonia and later died of kidney failure . The early reports of the disease were similar to SARS as the symptoms are similar, but it was quickly determined these cases were caused by a new strain called MERS coronavirus (MERS-CoV). Given Lipkin's expertise with the SARS outbreak in China nearly ten years prior, the Saudi Arabian Ministry of Health granted Lipkin and his lab local access to animal samples related to the initial reported cases. With the rare opportunity, Lipkin's team created a mobile lab able to fit in six pieces of personal luggage and was transported from New York to Saudi Arabia via commercial flight to complete the analysis of samples. It seemed unlikely that bats were directly infecting humans, as the direct physical interaction between the two is limited at best. A study was completed in more local proximity, examining the diverse bat populations in southeastern Mexico and determining how diverse the viruses they carry could be. However, it became apparent that dromedary camels were the intermediary in the transmission between bats and humans, since camel milk and meat are dietary staples in the Saudi Arabian region. The instances of human-to-human transmission appeared to be isolated to case-patients and anyone in close direct contact with them, as opposed to a broad open-air transmission. By 2017, it was determined that bats are most likely the evolutionary original source for MERS-CoV along with several other coronaviruses, though not all of those types of zoonotic viruses are direct threats to humans like MERS-CoV and "[c]ollectively, these examples demonstrate that the MERS-related coronaviruses are high associated with bats and are geographically widespread." Myalgic encephalomyelitis/chronic fatigue syndrome ( ME/CFS ) is a chronic condition characterized by extreme fatigue after exertion that is not relieved by rest and includes other symptoms, such as muscle and joint pain and cognitive dysfunction. In September 2017, the NIH awarded a $9.6 million grant to Columbia University for the "CfS for ME/CFS" intended for the pursuit of basic research and the development of tools to help both physicians and patients effectively monitor the course of the illness. This collaboration effort led by Lipkin includes other institutions, such as the Bateman Horne Center (Lucinda Bateman), Harvard University ( Anthony L. Komaroff ), Stanford University (Kegan Moneghetti), Sierra Internal Medicine ( Daniel Peterson ), University of California, Davis (Oliver Fiehn), and Albert Einstein College of Medicine (John Greally), along with private clinicians in New York City. The team of researchers and clinicians initially collaborated to de-link xenotropic murine leukemia virus-related virus (XMRV) to ME/CFS after the NIH requested research into the conflicting reports between XMRV and ME/CFS. The group "consolidated its vision with support from the Hutchins Family Foundation Chronic Fatigue Initiative and a crowd-funding organization, The Microbe Discovery Project, to explore the role of infection and immunity in disease and identify biomarkers for diagnosis through functional genomic , proteomic , and metabolomic discovery." The project will collect a large clinical database and sample repository representing oral, fecal, and blood samples from well-characterized ME/CFS subjects and frequency-matched controls collected nationwide over a period of several years. Additionally, researchers are working with ME/CFS community and advocacy groups as the project progresses. Acute flaccid myelitis (AFM) is a serious condition of the spinal cord with symptoms including rapid onset of arm or leg weakness, decreased reflexes, difficulty moving the eyes, speaking, or swallowing may also occur. Occasionally numbness or pain may be present and complications can include trouble breathing. In August 2019, Lipkin and Dr. Nischay Mishra published a collaborative study with the CDC in analyzing serological data for serum and cerebrospinal fluid (CSF) samples of AFM patients. The Lipkin team utilized high-density peptide arrays (also known as Serochips) to identify antibodies to EV-D68 in those samples. The technology was featured on the Dr. Oz Show in mid-September, illustrating how the enterovirus affects the CSF and the actual Serochip used to do the analysis. In October, the University of California, San Francisco published a separate collaborative study with the CDC that confirmed the presence of antibodies to enterovirus in AFM patient CSF samples using phage display (VirScan). "It's always good to see reproducibility. It gives more confidence in the findings for sure," commented Lipkin in an October 2019 CNN article. "This gives us more support of what we found." According to the Financial Times , Lipkin first learnt of COVID-19 from contacts in China, where it first emerged, in mid-December. In early January he repeatedly urged his Chinese counterparts to publish the virus's genetic sequencing to aid research, and visited senior Chinese officials, including Premier Li Keqiang , to discuss the disease. Lipkin described his engagement with the early COVID-19 investigations during an April 2023 interview with the U.S. House of Representatives Select Committee on the Coronavirus Pandemic . On January 29, 2020, Lipkin flew into Guangzhou , China to learn about the outbreak of SARS-CoV-2 . Lipkin met with the epidemiologist and pulmonologist Zhong Nanshan , the lead advisor to the Chinese government during the outbreak. Lipkin also worked with the China CDC to access blood samples from across the country for further study into the origin and spread of the virus. Lipkin did not travel to Wuhan , the epicenter of the outbreak, due to fears that this would prevent him from returning to the United States. On returning to the United States, Lipkin self-quarantined for 14 days. Lipkin later contracted SARS-CoV-2 in New York City, refusing to go to hospital and treating himself with hydroxychloroquine at home. Lipkin criticized what he considered a xenophobic response that blames China for the virus, specifically the words of US president Donald Trump calling it the "China virus" and his decision to suspend funding to the World Health Organization for being "China-centric", calling for "global problems" to be addressed by "global solutions". He said that a series of government missteps helped spread the virus around the world very rapidly, and criticized the US and UK's responses, calling them slow, and blamed insufficient and inadequate testing and tracing for rising fatality numbers. In the US, he singled out as an issue what he saw as an inconsistency in advice, including by president Trump, and highlighted the need for national leadership, while acknowledging states had the ability to make decisions in certain areas. He praised his NIAID superior Anthony Fauci for his integrity. He also warned about the danger of future emergence of new deadly viruses. After his trip to China, Lipkin maintained links with Lu Jiahai, his research partner at Sun Yat-sen University in Guangzhou , and Zhong Nanshan, to try to establish the origins of the virus. Their efforts, aimed at finding out whether the virus emerged in other parts of China and circulated before it was first discovered in Wuhan in December, include antibody tests of nationwide blood bank samples from pneumonia patients which predate the pandemic, which led to a collaboration with the Chinese Centers for Disease Control and Prevention. According to Lipkin, this research began in early February. The international research team also began studying blood samples from different wild animals which it deemed potential origins of the virus, in order to understand animal-to-human transmission. Lipkin thinks the virus could have originated in the wild animal trade and undergone "repeated jumps" from animal to human in the weeks before the first cases were logged, such a stream of events having recent precedents in the emergence of MERS-CoV, which jumped from dromedary camels to humans in 2012, and SARS-CoV, from civet cats to humans in 2003. Lipkin co-authored a paper on "The proximal origin of SARS-CoV-2", which was published in Nature Medicine in March 2020. The conclusion of the genomic analyses was that COVID-19 was not a case of lab leak or human-made infection. In 2023, the paper was alleged by the US Republicans as a coverup based on certain misconducts to eliminate the lab leak theory . The paper and the controversy became known as the " Proximal Origin ". Gain-of-function experiments aim to increase the virulence and/or transmissibility of pathogens, in order to better understand them and inform public health preparedness efforts. This includes targeted genetic modification (to create hybrid viruses), the serial passaging of a virus through a host animal (to generate adaptive mutations), and targeted mutagenesis (to introduce mutations). Lipkin is a listed "supporter" of the gain-of-function advocate group, Scientists for Science , which was co-founded by Columbia colleague Vincent Racaniello. The US National Institutes of Health placed a moratorium on gain-of-function research in October 2014, and lifted the moratorium in December 2017, after the implementation of stricter controls. Lipkin, while not endorsing every gain-of-function experiment, has said that "[t]here clearly are going to be instances where gain-of-function research is necessary and appropriate." In the example of Ebola, which is incapable of airborne transfer, Lipkin believes that "researchers could make a case for the need to determine how the virus could evolve in nature by engineering a more dangerous version in the lab." Lipkin believes that there should be guidelines in place to govern gain-of-function experiments. Lipkin has called for the World Health Organization to establish strict biocontainment criteria that can be applied globally – including in the developing world – to gain-of-function research.

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Lisa Whelchel

Lisa Diane Whelchel (born May 29, 1963) is an American actress, singer, songwriter, author, and life coach. She is known for her appearances as a Mouseketeer on The New Mickey Mouse Club and her nine-year role as the preppy and wealthy Blair Warner on The Facts of Life . In 1984, she was nominated for a Grammy Award for Best Inspirational Performance for her contemporary Christian album All Because of You . In 2012, Whelchel participated as a contestant on the CBS competitive reality series Survivor: Philippines and tied for second place. She was also voted fan favorite and was awarded $100,000. Lisa Whelchel was born on May 29, 1963, in Littlefield, Texas . She is the daughter of Virginia "Genny" (née French), a real estate agent, and James "Jimmy" Whelchel Sr., an electrician. Her parents divorced in 1981, and her mother married Roy Coleman in 1983. Lisa is the elder sister of James "Cody" Whelchel Jr., and the elder half-sister of Casey Justice Coleman. She also has a nephew, Chasin (Cody's son). Lisa and Cody were raised for most of their childhood in Fort Worth, Texas , and she was in the class of 1980.At age 13, Whelchel was recruited in Texas by talent scouts who were looking for children interested in working with Disney Studios as a Mouseketeer on The New Mickey Mouse Club . She moved to California the next year and appeared on the show in syndication from 1977 to 1978. Whelchel is probably best known for being a main cast member of The Facts of Life where she portrayed Blair Warner , an uptight prep student. She also played the character on Diff'rent Strokes , the show from which The Facts of Life spun off. Whelchel once refused a storyline that would have made her character the first among the four main young women on the show to lose her virginity. Having become a Christian when she was ten years old, Whelchel declined due to her religious beliefs, and the storyline was rewritten for the character of Natalie, portrayed by Mindy Cohn . This was the only episode of the series in which Whelchel did not appear. In 2001, Whelchel reprised her role as Blair Warner for the made-for-television movie, The Facts of Life Reunion . On March 7, 2004, Whelchel was reunited with Charlotte Rae to perform The Facts of Life theme song at the 2nd Annual TV Land Awards at the Hollywood Palladium in Hollywood. In spring 2006, she appeared with two of her Facts of Life co-stars on The Today Show to promote the show's DVD releases of the first and second seasons, admitting to being "really bummed out" that Kim Fields was unable to attend. On February 1, 2007, Whelchel was reunited with Fields on WFAA-TV 's Good Morning Texas . Fields was in Dallas to promote her appearance in the production Issues: We've All Got 'Em ' , when Whelchel was introduced as a surprise guest. On April 10, 2011, Whelchel and the cast of The Facts of Life , including Charlotte Rae, Nancy McKeon , Mindy Cohn, Kim Fields, Geri Jewell , and Cloris Leachman were honored with the Pop Culture Award at the 9th Annual TV Land Awards at the Javits Center in New York City. In 2021, Whelchel, Fields, and Cohn reunited again on the set of Live in Front of a Studio Audience ' s reenactment of the show's third season episode "Kids Can Be Cruel". Whelchel also sang the show's theme song that evening. At age 13, Whelchel was recruited in Texas by talent scouts who were looking for children interested in working with Disney Studios as a Mouseketeer on The New Mickey Mouse Club . She moved to California the next year and appeared on the show in syndication from 1977 to 1978.Whelchel is probably best known for being a main cast member of The Facts of Life where she portrayed Blair Warner , an uptight prep student. She also played the character on Diff'rent Strokes , the show from which The Facts of Life spun off. Whelchel once refused a storyline that would have made her character the first among the four main young women on the show to lose her virginity. Having become a Christian when she was ten years old, Whelchel declined due to her religious beliefs, and the storyline was rewritten for the character of Natalie, portrayed by Mindy Cohn . This was the only episode of the series in which Whelchel did not appear. In 2001, Whelchel reprised her role as Blair Warner for the made-for-television movie, The Facts of Life Reunion . On March 7, 2004, Whelchel was reunited with Charlotte Rae to perform The Facts of Life theme song at the 2nd Annual TV Land Awards at the Hollywood Palladium in Hollywood. In spring 2006, she appeared with two of her Facts of Life co-stars on The Today Show to promote the show's DVD releases of the first and second seasons, admitting to being "really bummed out" that Kim Fields was unable to attend. On February 1, 2007, Whelchel was reunited with Fields on WFAA-TV 's Good Morning Texas . Fields was in Dallas to promote her appearance in the production Issues: We've All Got 'Em ' , when Whelchel was introduced as a surprise guest. On April 10, 2011, Whelchel and the cast of The Facts of Life , including Charlotte Rae, Nancy McKeon , Mindy Cohn, Kim Fields, Geri Jewell , and Cloris Leachman were honored with the Pop Culture Award at the 9th Annual TV Land Awards at the Javits Center in New York City. In 2021, Whelchel, Fields, and Cohn reunited again on the set of Live in Front of a Studio Audience ' s reenactment of the show's third season episode "Kids Can Be Cruel". Whelchel also sang the show's theme song that evening. In 1984, Whelchel released a Christian pop album entitled All Because of You . The album reached No. 17 on the Billboard Contemporary Christian music charts. She was nominated for a Grammy Award for Best Inspirational Performance and was recognized as the writer of the title song, "All Because of You". Among the songs featured on the album were "All Because of You", "Just Obey", "Cover Me Lord", and "Good Girl". She did not record a second album. While she was appearing on The Facts of Life , she made a cameo appearance in the music video for contemporary Christian music singer-songwriter Steve Taylor 's song "Meltdown (at Madame Tussaud's)". The song was the title track from the album Meltdown .For years, Whelchel was a regular inspirational speaker at churches and conferences nationwide. In 2000, she founded Momtime Ministries, a religious network of mothers' groups who met weekly to "equip and refresh and encourage" each other. In 2021, Whelchel appeared on friend and The Facts of Life co-star Mindy Cohn's podcast, Mondays with Mindy , on which she talked about how her faith has changed and evolved over time. She explained that her speaking commitments have shifted over the years, as she no longer operates from a "fear-based, punishment-based" mentality. She explained, "Jesus came, ultimately, to bring grace. I can speak that message in any situation, but a lot of churches — when they find out that I believe that there are many ways to experience God, not just Jesus, then the invitations kind of dry up." Whelchel has written ten books on motherhood, child discipline, adult friendships, homeschooling, and finding Jesus through the development of holiday traditions. Additional topics from a spiritual point of view include prayer and wisdom. She is the bestselling author of So You're Thinking About Homeschooling and The Facts of Life (and Other Lessons My Father Taught Me) .On August 20, 2012, Whelchel was announced as a contestant in Survivor: Philippines as a member of the Tandang tribe. She joined retired Major League Baseball star Jeff Kent as one of the season's two "celebrity" contestants. A former television star, she elected to keep her true identity a secret from the other contestants, many of whom were too young to have watched The Facts of Life during its original run and thus did not recognize her. Michael Skupin and Jonathan Penner , who were around Whelchel's age, as well as eventual winner Denise Stapley , were the only ones to recognize her as "Blair Warner". On November 14, 2012, Whelchel announced via her Twitter account that she was suffering from West Nile fever and had been advised by her doctor that recovery would take approximately one year. She did not specify whether she had contracted the arbovirus while in the Philippines shooting Survivor . On December 16, 2012, Whelchel made it to the Final Tribal Council, where fellow contestant and jury member Jonathan Penner revealed to the rest of the jury that she was a former child star. In the end, she received one jury vote from RC Saint-Amour and tied with returning contestant Michael Skupin for runner-up, both losing to eventual winner Denise Stapley. She was also voted the Sprint Player of the Season, winning $100,000 by a margin of about .7 percent against Malcolm Freberg.On January 14, 2013, Whelchel co-hosted several episodes of The Jeff Probst Show with Survivor host, Jeff Probst. In April 2019, Whelchel hosted a The Facts of Life marathon on the MeTV television network, as a lead-in for a preview of her series Collector's Call that debuted later that year and is in Season 4 as of 2024 On July 9, 1988, Whelchel married Steven Cauble, who was an associate pastor at The Church on the Way in Van Nuys, California , which Whelchel attended at the time. The couple, who have three adult children, divorced in March 2012. In 2019, Whelchel married Pete Harris, who is a psychologist based in Nashville, Tennessee.

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West Nile

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House finch

Burrica mexicana Carpodacus mexicanus The House finch ( Haemorhous mexicanus ) is a North American bird in the finch family . It is native to Mexico and southwestern United States , but has since been introduced to the eastern part of North America and Hawaii; it is now found year-round in all parts of the United States and most of Mexico, with some residing near the border of Canada . There are estimated to be 40 million house finches across North America, making it the second-most populous finch, just behind the American goldfinch . The house finch and the other two American rosefinches are placed in the genus Haemorhous .The house finch is a moderate-sized finch , 12.5 to 15 cm (5 to 6 in) long, with a wingspan of 20 to 25 cm (8 to 10 in) . Body mass can vary from 16 to 27 g ( 9 ⁄ 16 to 15 ⁄ 16 oz) , with an average weight of 21 g ( 3 ⁄ 4 oz) . Among standard measurements, the wing chord is 7 to 8.4 cm ( 2 + 3 ⁄ 4 to 3 + 1 ⁄ 4 in) , the tail is 5.7 to 6.5 cm ( 2 + 1 ⁄ 4 to 2 + 1 ⁄ 2 in) , the culmen is 0.9 to 1.1 cm ( 3 ⁄ 8 to 7 ⁄ 16 in) and the tarsus is 1.6 to 1.8 cm ( 5 ⁄ 8 to 11 ⁄ 16 in) . Adults have a long, square-tipped brown tail and are a brown or dull-brown color across the back with some shading into deep gray on the wing feathers. Breast and belly feathers may be streaked; the flanks usually are. In most cases, adult males' heads, necks and shoulders are reddish. This color sometimes extends to the belly and down the back, between the wings. Male coloration varies in intensity with the seasons and is derived from the berries and fruits in its diet. As a result, the colors range from pale straw-yellow through bright orange (both rare) to deep, intense red. Adult females have brown upperparts and streaked underparts. The house finch's songs typically consist of a series of high-pitched musical jumbles ending with a distinct high note, wheer. Calls from flight include a soft cheet or wheat , with perched birds giving a more drawn-out version. House finches are mainly permanent residents throughout their range, some birds migrate to the south, with adult females moving longer distances than males. Their breeding habitat is urban and suburban areas across North America, as well as various semi-open areas in the west from southern Canada to the Mexican state of Oaxaca ; the population in central Chiapas may be descended from escaped cagebirds. Analyses of nest records from house finches in California spanning more than a century found that egg‐laying occurred significantly earlier in warmer springs. Originally only a resident of Mexico and the southwestern United States , house finches were introduced to eastern North America in the 1940s. The birds were sold illegally in New York City as "Hollywood Finches", a marketing artifice. To avoid prosecution under the Migratory Bird Treaty Act of 1918 , vendors and owners released the birds. They have since become naturalized; in largely unforested land across the eastern U.S. they have displaced the native purple finch and even the non-native house sparrow . Sometime in the 19th century, they were introduced to Hawaii and are now abundant on all its major islands. According to the Partners in Flight database, there are estimated to be 40 million house finches across North America . Instances of naturalization originating in escapes or releases of cage birds have been recorded in Europe, such as in 2020 in Murcia , (Spain). House finches forage on the ground or in vegetation normally. They primarily eat grains , seeds and berries , being voracious consumers of weed seeds such as nettle and dandelion ; included are incidental small insects such as aphids . They are frequent visitors to bird feeders throughout the year, particularly if stocked with sunflower or nyjer seed, and will congregate at hanging nyjer sock feeders. The house finch is known to damage orchard fruit and consume commercially grown grain, but is generally considered an annoyance rather than a significant pest. Nests are made in cavities , including openings in buildings, hanging plants, and other cup-shaped outdoor decorations. Sometimes nests abandoned by other birds are used. Nests may be re-used for subsequent broods or in following years. The nest is built by the female, sometimes in as little as two days. It is well made of twigs and debris, forming a cup shape, usually 1.8 to 2.7 m (5 ft 11 in to 8 ft 10 in) above the ground. During courtship, the male will touch bills with the female. He may then present the female with choice bits of food, and if she mimics the behavior of a hungry chick, he may feed her. The male also feeds the female during breeding and incubation of the eggs, and raising of the young, and the male is the primary feeder of the fledglings (who can be differentiated from the females by the pin feathers remaining on their heads). Females are typically attracted to the males with the deepest pigment of red to their head, more so than the occasional orange or yellowish-headed males that sometimes occur. The female lays clutches of eggs from February through August, two or more broods per year with 2 to 6 eggs per brood, most commonly 4 or 5. The egg laying usually takes place in the morning, at one egg per day. The eggs are pale bluish-green with few black spots and a smooth, somewhat glossy surface. In response to mite infestation, which has a more deleterious effect on male chicks than on females, the mother finch may lay eggs containing females first, to reduce the length of time male chicks are exposed to mites. This strategy increases the likelihood that representative numbers of both sexes will survive. The female incubates the eggs for 12 to 14 days. Shortly after hatching, she removes the empty eggshells from the nest. The hatchlings are pink with closed eyes and tufts of fluffy down. The female always feeds the young. The male usually joins in. The young are silent for the first seven or eight days, and subsequently start peeping during feedings. Initially, the mother carries fecal sacs out of the nest, but when the young become older, she no longer carries them all away, allowing droppings to accumulate around the edge of the nest. Before flying, the young often climb into adjacent plants and usually fledge at about 11 to 19 days after hatching. Dandelion seeds are among the preferred seeds for the young. Contrary to the way most birds, even ones with herbivorous leanings as adults, tend to feed their nestlings animal matter to give them the protein necessary to grow, house finches are one of the few birds who feed their young only plant matter. House finches are aggressive enough to drive other birds away from places such as feeders. The house finch may be infected by several parasites including Plasmodium relictum and Mycoplasma gallisepticum , which caused the population of house finches in eastern North America to crash during the 1990s. The mite Pellonyssus reedi is often found on house finch nestlings, particularly for nests later in the season. The brown-headed cowbird , a brood parasite , will lay its eggs in house finch nests, although the diet house finches feed their young is inadequate for the young cowbirds, which rarely survive. In 2012, house finches positive for West Nile virus were found in northwestern Riverside County , CA.

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West Nile

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Wolbachia

" Candidatus Wolbachia bourtzisii " Ramirez-Puebla et al. 2015 " Candidatus Wolbachia brugii " Ramirez-Puebla et al. 2015 " Candidatus Wolbachia collembolicola " Ramirez-Puebla et al. 2015 " Candidatus Wolbachia ivorensis " Ehounoud et al. 2016 Wolbachia melophagi (Nöller 1917) Philip 1956 (Approved Lists 1980) " Candidatus Wolbachia multihospitum " Ramirez-Puebla et al. 2015 " Candidatus Wolbachia onchocercicola " Ramirez-Puebla et al. 2015 Wolbachia pipientis Hertig 1936 (Approved Lists 1980) Wolbachia is a genus of gram-negative bacteria that can either infect many species of arthropod as an intracellular parasite , or act as a mutualistic microbe in filarial nematodes . It is one of the most common parasitic microbes of arthropods, and is possibly the most common reproductive parasite in the biosphere . Its interactions with its hosts are often complex. Some host species cannot reproduce, or even survive, without Wolbachia colonisation . One study concluded that more than 16% of neotropical insect species carry bacteria of this genus, and as many as 25 to 70% of all insect species are estimated to be potential hosts. The genus was first identified in 1924 by Marshall Hertig and Simeon Burt Wolbach in the common house mosquito . They described it as "a somewhat pleomorphic , rodlike , Gram-negative , intracellular organism [that] apparently infects only the ovaries and testes ". Hertig formally described the species in 1936, and proposed both the generic and specific names: Wolbachia pipientis . Research on Wolbachia intensified after 1971, when Janice Yen and A. Ralph Barr of UCLA discovered that Culex mosquito eggs were killed by a cytoplasmic incompatibility when the sperm of Wolbachia -infected males fertilized infection-free eggs. The genus Wolbachia is of considerable interest today due to its ubiquitous distribution, its many different evolutionary interactions, and its potential use as a biocontrol agent . Phylogenetic studies have shown that Wolbachia persica (now Francisella persica ) was closely related to species in the genus Francisella and that Wolbachia melophagi (now Bartonella melophagi ) was closely related to species in the genus Bartonella , leading to a transfer of these species to these respective genera. Furthermore, unlike true Wolbachia , which needs a host cell to multiply, F. persica and B. melophagi can be cultured on agar plates . These bacteria can infect many different types of organs, but are most notable for the infections of the testes and ovaries of their hosts. Wolbachia species are ubiquitous in mature eggs, but not mature sperm. Only infected females, therefore, pass the infection on to their offspring. Wolbachia bacteria maximize their spread by significantly altering the reproductive capabilities of their hosts, with four different phenotypes :Several host species, such as those within the genus Trichogramma , are so dependent on sexual differentiation of Wolbachia that they are unable to reproduce effectively without the bacteria in their bodies, and some might even be unable to survive uninfected. One study on infected woodlice showed the broods of infected organisms had a higher proportion of females than their uninfected counterparts. Wolbachia , especially Wolbachia -caused cytoplasmic incompatibility, may be important in promoting speciation. Wolbachia strains that distort the sex ratio may alter their host's pattern of sexual selection in nature, and also engender strong selection to prevent their action, leading to some of the fastest examples of natural selection in natural populations. The male killing and feminization effects of Wolbachia infections can also lead to speciation in their hosts. For example, populations of the pill woodlouse, Armadillidium vulgare which are exposed to the feminizing effects of Wolbachia , have been known to lose their female-determining chromosome. In these cases, only the presence of Wolbachia can cause an individual to develop into a female. Cryptic species of ground wētā ( Hemiandrus maculifrons complex) are host to different lineages of Wolbachia which might explain their speciation without ecological or geographical separation. The enzyme aromatase is found to mediate sex-change in many species of fish. Wolbachia can affect the activity of aromatase in developing fish embryos. The enzyme aromatase is found to mediate sex-change in many species of fish. Wolbachia can affect the activity of aromatase in developing fish embryos. Wolbachia may transfer from prey to predator through the digestive system. To do so, Wolbachia needs to first survive through the lumen secretion and then enter the host tissue through the gut epithelium. This route does not seem to occur frequently due to little evidence. This may be one of the most common routes of Wolbachia host shifts. Compared to predator-prey interactions, the physical association between the host and parasites typically lasts longer, occurs at various developmental stages, and enables Wolbachia to directly contact various tissues. Since this interaction may expose both sides to microbial exchange, one strategy for understanding the direction of transfer is to assess Wolbachia 's presence in close relatives on both sides, as the donor side generally has a larger diversity of infection. One parasitoid species can infect multiple shared hosts, and one host species can infect multiple parasitoids. For instance, parthenogenesis-inducing Wolbachia can spread between Trichogramma parasitoid wasps sharing host eggs. Parasites can also serve as a vector between infected and uninfected hosts without being infected. When the mouthparts and ovipositors of aphelinid parasitoid wasps become contaminated through feeding Wolbachia -infected Bemisia tabaci , it can infect the next host. This route applies to microbes that can survive either within or on the surface of the food. Experiments demonstrated that the Wolbachia wAlbB strain can survive extracellularly for up to 7 days, and up to 50 days for some strains in cotton leaf phloem vessels. Plants are one of the best platforms for this route. By physical contact between arthropod mouthparts and plant tissue, the Wolbachia inhabiting the salivary glands of some insects may be transferred to the plants. As a result, arthropod species feeding on the same plants may share common Wolbachia strains. Other insect food sources may also mediate Wolbachia horizontal transfer, such as the sharing of dung patches between two Malagasy dung beetle species. The pathogen-associated molecular patterns (PAMPs) in the bacteria, such as peptidoglycan, can activate the host's innate immune responses. In response, some Wolbachia strains have a unique functional peptidoglycan amidase (AmiDwol) that cleaves its bacterial cell wall so that it can escape from immune responses. Besides the peptidoglycans, cell-to-cell movements of Wolbachia can also cause oxidative stress to the host and trigger the host's immune response. Therefore, Wolbachia has a triple-layer vacuole that acts as a mechanical shield to protect it from cellular immune responses. Vertical transmission requires Wolbachia to reach germ line cells and maintain in the zygote. Wolbachia may initially occupy somatic stem cells as a stable reservoir and then use the host's vitellogenin transovarial transportation system to enter the oocyte. Once Wolbachia enter the zygote, they need to reach important host tissues without disrupting the embryo's development. This can be achieved using the host cytoskeleton, by bundling Wolbachia protein WD0830 to host actin filaments. They can also increase the division rate of germ-line stem cells to localize and increase their titer. Under natural conditions, successful vertical transmission of Wolbachia is challenging. Invasion of a new population likely stems from specific phenotypic effects, including reproductive manipulations and/or providing direct fitness benefits to their female hosts. Upon transferring into a new host, Wolbachia may retain its original phenotypic effects, induce a different phenotype, or have no detectable effect. For instance, a strain that induce male killing in the moth Cadra cautella induced Cytoplasmic incompatibility in a novel moth host Ephestia kuehniella . Wolbachia may transfer from prey to predator through the digestive system. To do so, Wolbachia needs to first survive through the lumen secretion and then enter the host tissue through the gut epithelium. This route does not seem to occur frequently due to little evidence. This may be one of the most common routes of Wolbachia host shifts. Compared to predator-prey interactions, the physical association between the host and parasites typically lasts longer, occurs at various developmental stages, and enables Wolbachia to directly contact various tissues. Since this interaction may expose both sides to microbial exchange, one strategy for understanding the direction of transfer is to assess Wolbachia 's presence in close relatives on both sides, as the donor side generally has a larger diversity of infection. One parasitoid species can infect multiple shared hosts, and one host species can infect multiple parasitoids. For instance, parthenogenesis-inducing Wolbachia can spread between Trichogramma parasitoid wasps sharing host eggs. Parasites can also serve as a vector between infected and uninfected hosts without being infected. When the mouthparts and ovipositors of aphelinid parasitoid wasps become contaminated through feeding Wolbachia -infected Bemisia tabaci , it can infect the next host. This route applies to microbes that can survive either within or on the surface of the food. Experiments demonstrated that the Wolbachia wAlbB strain can survive extracellularly for up to 7 days, and up to 50 days for some strains in cotton leaf phloem vessels. Plants are one of the best platforms for this route. By physical contact between arthropod mouthparts and plant tissue, the Wolbachia inhabiting the salivary glands of some insects may be transferred to the plants. As a result, arthropod species feeding on the same plants may share common Wolbachia strains. Other insect food sources may also mediate Wolbachia horizontal transfer, such as the sharing of dung patches between two Malagasy dung beetle species. Wolbachia may transfer from prey to predator through the digestive system. To do so, Wolbachia needs to first survive through the lumen secretion and then enter the host tissue through the gut epithelium. This route does not seem to occur frequently due to little evidence. This may be one of the most common routes of Wolbachia host shifts. Compared to predator-prey interactions, the physical association between the host and parasites typically lasts longer, occurs at various developmental stages, and enables Wolbachia to directly contact various tissues. Since this interaction may expose both sides to microbial exchange, one strategy for understanding the direction of transfer is to assess Wolbachia 's presence in close relatives on both sides, as the donor side generally has a larger diversity of infection. One parasitoid species can infect multiple shared hosts, and one host species can infect multiple parasitoids. For instance, parthenogenesis-inducing Wolbachia can spread between Trichogramma parasitoid wasps sharing host eggs. Parasites can also serve as a vector between infected and uninfected hosts without being infected. When the mouthparts and ovipositors of aphelinid parasitoid wasps become contaminated through feeding Wolbachia -infected Bemisia tabaci , it can infect the next host. This route applies to microbes that can survive either within or on the surface of the food. Experiments demonstrated that the Wolbachia wAlbB strain can survive extracellularly for up to 7 days, and up to 50 days for some strains in cotton leaf phloem vessels. Plants are one of the best platforms for this route. By physical contact between arthropod mouthparts and plant tissue, the Wolbachia inhabiting the salivary glands of some insects may be transferred to the plants. As a result, arthropod species feeding on the same plants may share common Wolbachia strains. Other insect food sources may also mediate Wolbachia horizontal transfer, such as the sharing of dung patches between two Malagasy dung beetle species. The pathogen-associated molecular patterns (PAMPs) in the bacteria, such as peptidoglycan, can activate the host's innate immune responses. In response, some Wolbachia strains have a unique functional peptidoglycan amidase (AmiDwol) that cleaves its bacterial cell wall so that it can escape from immune responses. Besides the peptidoglycans, cell-to-cell movements of Wolbachia can also cause oxidative stress to the host and trigger the host's immune response. Therefore, Wolbachia has a triple-layer vacuole that acts as a mechanical shield to protect it from cellular immune responses. Vertical transmission requires Wolbachia to reach germ line cells and maintain in the zygote. Wolbachia may initially occupy somatic stem cells as a stable reservoir and then use the host's vitellogenin transovarial transportation system to enter the oocyte. Once Wolbachia enter the zygote, they need to reach important host tissues without disrupting the embryo's development. This can be achieved using the host cytoskeleton, by bundling Wolbachia protein WD0830 to host actin filaments. They can also increase the division rate of germ-line stem cells to localize and increase their titer. Under natural conditions, successful vertical transmission of Wolbachia is challenging.Invasion of a new population likely stems from specific phenotypic effects, including reproductive manipulations and/or providing direct fitness benefits to their female hosts. Upon transferring into a new host, Wolbachia may retain its original phenotypic effects, induce a different phenotype, or have no detectable effect. For instance, a strain that induce male killing in the moth Cadra cautella induced Cytoplasmic incompatibility in a novel moth host Ephestia kuehniella . Wolbachia infection has been linked to viral resistance in Drosophila melanogaster , Drosophila simulans , and mosquito species. Flies, including mosquitoes, infected with the bacteria are more resistant to RNA viruses such as Drosophila C virus , norovirus , flock house virus , cricket paralysis virus , chikungunya virus , and West Nile virus . In the common house mosquito, higher levels of Wolbachia were correlated with more insecticide resistance. In leafminers of the species Phyllonorycter blancardella , Wolbachia bacteria help their hosts produce green islands on yellowing tree leaves, that is, small areas of leaf remaining fresh, allowing the hosts to continue feeding while growing to their adult forms. Larvae treated with tetracycline , which kills Wolbachia , lose this ability and subsequently only 13% emerge successfully as adult moths. Muscidifurax uniraptor , a parasitoid wasp , also benefits from hosting Wolbachia bacteria. In the parasitic filarial nematode species responsible for elephantiasis , such as Brugia malayi and Wuchereria bancrofti , Wolbachia has become an obligate endosymbiont and provides the host with chemicals necessary for its reproduction and survival. Elimination of the Wolbachia symbionts through antibiotic treatment therefore prevents reproduction of the nematode, and eventually results in its premature death. Some Wolbachia species that infect arthropods also provide some metabolic provisioning to their hosts. In Drosophila melanogaster , Wolbachia is found to mediate iron metabolism under nutritional stress and in Cimex lectularius , the Wolbachia strain cCle helps the host to synthesize B vitamins . Some Wolbachia strains have increased their prevalence by increasing their hosts' fecundity. Wolbachia strains captured from 1988 in southern California still induce a fecundity deficit, but nowadays the fecundity deficit is replaced with a fecundity advantage such that infected Drosophila simulans produces more offspring than the uninfected ones. Wolbachia often manipulates host reproduction and life-history in a way that favours its own propagation. In the Pharaoh ant , Wolbachia infection correlates with increased colony-level production of reproductives (i.e., greater reproductive investment), and earlier onset of reproductive production (i.e., shorter life-cycle). Infected colonies also seem to grow more rapidly. There is substantial evidence that the presence of Wolbachia that induce parthenogenesis have put pressure on species to reproduce primarily or entirely this way. Additionally, Wolbachia has been seen to decrease the lifespan of Aedes aegypti , carriers of mosquito-borne diseases, and it decreases their efficacy of pathogen transmission because older mosquitoes are more likely to have become carriers of one of those diseases. This has been exploited as a method for pest control.The first Wolbachia genome to be determined was that of strain wMel, which infects D. melanogaster fruit flies. This genome was sequenced at The Institute for Genomic Research in a collaboration between Jonathan Eisen and Scott O'Neill. The second Wolbachia genome to be determined was of strain wBm, which infects Brugia malayi nematodes. Genome sequencing projects for several other Wolbachia strains are in progress. Wolbachia species also harbor a bacteriophage called bacteriophage WO or phage WO. Comparative sequence analyses of bacteriophage WO offer some of the most compelling examples of large-scale horizontal gene transfer between Wolbachia coinfections in the same host. It is the first bacteriophage implicated in frequent lateral transfer between the genomes of bacterial endosymbionts . Gene transfer by bacteriophages could drive significant evolutionary change in the genomes of intracellular bacteria that were previously considered highly stable or prone to loss of genes over time. Wolbachia also transfers genes to the host. A nearly complete copy of the Wolbachia genome sequence was found within the genome sequence of the fruit fly Drosophila ananassae and large segments were found in seven other Drosophila species. In an application of DNA barcoding to the identification of species of Protocalliphora flies, several distinct morphospecies had identical cytochrome c oxidase I gene sequences, most likely through horizontal gene transfer (HGT) by Wolbachia species as they jump across host species. As a result, Wolbachia can cause misleading results in molecular cladistical analyses. It is estimated that between 20 and 50 percent of insect species have evidence of HGT from Wolbachia —passing from microbes to animal (i.e. insects). Wolbachia species also harbor a bacteriophage called bacteriophage WO or phage WO. Comparative sequence analyses of bacteriophage WO offer some of the most compelling examples of large-scale horizontal gene transfer between Wolbachia coinfections in the same host. It is the first bacteriophage implicated in frequent lateral transfer between the genomes of bacterial endosymbionts . Gene transfer by bacteriophages could drive significant evolutionary change in the genomes of intracellular bacteria that were previously considered highly stable or prone to loss of genes over time. Wolbachia also transfers genes to the host. A nearly complete copy of the Wolbachia genome sequence was found within the genome sequence of the fruit fly Drosophila ananassae and large segments were found in seven other Drosophila species. In an application of DNA barcoding to the identification of species of Protocalliphora flies, several distinct morphospecies had identical cytochrome c oxidase I gene sequences, most likely through horizontal gene transfer (HGT) by Wolbachia species as they jump across host species. As a result, Wolbachia can cause misleading results in molecular cladistical analyses. It is estimated that between 20 and 50 percent of insect species have evidence of HGT from Wolbachia —passing from microbes to animal (i.e. insects). The small non-coding RNAs WsnRNA-46 and WsnRNA-59 in Wolbachia were detected in Aedes aegypti mosquitoes and Drosophila melanogaster . The small RNAs (sRNAs) may regulate bacterial and host genes. Highly conserved intragenic region sRNA called ncrwmel02 was also identified in Wolbachia pipientis. It is expressed in four different strains in a regulated pattern that differs according to the sex of the host and the tissue localisation. This suggested that the sRNA may play important roles in the biology of Wolbachia. Outside of insects, Wolbachia infects a variety of isopod species, spiders , mites , and many species of filarial nematodes (a type of parasitic worm ), including those causing onchocerciasis (river blindness) and elephantiasis in humans, as well as heartworms in dogs. Not only are these disease-causing filarial worms infected with Wolbachia , but Wolbachia also seems to play an inordinate role in these diseases. A large part of the pathogenicity of filarial nematodes is due to host immune response toward their Wolbachia . Elimination of Wolbachia from filarial nematodes generally results in either death or sterility of the nematode. Consequently, current strategies for control of filarial nematode diseases include elimination of their symbiotic Wolbachia via the simple doxycycline antibiotic, rather than directly killing the nematode with often more toxic antinematode medications. Naturally existing strains of Wolbachia have been shown to be a route for vector control strategies because of their presence in arthropod populations, such as mosquitoes. Due to the unique traits of Wolbachia that cause cytoplasmic incompatibility , some strains are useful to humans as a promoter of genetic drive within an insect population. Wolbachia -infected females are able to produce offspring with uninfected and infected males; however, uninfected females are only able to produce viable offspring with uninfected males. This gives infected females a reproductive advantage that is greater the higher the frequency of Wolbachia in the population. Computational models predict that introducing Wolbachia strains into natural populations will reduce pathogen transmission and reduce overall disease burden. An example includes a life-shortening Wolbachia that can be used to control dengue virus and malaria by eliminating the older insects that contain more parasites. Promoting the survival and reproduction of younger insects lessens selection pressure for evolution of resistance. In addition, some Wolbachia strains are able to directly reduce viral replication inside the insect. For dengue they include wAllbB and wMelPop with Aedes aegypti , wMel with Aedes albopictus and Aedes aegypti . Wolbachia has also been identified to inhibit replication of chikungunya virus (CHIKV) in A. aegypti . The w Mel strain of Wolbachia pipientis significantly reduced infection and dissemination rates of CHIKV in mosquitoes, compared to Wolbachia uninfected controls and the same phenomenon was observed in yellow fever virus infection converting this bacterium in an excellent promise for YFV and CHIKV suppression. Wolbachia also inhibits the secretion of West Nile virus (WNV) in cell line Aag2 derived from A. aegypti cells. The mechanism is somewhat novel, as the bacteria actually enhances the production of viral genomic RNA in the cell line Wolbachia . Also, the antiviral effect in intrathoracically infected mosquitoes depends on the strain of Wolbachia , and the replication of the virus in orally fed mosquitoes was completely inhibited in wMelPop strain of Wolbachia . The effect of Wolbachia infection on virus replication in insect hosts is complex and depends on the Wolbachia strain and virus species. While several studies have indicated consistent refractory phenotypes of Wolbachia infection on positive-sense RNA viruses in Drosophila melanogaster , the yellow fever mosquito Aedes aegypti and the Asian tiger mosquito Aedes albopictus , this effect is not seen in DNA virus infection and in some cases Wolbachia infection has been associated or shown to increase single stranded DNA and double-stranded DNA virus infection. There is also currently no evidence that Wolbachia infection restricts any tested negative-sense RNA viruses indicating Wolbachia would be unsuitable for restriction of negative-sense RNA arthropod borne viruses. Wolbachia infection can also increase mosquito resistance to malaria, as shown in Anopheles stephensi where the w AlbB strain of Wolbachia hindered the lifecycle of Plasmodium falciparum . However, Wolbachia infections can also enhance pathogen transmission. Wolbachia has enhanced multiple arboviruses in Culex tarsalis mosquitoes. In another study, West Nile Virus (WNV) infection rate was significantly higher in Wolbachia (strain wAlbB)-infected C. tarsalis compared to controls. Wolbachia may induce reactive oxygen species –dependent activation of the Toll (gene family) pathway, which is essential for activation of antimicrobial peptides , defensins , and cecropins that help to inhibit virus proliferation. Conversely, certain strains actually dampen the pathway, leading to higher replication of viruses. One example is with strain wAlbB in Culex tarsalis , where infected mosquitoes actually carried the west nile virus (WNV) more frequently. This is because wAlbB inhibits REL1, an activator of the antiviral Toll immune pathway. As a result, careful studies of the Wolbachia strain and ecological consequences must be done before releasing artificially-infected mosquitoes in the environment. The World Mosquito Program (WMP) uses Wolbachia strain wMel to infect Aedes mosquitos. The mixed-sex mosquitos are intended to infect the local population with wMel, giving them transmission resistance. In 2014, WMP released infected mosquitos in Townsville , an Australia city with 187,000 inhabitants plagued by dengue. For four years after introduction, no cases of dengue were reported. Trials in much smaller areas had been carried out, but a larger area had not been tested. No environmental ill-effects were reported. The cost was A$ 15 per inhabitant, but it was hoped that it could be reduced to US$ 1 in poorer countries with lower labor costs. In 2016, WMP scientist Scott Ritchie proposed using wMel mosquitos to combat the spread of the Zika virus . A study reported that Wolbachia wMel has the ability to block Zika in Brazil. In October 2016, it was announced that US$18 million in funding was being allocated for the use of Wolbachia -infected mosquitoes to fight Zika and dengue viruses. Deployment is slated for early 2017 in Colombia and Brazil. Between 2016 and 2020, WMP conducted its first randomized controlled trial in Yogyakarta , an Indonesian city of about 400,000 inhabitants. In August 2020, the trial's Indonesian lead scientist Adi Utarini announced that the trial showed a 77% reduction in dengue cases compared to the control areas. This trial was the "strongest evidence yet" for the technique. In 2017 – 2019, WMP released mosquitos in Niterói, Brazil. In March 2023, Brazil's Oswaldo Cruz Foundation signed an agreement with WMP to provide funds for a large "mosquito factory" producing infected insects. Another method to use Wolbachia in mosquitos exploits the cytoplamic incompatibility between infected males and uninfected females. If an uninfected female mates with an infected male, her eggs become infertile. With enough infected males released, the mosquito population would be reduced temporarily. Verily , the life sciences arm of Google's parent company Alphabet Inc. , uses this method. In July 2017, it announced a plan to release about 20 million Wolbachia -infected male Aedes aegypti mosquitoes in Fresno , California , in an attempt to combat the Zika virus. Singapore's National Environment Agency has teamed up with Verily to come up with an advanced, more efficient way to release male Wolbachia mosquitoes for Phase 2 of its study to suppress the urban Aedes aegypti mosquito population and fight dengue. On November 3, 2017, the US Environmental Protection Agency (EPA) registered Mosquito Mate, Inc. to release Wolbachia strain "ZAP"-infected male mosquitoes in 20 US states and the District of Columbia. Outside of insects, Wolbachia infects a variety of isopod species, spiders , mites , and many species of filarial nematodes (a type of parasitic worm ), including those causing onchocerciasis (river blindness) and elephantiasis in humans, as well as heartworms in dogs. Not only are these disease-causing filarial worms infected with Wolbachia , but Wolbachia also seems to play an inordinate role in these diseases. A large part of the pathogenicity of filarial nematodes is due to host immune response toward their Wolbachia . Elimination of Wolbachia from filarial nematodes generally results in either death or sterility of the nematode. Consequently, current strategies for control of filarial nematode diseases include elimination of their symbiotic Wolbachia via the simple doxycycline antibiotic, rather than directly killing the nematode with often more toxic antinematode medications. Naturally existing strains of Wolbachia have been shown to be a route for vector control strategies because of their presence in arthropod populations, such as mosquitoes. Due to the unique traits of Wolbachia that cause cytoplasmic incompatibility , some strains are useful to humans as a promoter of genetic drive within an insect population. Wolbachia -infected females are able to produce offspring with uninfected and infected males; however, uninfected females are only able to produce viable offspring with uninfected males. This gives infected females a reproductive advantage that is greater the higher the frequency of Wolbachia in the population. Computational models predict that introducing Wolbachia strains into natural populations will reduce pathogen transmission and reduce overall disease burden. An example includes a life-shortening Wolbachia that can be used to control dengue virus and malaria by eliminating the older insects that contain more parasites. Promoting the survival and reproduction of younger insects lessens selection pressure for evolution of resistance. In addition, some Wolbachia strains are able to directly reduce viral replication inside the insect. For dengue they include wAllbB and wMelPop with Aedes aegypti , wMel with Aedes albopictus and Aedes aegypti . Wolbachia has also been identified to inhibit replication of chikungunya virus (CHIKV) in A. aegypti . The w Mel strain of Wolbachia pipientis significantly reduced infection and dissemination rates of CHIKV in mosquitoes, compared to Wolbachia uninfected controls and the same phenomenon was observed in yellow fever virus infection converting this bacterium in an excellent promise for YFV and CHIKV suppression. Wolbachia also inhibits the secretion of West Nile virus (WNV) in cell line Aag2 derived from A. aegypti cells. The mechanism is somewhat novel, as the bacteria actually enhances the production of viral genomic RNA in the cell line Wolbachia . Also, the antiviral effect in intrathoracically infected mosquitoes depends on the strain of Wolbachia , and the replication of the virus in orally fed mosquitoes was completely inhibited in wMelPop strain of Wolbachia . The effect of Wolbachia infection on virus replication in insect hosts is complex and depends on the Wolbachia strain and virus species. While several studies have indicated consistent refractory phenotypes of Wolbachia infection on positive-sense RNA viruses in Drosophila melanogaster , the yellow fever mosquito Aedes aegypti and the Asian tiger mosquito Aedes albopictus , this effect is not seen in DNA virus infection and in some cases Wolbachia infection has been associated or shown to increase single stranded DNA and double-stranded DNA virus infection. There is also currently no evidence that Wolbachia infection restricts any tested negative-sense RNA viruses indicating Wolbachia would be unsuitable for restriction of negative-sense RNA arthropod borne viruses. Wolbachia infection can also increase mosquito resistance to malaria, as shown in Anopheles stephensi where the w AlbB strain of Wolbachia hindered the lifecycle of Plasmodium falciparum . However, Wolbachia infections can also enhance pathogen transmission. Wolbachia has enhanced multiple arboviruses in Culex tarsalis mosquitoes. In another study, West Nile Virus (WNV) infection rate was significantly higher in Wolbachia (strain wAlbB)-infected C. tarsalis compared to controls. Wolbachia may induce reactive oxygen species –dependent activation of the Toll (gene family) pathway, which is essential for activation of antimicrobial peptides , defensins , and cecropins that help to inhibit virus proliferation. Conversely, certain strains actually dampen the pathway, leading to higher replication of viruses. One example is with strain wAlbB in Culex tarsalis , where infected mosquitoes actually carried the west nile virus (WNV) more frequently. This is because wAlbB inhibits REL1, an activator of the antiviral Toll immune pathway. As a result, careful studies of the Wolbachia strain and ecological consequences must be done before releasing artificially-infected mosquitoes in the environment. The World Mosquito Program (WMP) uses Wolbachia strain wMel to infect Aedes mosquitos. The mixed-sex mosquitos are intended to infect the local population with wMel, giving them transmission resistance. In 2014, WMP released infected mosquitos in Townsville , an Australia city with 187,000 inhabitants plagued by dengue. For four years after introduction, no cases of dengue were reported. Trials in much smaller areas had been carried out, but a larger area had not been tested. No environmental ill-effects were reported. The cost was A$ 15 per inhabitant, but it was hoped that it could be reduced to US$ 1 in poorer countries with lower labor costs. In 2016, WMP scientist Scott Ritchie proposed using wMel mosquitos to combat the spread of the Zika virus . A study reported that Wolbachia wMel has the ability to block Zika in Brazil. In October 2016, it was announced that US$18 million in funding was being allocated for the use of Wolbachia -infected mosquitoes to fight Zika and dengue viruses. Deployment is slated for early 2017 in Colombia and Brazil. Between 2016 and 2020, WMP conducted its first randomized controlled trial in Yogyakarta , an Indonesian city of about 400,000 inhabitants. In August 2020, the trial's Indonesian lead scientist Adi Utarini announced that the trial showed a 77% reduction in dengue cases compared to the control areas. This trial was the "strongest evidence yet" for the technique. In 2017 – 2019, WMP released mosquitos in Niterói, Brazil. In March 2023, Brazil's Oswaldo Cruz Foundation signed an agreement with WMP to provide funds for a large "mosquito factory" producing infected insects. Another method to use Wolbachia in mosquitos exploits the cytoplamic incompatibility between infected males and uninfected females. If an uninfected female mates with an infected male, her eggs become infertile. With enough infected males released, the mosquito population would be reduced temporarily. Verily , the life sciences arm of Google's parent company Alphabet Inc. , uses this method. In July 2017, it announced a plan to release about 20 million Wolbachia -infected male Aedes aegypti mosquitoes in Fresno , California , in an attempt to combat the Zika virus. Singapore's National Environment Agency has teamed up with Verily to come up with an advanced, more efficient way to release male Wolbachia mosquitoes for Phase 2 of its study to suppress the urban Aedes aegypti mosquito population and fight dengue. On November 3, 2017, the US Environmental Protection Agency (EPA) registered Mosquito Mate, Inc. to release Wolbachia strain "ZAP"-infected male mosquitoes in 20 US states and the District of Columbia. The World Mosquito Program (WMP) uses Wolbachia strain wMel to infect Aedes mosquitos. The mixed-sex mosquitos are intended to infect the local population with wMel, giving them transmission resistance. In 2014, WMP released infected mosquitos in Townsville , an Australia city with 187,000 inhabitants plagued by dengue. For four years after introduction, no cases of dengue were reported. Trials in much smaller areas had been carried out, but a larger area had not been tested. No environmental ill-effects were reported. The cost was A$ 15 per inhabitant, but it was hoped that it could be reduced to US$ 1 in poorer countries with lower labor costs. In 2016, WMP scientist Scott Ritchie proposed using wMel mosquitos to combat the spread of the Zika virus . A study reported that Wolbachia wMel has the ability to block Zika in Brazil. In October 2016, it was announced that US$18 million in funding was being allocated for the use of Wolbachia -infected mosquitoes to fight Zika and dengue viruses. Deployment is slated for early 2017 in Colombia and Brazil. Between 2016 and 2020, WMP conducted its first randomized controlled trial in Yogyakarta , an Indonesian city of about 400,000 inhabitants. In August 2020, the trial's Indonesian lead scientist Adi Utarini announced that the trial showed a 77% reduction in dengue cases compared to the control areas. This trial was the "strongest evidence yet" for the technique. In 2017 – 2019, WMP released mosquitos in Niterói, Brazil. In March 2023, Brazil's Oswaldo Cruz Foundation signed an agreement with WMP to provide funds for a large "mosquito factory" producing infected insects. Another method to use Wolbachia in mosquitos exploits the cytoplamic incompatibility between infected males and uninfected females. If an uninfected female mates with an infected male, her eggs become infertile. With enough infected males released, the mosquito population would be reduced temporarily. Verily , the life sciences arm of Google's parent company Alphabet Inc. , uses this method. In July 2017, it announced a plan to release about 20 million Wolbachia -infected male Aedes aegypti mosquitoes in Fresno , California , in an attempt to combat the Zika virus. Singapore's National Environment Agency has teamed up with Verily to come up with an advanced, more efficient way to release male Wolbachia mosquitoes for Phase 2 of its study to suppress the urban Aedes aegypti mosquito population and fight dengue. On November 3, 2017, the US Environmental Protection Agency (EPA) registered Mosquito Mate, Inc. to release Wolbachia strain "ZAP"-infected male mosquitoes in 20 US states and the District of Columbia. The World Mosquito Program (WMP) uses Wolbachia strain wMel to infect Aedes mosquitos. The mixed-sex mosquitos are intended to infect the local population with wMel, giving them transmission resistance. In 2014, WMP released infected mosquitos in Townsville , an Australia city with 187,000 inhabitants plagued by dengue. For four years after introduction, no cases of dengue were reported. Trials in much smaller areas had been carried out, but a larger area had not been tested. No environmental ill-effects were reported. The cost was A$ 15 per inhabitant, but it was hoped that it could be reduced to US$ 1 in poorer countries with lower labor costs. In 2016, WMP scientist Scott Ritchie proposed using wMel mosquitos to combat the spread of the Zika virus . A study reported that Wolbachia wMel has the ability to block Zika in Brazil. In October 2016, it was announced that US$18 million in funding was being allocated for the use of Wolbachia -infected mosquitoes to fight Zika and dengue viruses. Deployment is slated for early 2017 in Colombia and Brazil. Between 2016 and 2020, WMP conducted its first randomized controlled trial in Yogyakarta , an Indonesian city of about 400,000 inhabitants. In August 2020, the trial's Indonesian lead scientist Adi Utarini announced that the trial showed a 77% reduction in dengue cases compared to the control areas. This trial was the "strongest evidence yet" for the technique. In 2017 – 2019, WMP released mosquitos in Niterói, Brazil. In March 2023, Brazil's Oswaldo Cruz Foundation signed an agreement with WMP to provide funds for a large "mosquito factory" producing infected insects. Another method to use Wolbachia in mosquitos exploits the cytoplamic incompatibility between infected males and uninfected females. If an uninfected female mates with an infected male, her eggs become infertile. With enough infected males released, the mosquito population would be reduced temporarily. Verily , the life sciences arm of Google's parent company Alphabet Inc. , uses this method. In July 2017, it announced a plan to release about 20 million Wolbachia -infected male Aedes aegypti mosquitoes in Fresno , California , in an attempt to combat the Zika virus. Singapore's National Environment Agency has teamed up with Verily to come up with an advanced, more efficient way to release male Wolbachia mosquitoes for Phase 2 of its study to suppress the urban Aedes aegypti mosquito population and fight dengue. On November 3, 2017, the US Environmental Protection Agency (EPA) registered Mosquito Mate, Inc. to release Wolbachia strain "ZAP"-infected male mosquitoes in 20 US states and the District of Columbia.

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West Nile

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Barred owl

S. v. georgica S. v. helveola S. v. varia Syrnium varium The barred owl ( Strix varia ), also known as the northern barred owl , striped owl or, more informally, hoot owl or eight-hooter owl , is a North American large species of owl . A member of the true owl family, Strigidae, they belong to the genus Strix , which is also the origin of the family's name under Linnaean taxonomy . Barred owls are largely native to eastern North America , but have expanded their range to the west coast of North America where they are considered invasive. Mature forests are their preferred habitat, but they can also acclimatise to various gradients of open woodlands . Their diet consists mainly of small mammals , but this species is an opportunistic predator and is known to prey upon other small vertebrates such as birds , reptiles , and amphibians , as well as a variety of invertebrates . Barred owls are brown to gray overall, with dark striping on the underside. Barred owls have typical nesting habits for a true owl, tending to raise a relatively small brood often in a tree hollow or snag (but sometimes also in other nesting sites) in forested areas. As a result of the barred owl's westward expansion, the species has begun to encroach on the range of the related and threatened spotted owl ( Strix occidentalis ). Evidence shows the assorted threats posed by the invading barred species are only increasing. In response, biologists have recommended culling operations to mitigate the negative effect of the barred on the spotted owl species. The barred owl was first described by Philadelphia naturalist Benjamin Smith Barton in 1799. The species was named due to the varied directions the dusky markings take on their underside. The barred owl is roughly intermediate in size between the larger Ural and the smaller tawny owl, but the structural features of its relatively short and decurved claws more so resemble the tawny species as does their dietary and habitat ecology. The spotted owl has been hypothesized to be within a superspecies with the barred owl. However, genetic testing reveals very early divergence (likely at or near their ancestor's entry to North America) between spotted and barred owls. A fossil species once called Strix brea from the early Pleistocene in California does little to resolve the ancestry of modern species, given its ambiguous relation to any living Strix . The fossil species was larger (more similar in size and slenderness to the spotted owl, albeit with a slightly smaller skull and geographically isolated from that species) and longer-legged than either the spotted and barred owls, and is now considered to be in a separate genus, Oraristrix . Pleistocene era fossils of probable barred owls are known from Florida, Tennessee and Ontario. The subspecies of the barred owl vary mostly by region, with slight to moderate variation by coloring, size and extent of feathering on the toes. Although several have been described in the past, the barred owl may include only three subspecies, subsequent to the separation of the fulvous and cinereous forms. The subspecies of the barred owl vary mostly by region, with slight to moderate variation by coloring, size and extent of feathering on the toes. Although several have been described in the past, the barred owl may include only three subspecies, subsequent to the separation of the fulvous and cinereous forms. The barred owl is considered somewhat subdued and drab in coloration compared to the sometimes rich coloring of other sympatric owls. Overall, this owl is greyish-brown or brown. The brownish color extends from the head to the back. Barred owls are scalloped with white bars on the mantle and the back, bearing as well some whitish spotting on the wing coverts . The underside has a pale creamy gray-brown base color (ranging into dirty white in the palest individuals) overlaid about the throat and upper chest with horizontal, slightly crescent-shaped barring (hence its common name), while the belly is boldly streaked in a vertical pattern. The streaking is usually blackish, dusky brown, or sometimes rufescent- (reddish-) brown. The head is fairly large (although not especially so for a species in Strix ) and rounded with no ear tufts . The facial disc is pale grayish-brown with darker yet subtle concentric lines . The bill is pale straw-yellow (occasionally showing a mild greenish tint) while the cere (a bare structure at the base of the beak) is "horn-colored". Its eyes are a dark brown color; the eyes may appear intensely black in the field and, although large, are fairly closely set. The barred owl has well-developed eye anatomy. As is typical of owls, their ocular anatomy is quite distinct from diurnal raptors especially in terms of their photoreceptor cells , as they have a very large number of rod cells in their quite sensitive retina . However, their pecten oculi is smaller relative to the size of their large ocular globe (other large owls are known to have similar pecten proportions). The vision in limited or almost no light during a laboratory study of a barred owl was found to be similar to that of other owls, including the long-eared owl ( Asio otus ) and the barn owl ( Tyto alba ). The tarsi and toes are feathered up to the dark gray, black-tipped talons. These feathers are more sparse and bristled in the southern races. On individuals with bare sections of their toes, the toes are yellowish-gray in color. The flight feathers are barred with whitish buff and brown while the tail is brown or grayish-brown with 4–5 whitish bars. Young barred owls with their second set of down feathers are fluffy brownish-white, with indistinct darker barring on their head, back and mantle. They quickly become juveniles which resemble adults but have less distinct markings (especially about the head and neck), more buff coloring overall, often some remnant down, pinkish skin and a pale, blue-green cere. Also the tail at this age may have as many as seven bands (though sometimes have four like adults). Full adult plumage is obtained via molt after about a year as well as adult bare part characteristics. A study of tail molt in Washington showed that molt tends to occur relatively quickly, and that young individuals are difficult to age by state of molt alone. Southern barred owls tend to be darker and slightly smaller than northerly ones. Rare captive and wild barred owls with albinism have been described and are pure white but tend to retain their brown eyes. The barred owl is a large species. The adult measures anywhere from 40 to 63 cm (16 to 25 in) in length while the wingspan may range from 96 to 125 cm (38 to 49 in) . The wing area (measured by square centimeter relative to the body mass) is quite intermediate among American owls, with the wing loading being lower than larger, but proportionately small-winged larger owls and even than some smaller owls . The barred has high wing-loading. Wing-loading is related to hunting technique, with higher wing-loading owls typically hunting from a perch, with only a brief flight necessary to obtain food, whilst lower wing-loading owls often hunt their prey from active flight. As is the case in most owls, the various wing feathers of barred owls are uncharacteristically soft and bear a comb -like shape, which in turn renders their flight functionally silent during their hunts. Like most birds of prey , the female is larger than the male barred owl, sometimes described as reverse sexual dimorphism (due to the fact that males average larger than females in most non-raptorial birds). Among standard measurements, the wing chord of grown males varies from 303 to 340 mm (11.9 to 13.4 in) , with an average from three sources of 326.2 mm (12.84 in) , the tail may measure from 182 to 250 mm (7.2 to 9.8 in) , with an average of 219.6 mm (8.65 in) and the culmen from the cere may measure from 22 to 27 mm (0.87 to 1.06 in) , with an average of 24.3 mm (0.96 in) . Meanwhile, for the female, the wing chord may range from 318 to 357 mm (12.5 to 14.1 in) , averaging 335.8 mm (13.22 in) , the tail from 204 to 257 mm (8.0 to 10.1 in) , averaging 223.3 mm (8.79 in) and the culmen from the cere 20 to 30.7 mm (0.79 to 1.21 in) , averaging 25.1 mm (0.99 in) . Sexual dimorphism is particularly pronounced in barred owls by body mass as males within a population are sometimes a third lighter in weight. In the nominate subspecies ( S. v. varia ), average weights for males have been reported as 621.9 g (1.371 lb) (sample size 12), 632 g (1.393 lb) (sample size 20) and 681 g (1.501 lb) (sample size unknown) in three samples. The weight range for adult males is known to vary from 468 to 812 g (1.032 to 1.790 lb) . The considerably larger female of the nominate subspecies has been reported to average 801 g (1.766 lb) (sample size 24), 872.6 g (1.924 lb) (sample size 14) and 909.5 g (2.005 lb) (sample size unknown). Altogether, fully-grown female barred owls may weigh from 610 to 1,150 g (1.34 to 2.54 lb) . The barred owl is a powerful vocalist, with an array of calls that are considered "spectacular, loud and emphatic". Calls probably carry well over 0.8 km (0.50 mi) . Its usual call is a series of eight accented hoots ok-ok-ok-ok ok-ok-buhooh , or the "typical two-phrase hoot" with a downward pitch at the end. The most common mnemonic device for remembering the call is "Who cooks for you, who cooks for you all." Due to its best known call, the barred owl is sometimes colloquially referred to as Old Eight-Hooter . At 80% of study posts in Virginia , barred owls responded to playback of this call. A further call is the "ascending type" or the " legato " call, a series of variable notes ending in oo-aw or hoo-aah . At least two other variations on the legato/ascending call are known. 56% of studied owls in Virginia engaged in the ascending type call but 36% uttered only the closing notes. The isolated hoo-aah , sometimes called the "inspection call", was the most common song type in north Florida and the most likely to be heard during daylight. Several other calls, although some are not dissimilar variations on the main calls, are known. Some of these vary into cackles, hoots, caws and gurgles, at times described as "sudden demonic laughter", "cat-like screams" and "prolonged outbursts of cackling" and seem to be, among Strix species, an idiosyncrasy endemic to the barred owl. Another call type is the "mumble", a grumbling, slurred and subtle err-ERR-err , also an up-and-down "twitter" call at a high pitch. When agitated, this species will make a buzzy, rasping hiss about three times in three seconds, repeating every 10–30 seconds, and will click its beak together forcefully. Females and juveniles beg with high scratching skreeechch notes. The voice of the two sexes is similar, but the female has a higher-pitched voice with longer terminal notes. Of calls, 87 to 94% are identifiable to sex per one study. While calls are most common at night, the birds do call during the day as well, especially when provoked by human playback or imitation. They are more responsive than any hawk in the east to playback of calls of their own species. The barred owl is noisy in most seasons but peak vocalization times for barred owls tend to be between late January (in Florida) and early April (in Canada). Two seasonal peaks in vocalizations, one right before breeding and another after the young have dispersed, was detected in Connecticut , with peak vocalizations on nights with extensive cloud cover. Peak times for vocalizations are between 6:00 pm and 6:00 am, with the least frequent vocalizations around mid-afternoon. The barred owl is a powerful vocalist, with an array of calls that are considered "spectacular, loud and emphatic". Calls probably carry well over 0.8 km (0.50 mi) . Its usual call is a series of eight accented hoots ok-ok-ok-ok ok-ok-buhooh , or the "typical two-phrase hoot" with a downward pitch at the end. The most common mnemonic device for remembering the call is "Who cooks for you, who cooks for you all." Due to its best known call, the barred owl is sometimes colloquially referred to as Old Eight-Hooter . At 80% of study posts in Virginia , barred owls responded to playback of this call. A further call is the "ascending type" or the " legato " call, a series of variable notes ending in oo-aw or hoo-aah . At least two other variations on the legato/ascending call are known. 56% of studied owls in Virginia engaged in the ascending type call but 36% uttered only the closing notes. The isolated hoo-aah , sometimes called the "inspection call", was the most common song type in north Florida and the most likely to be heard during daylight. Several other calls, although some are not dissimilar variations on the main calls, are known. Some of these vary into cackles, hoots, caws and gurgles, at times described as "sudden demonic laughter", "cat-like screams" and "prolonged outbursts of cackling" and seem to be, among Strix species, an idiosyncrasy endemic to the barred owl. Another call type is the "mumble", a grumbling, slurred and subtle err-ERR-err , also an up-and-down "twitter" call at a high pitch. When agitated, this species will make a buzzy, rasping hiss about three times in three seconds, repeating every 10–30 seconds, and will click its beak together forcefully. Females and juveniles beg with high scratching skreeechch notes. The voice of the two sexes is similar, but the female has a higher-pitched voice with longer terminal notes. Of calls, 87 to 94% are identifiable to sex per one study. While calls are most common at night, the birds do call during the day as well, especially when provoked by human playback or imitation. They are more responsive than any hawk in the east to playback of calls of their own species. The barred owl is noisy in most seasons but peak vocalization times for barred owls tend to be between late January (in Florida) and early April (in Canada). Two seasonal peaks in vocalizations, one right before breeding and another after the young have dispersed, was detected in Connecticut , with peak vocalizations on nights with extensive cloud cover. Peak times for vocalizations are between 6:00 pm and 6:00 am, with the least frequent vocalizations around mid-afternoon. The barred owl is distributed throughout most of the eastern United States , as well as much of southern Canada . They are found as far northeast as much of Nova Scotia (western two-thirds), New Brunswick and Sept-Îles , in much of Quebec , up to Lake Mistassini , and Ontario , up to Moosonee . The barred owl has been recorded as ended up as far north as central Labrador , though the species is not yet confirmed to breed in the province. The barred owl ranges in every part of the eastern United States continuously from northernmost Maine down throughout New England , the Mid-Atlantic states , much of the Midwest , the Southeast United States and all of Florida . They are found to as far west without substantial gaps to the limits of western Minnesota , easternmost South Dakota , the southeastern corner of Nebraska , the eastern half roughly of Kansas , most of Oklahoma and east Texas to as far west as Cisco and Burnet . Arguably and discontinuously from Texas, the species may range into central and southern Mexico but these populations are now often considered a separate species . These initial parts of the range in the eastern and central stretches would be considered as where the species is "native". A wandering barred owl was once seen flying over Lake Michigan 48 km (30 mi) from the nearest land. The remaining parts of the range are considered where the barred owl introduced itself in the last century or so. The historical lack of trees in the Great Plains presumably acted as a barrier to the range expansion, and recent increases in forests broke down this barrier. Increases in forest distribution along the Missouri River and its tributaries provided barred owls with sufficient foraging habitat, protection from the weather, and concealment from avian predators. This allowed barred owls to move westward, initially solely along other forested river corridors (e.g. the Yellowstone and Musselshell ), but increases in forests in the northern Great Plains decades later would allow them to connect their eastern and western distributions across southern Canada. These increases in forests were caused by European-American settlers via wildfire suppression and ceasing the fires historically set by Native Americans , as well as by increased tree-planting. In Canada, the barred owls with range expansion now range through southern Manitoba (excluding the southwest corner), a broad section of south-central Saskatchewan , and east-central and nearly all of western Alberta , now up to High Level . The barred owl has been present in Manitoba at least since 1886, Alberta since 1932 and Saskatchewan since 1948. However, a study in Alberta has shown that barred owls have likely been present for no less than 100 years. This owl species currently ranges through much of British Columbia , where they have been expanding their range since at least 1943, including Vancouver Island and as far north as Fort St. John . The barred owl has had a further northward expansion in the west to southeastern Alaska ( Skagway to Ketchikan ) and extreme southwestern Yukon . In the western United States they also range into northwestern Montana and northern Idaho . Barred owls were first verified in southwest Montana in 1909 and in northwest Montana in 1921 (although reports of the species may date back to the 1870s) but not in Idaho until 1968. Of unknown origin, barred owls have been seen in Colorado since around the turn of the 20th century. They range broadly in eastern and western Washington (reached by 1965) and western Oregon (reached by 1972) (mostly along the forested corridors hugging the montane areas of the Cascade , Olympic and Blue ranges), and northern California (reached by 1976), now down to the Redwood National Forest , the Sierra Nevada and outer San Francisco . The habitat used by barred owl is largely old deciduous , mixed forests and, occasionally, coniferous forests . Old growth forests are preferred due to more extensive potential nest sites, less lower-branch density to impede hunting (and perhaps superior structural complexity to aid hunting), greater security from mobbing and perhaps greater thermoregulation . They are often found in bottomland hardwood forests in the largest swath of the native breeding range, often (particularly from Virginia south and west) with deep, dark stands of oak , gum and cypress . Secondary habitat, often used during foraging forays in the south, are often oak savanna or cabbage-palm areas. Regardless of area, some variety of water is frequently present, including riparian areas or swampy ground. Closed canopy forests were preferred in a study from Oklahoma (62.8% of habitat used), followed by fallow agricultural fields (10.6%), wetlands (8.1%) and open terrain (6.2%). The latter three were visited during hunting forays, and wetlands and open terrain areas were not used outside of the breeding season. Along the Atlantic coast area from New England to New Jersey , barred owls are often found in mixed swamps areas with cedars , seldom wandering to adjacent wetlands or farmland . The species may be at home in wooded areas in mountainous regions . More upland wooded habitats, often in mixed woods containing hemlock , alder , poplar , pine and oak , are typical in the northern part of the range. A study in northern New Jersey found at least 15 species of both conifer and deciduous trees were routinely used for differing purposes. In Michigan, barred owl habitat usually consists largely of some combination of hemlock and maple trees, with mixed forest usage being use disproportionately to its prevalence in the environment. Large oak stands were preferred in Minnesota , a bit ahead of mixed forest and far ahead of white cedar swamps and other habitat types, which were either too dense, too open or had too few attractive nesting sites. Barred owls are not confined to extensive forest, also dwelling extensively in semi-open wooded areas , locally in large parks with mature trees, and in forest adjacent regions recently logged . Recent studies show suburban neighborhoods can be ideal habitat for barred owls, and the species may be considered a local synanthrope . Using transmitters, scientists found that some regional populations, such as in Charlotte, North Carolina , increased faster in the suburban settings than in old growth forest . A factor of this suburban success may be easily accessible rodent prey in such settings. However, for breeding and roosting needs, this species needs at least some large trees and can be locally absent in some urban areas for this reason. The increased offspring offset the death rate due to impacts from cars, other types of collisions and disease. Similarly, in Piedmont, South Carolina , productivity of the owls was higher in suburban areas and they comprised 41% of the territories of the local owls but various sorts of anthropogenic mortality were seemingly higher. In suburban areas of Ohio , 41.4% of barred owl range was forested, 29.8% was low-density residential areas and less than 15% was pasture . On the other hand, studies from the Northeastern United States , such as in New Jersey , found barred owls breeding mainly in plots of old-growth woodlands, and rarely successfully breeding in peri-urban areas , in part because of competitive and predatory displacement by great horned owls . Furthermore, a study in North Carolina showed most barred owls appear to favor areas with at least 86 to 370 ha (210 to 910 acres) of woods but did not seem to be affected by the presence of roadways. In the Pacific Northwest , they can be quite adaptive to secondary forests . On the other hand, in Ontario where the barred owl is native, secondary forest seemed to be largely avoided per a study. In the recent western part of the range, barred owls often dwell in mixed wood areas, often where there are lowland stands of balsam poplar , trembling aspen and white spruce , occasionally but not commonly in pure conifer boreal stands . Barred owls in California preferred stands of red alder . More so confined to inland areas, as in eastern Washington, Idaho, Manitoba and Montana, they prefer Douglas fir, ponderosa pine , paper birch , burr oak and western larch . In north-central Alberta, the use of old growth forest was far more prevalent than its occurrence in the wild. In the Cascades Range of Washington, barred owls usually dwell in areas with more grand firs , taller and more diverse tree heights, more enclosed canopies, higher numbers of trees per acre and less ground cover. In Saskatchewan, barred owls preferred areas with a minimum of 66% forest cover. The remaining parts of the range are considered where the barred owl introduced itself in the last century or so. The historical lack of trees in the Great Plains presumably acted as a barrier to the range expansion, and recent increases in forests broke down this barrier. Increases in forest distribution along the Missouri River and its tributaries provided barred owls with sufficient foraging habitat, protection from the weather, and concealment from avian predators. This allowed barred owls to move westward, initially solely along other forested river corridors (e.g. the Yellowstone and Musselshell ), but increases in forests in the northern Great Plains decades later would allow them to connect their eastern and western distributions across southern Canada. These increases in forests were caused by European-American settlers via wildfire suppression and ceasing the fires historically set by Native Americans , as well as by increased tree-planting. In Canada, the barred owls with range expansion now range through southern Manitoba (excluding the southwest corner), a broad section of south-central Saskatchewan , and east-central and nearly all of western Alberta , now up to High Level . The barred owl has been present in Manitoba at least since 1886, Alberta since 1932 and Saskatchewan since 1948. However, a study in Alberta has shown that barred owls have likely been present for no less than 100 years. This owl species currently ranges through much of British Columbia , where they have been expanding their range since at least 1943, including Vancouver Island and as far north as Fort St. John . The barred owl has had a further northward expansion in the west to southeastern Alaska ( Skagway to Ketchikan ) and extreme southwestern Yukon . In the western United States they also range into northwestern Montana and northern Idaho . Barred owls were first verified in southwest Montana in 1909 and in northwest Montana in 1921 (although reports of the species may date back to the 1870s) but not in Idaho until 1968. Of unknown origin, barred owls have been seen in Colorado since around the turn of the 20th century. They range broadly in eastern and western Washington (reached by 1965) and western Oregon (reached by 1972) (mostly along the forested corridors hugging the montane areas of the Cascade , Olympic and Blue ranges), and northern California (reached by 1976), now down to the Redwood National Forest , the Sierra Nevada and outer San Francisco . The habitat used by barred owl is largely old deciduous , mixed forests and, occasionally, coniferous forests . Old growth forests are preferred due to more extensive potential nest sites, less lower-branch density to impede hunting (and perhaps superior structural complexity to aid hunting), greater security from mobbing and perhaps greater thermoregulation . They are often found in bottomland hardwood forests in the largest swath of the native breeding range, often (particularly from Virginia south and west) with deep, dark stands of oak , gum and cypress . Secondary habitat, often used during foraging forays in the south, are often oak savanna or cabbage-palm areas. Regardless of area, some variety of water is frequently present, including riparian areas or swampy ground. Closed canopy forests were preferred in a study from Oklahoma (62.8% of habitat used), followed by fallow agricultural fields (10.6%), wetlands (8.1%) and open terrain (6.2%). The latter three were visited during hunting forays, and wetlands and open terrain areas were not used outside of the breeding season. Along the Atlantic coast area from New England to New Jersey , barred owls are often found in mixed swamps areas with cedars , seldom wandering to adjacent wetlands or farmland . The species may be at home in wooded areas in mountainous regions . More upland wooded habitats, often in mixed woods containing hemlock , alder , poplar , pine and oak , are typical in the northern part of the range. A study in northern New Jersey found at least 15 species of both conifer and deciduous trees were routinely used for differing purposes. In Michigan, barred owl habitat usually consists largely of some combination of hemlock and maple trees, with mixed forest usage being use disproportionately to its prevalence in the environment. Large oak stands were preferred in Minnesota , a bit ahead of mixed forest and far ahead of white cedar swamps and other habitat types, which were either too dense, too open or had too few attractive nesting sites. Barred owls are not confined to extensive forest, also dwelling extensively in semi-open wooded areas , locally in large parks with mature trees, and in forest adjacent regions recently logged . Recent studies show suburban neighborhoods can be ideal habitat for barred owls, and the species may be considered a local synanthrope . Using transmitters, scientists found that some regional populations, such as in Charlotte, North Carolina , increased faster in the suburban settings than in old growth forest . A factor of this suburban success may be easily accessible rodent prey in such settings. However, for breeding and roosting needs, this species needs at least some large trees and can be locally absent in some urban areas for this reason. The increased offspring offset the death rate due to impacts from cars, other types of collisions and disease. Similarly, in Piedmont, South Carolina , productivity of the owls was higher in suburban areas and they comprised 41% of the territories of the local owls but various sorts of anthropogenic mortality were seemingly higher. In suburban areas of Ohio , 41.4% of barred owl range was forested, 29.8% was low-density residential areas and less than 15% was pasture . On the other hand, studies from the Northeastern United States , such as in New Jersey , found barred owls breeding mainly in plots of old-growth woodlands, and rarely successfully breeding in peri-urban areas , in part because of competitive and predatory displacement by great horned owls . Furthermore, a study in North Carolina showed most barred owls appear to favor areas with at least 86 to 370 ha (210 to 910 acres) of woods but did not seem to be affected by the presence of roadways. In the Pacific Northwest , they can be quite adaptive to secondary forests . On the other hand, in Ontario where the barred owl is native, secondary forest seemed to be largely avoided per a study. In the recent western part of the range, barred owls often dwell in mixed wood areas, often where there are lowland stands of balsam poplar , trembling aspen and white spruce , occasionally but not commonly in pure conifer boreal stands . Barred owls in California preferred stands of red alder . More so confined to inland areas, as in eastern Washington, Idaho, Manitoba and Montana, they prefer Douglas fir, ponderosa pine , paper birch , burr oak and western larch . In north-central Alberta, the use of old growth forest was far more prevalent than its occurrence in the wild. In the Cascades Range of Washington, barred owls usually dwell in areas with more grand firs , taller and more diverse tree heights, more enclosed canopies, higher numbers of trees per acre and less ground cover. In Saskatchewan, barred owls preferred areas with a minimum of 66% forest cover. The barred owl, like most owls, is largely adapted to nocturnality . Between 5:00 am and 8:00 pm, juvenile barred owls were recorded to sleep an average of 28% of each hour. Peak times in Minnesota were found to be right after sunset and just before dawn. Nonetheless, they are not as fully nocturnal as many owls and rank around 6th amongst 19 regular North American owl species for the regularity of their activity outside of nightfall, especially in particular circumstances such as when a rival or a human impersonator is emitting barred owls calls or whilst hunting. Often daytime activity tends to be early in the morning or around dusk but potentially at any time ( overcast days being preferred). This species often spends the daytime hidden away in the dense foliage of a tree, often at minimum 5 m (16 ft) above the ground, but sometimes also roosts in a branch close to a broad trunk or in a natural tree hollow. Roost tree heights in Minnesota was typically 8 to 12 m (26 to 39 ft) while, in Illinois , they were up to 9 m (30 ft) . Recently fledged owls sometimes roost in tall grass, usually after falling from the nest tree. Roost site selection may be partially dictated by thermoregulation , as in spotted owls, with shadier roosts likely to mitigate heat stress . They seldom rely on camouflage , instead often flying at the least disturbance and not allowing close approaches, making them potentially difficult to observe. Yet, on the other hand, they can be surprisingly tame and seemingly curious of people in the wild; further they are considered "as mild and engaging" as a predator can be. Barred owls are regularly subject to mobbing by small birds, from several small passerines to corvids and woodpeckers , and mammals when discovered by them during the daytime, and such situations may lead to them being attacked by diurnal birds of prey. There are some records of barred owls engaging in allopreening , presumably between pairs, with each other in the wild. They are skilled and silent fliers and frequently use routine forest flyways with open understory and low branch densities. Like most species of owl in the Strix genus, the barred owl tends to be highly territorial regardless of the time of year. The territories are claimed by singing from different perches, often near the perimeter of its perceived home range. The boundaries are almost always well-maintained by barred owls and are generally stable from year to year and even generation to generation. Territory sizes have been determined via radio telemetry . The average territory size of 13 in Minnesota was 273 ha (670 acres) , of 7 in Michigan it was 282 ha (700 acres) and of 10 in Wisconsin was 337.9 ha (835 acres) . Another Minnesota study found pairs to occupy a mean of about 226 ha (560 acres) in mixed hardwood-conifer woods. Pairs in an Oklahoma study were reportedly found every 110 to 165 ha (270 to 410 acres) . The mean territory size from 10 studies was estimated from throughout the range. In this study, the breeding season mean area was calculated at 256.7 ha (634 acres) in males and 297.8 ha (736 acres) in females; whereas the means in nonbreeding season were 900.4 ha (2,225 acres) in males and 536.2 ha (1,325 acres) in females. Overall, the annual mean home range for males was 782 ha (1,930 acres) and for females was 538.7 ha (1,331 acres) . The breeding range's mean home size in Washington was 321 ha (790 acres) , while it was 971 ha (2,400 acres) in the non-breeding season. The ranges of pairs overlaps in the breeding season, at 87–95% range overlap, but decreases down to 45% after hatching. In a Florida study of barred owls, territorial responses, including several duets , by a pair were found to be provoked by researchers playing calls of both "stranger" owls and recordings of owls that were neighbors to the pair being tested. The aggressive response even to known neighbors in this study is unusual. In tawny owls in a study from Italy , for instance, they responded mildly or not at all to the calls of neighboring tawny owls known to them but with great aggression to the calls of "stranger" owls. Due to its rather stolidly territorial nature, the barred owl is not normally a migratory species. Claims in the past of "rather impressive" flights in New England in the past were lacking in verifiable details. Of 158 banded recoveries in the northern part of the range, movements during winter were found to cover no further than 10 km (6.2 mi) , while all those recovered in Saskatchewan and Alberta scarcely moved at all. There is little to no evidence of nomadic behavior as has been recorded in several other owls in the north. Barred owls are opportunistic predators of the woodlands. Like the tawny owl, the barred owl usually hunts from a perch. During hunting efforts, they glide briefly from perch to perch until prey is detected. The barred owl has incredibly large eyes that capture as much light as possible, allowing for better night vision. Attacks may be carried out merely 6 to 10 m (20 to 33 ft) away from the prey due to the effectiveness of the silencing wing feathers. The barred owl, especially compared to the predominantly arboreal prey of the spotted owl, usually prefers to target small animals that are terrestrial . However, barred owls will also flush and capture night-roosting birds, and capture bats on the wing as well. Daytime hunting has been reported several times, although peak hunting time is typically shortly after sunset. Although they usually hunt within woodlands, they also occasionally hunt in open terrain , more typical of the hunting areas of a bird like the long-eared owl. Cases of snow-plunging have been verified for barred owls, allowing them to capture prey like voles in subnivean zones that they use as hidden snow tunnels during winter, a hunting method once thought particular to great grey owls . While hunting squirrels in the Foothill Model Forest of Alberta , barred owls were seen to make several passes before succeeding. Hunting on the ground is usually done to obtain foods such as invertebrates or amphibians . These owls may wade into water to capture fish and may do an unusual amount of aquatic, for any Strix species or North American owl, foraging via wading into shallows. Due to its relatively modest foot size, it does not usually take particularly large prey. However, owls in general have proportionately larger feet and more powerful grips than similarly sized diurnal raptors, while the physiology of the daytime raptors differs . While the mechanism of the killing feet overlap, owls kill mainly with constriction and sacrifice velocity with their physiology while diurnal raptors have higher velocity and kill mainly by trauma inflicted by their enlarged talons. A majority of prey of barred owls is eaten outright but, with large prey, the barred owl may eat the head first and then return to consume the remainder of the body. Cases of owls of any variety scavenging on carrion are generally rare, but at least three instances of carrion-feeding by barred owls have been observed, more recently eating deer and squirrel roadkills on a remote camera in North Carolina. The pellet of the barred owl averages about 3.5 cm (1.4 in) in diameter and 7.2 cm (2.8 in) in length. The barred owl has been known to consume a diversity of animals from different taxonomic classes . Primarily, these owls live off of small mammals . Other vertebrates are rarely neglected though, especially birds and amphibians , but also occasionally reptiles and fish . For an owl its size, the barred owl also consumes a large amount of arthropods and other invertebrates . One study from a wide swath of the range found that among 2234 accrued prey items, 76% were mammals, 15.8% were invertebrates, 5.8% were birds and 2.5% were other vertebrates. In four other studies from different parts of the distribution, the mean balance of mammals in diet was around 64.9%, birds at around 13.4%, invertebrates at around 11.4% and different classes of vertebrates (mostly amphibians) at around 10.3%. A compilation study that included a total of 7077 prey items using all methodologies, 71.9% were mammals, 9.5% were birds, 0.6% reptiles, 6% amphibians, 1.89% fish, 1% earthworms , 0.2% gastropods , 6.5% insects and 2.4% crayfish . Barred owls tend to focus on fairly small-sized prey, although are capable of attacking larger than usual prey in infrequent cases. The mean size of prey taken is seldom estimated in the barred owls' eastern range, although one study estimated mean size of prey in the general east was 33.5 g (1.18 oz) . Many more studies have estimated mean prey masses in westerly areas of sympatry with spotted owls to understand how their diets may conflict. Different studies from the west (mainly Washington and Oregon ) have variously estimated the mean prey sizes for barred owls at 47.7 g (1.68 oz) , 56.1 g (1.98 oz) , 60.2 g (2.12 oz) , 103.5 g (3.65 oz) and 123.6 g (4.36 oz) . The predominant small mammals available in forest and woodland edges are generally small rodents , so the barred owl, like other Strix owls, most often relies on rodents as the primary type of food. Preferred rodents to be taken are voles , mice of the genus Peromyscus and assorted rats , including non-native Rattus species as well as unrelated native types like cotton rats , rice rats and woodrats . These all share with barred owls a penchant for nocturnality and crepuscular habits (although many voles are more correctly considered cathemeral ) While during other seasons, the diet of barred owls can be fairly diverse, the winter diet may be almost wholly rodents. This was the case in winter in Montana , where 97.6% of 1153 prey items were montane voles or meadow voles , with a possible slight mixture of other voles. The diet of barred owls in a much smaller study near Urbana, Illinois during winter was less homogeneous but still led by rodents, especially the meadow vole (32.3%) and white-footed mouse (23.5%). A winter food study in Essex County, New Jersey found that among 118 prey items, meadow voles comprised a great majority of the prey, at 91.5% of the balance. An unusual lack of diversity in barred owl pellets was found in several years of possibly an aseasonal study in Ann Arbor, Michigan where of 777 prey items, 83.3% were meadow voles. At Edwin S. George Preserve near the University of Michigan , the summer diet was also heavily rodent based, as among 146 prey items 37.9% were white-footed mice, 22.6% were southern bog lemming and 6.84% were meadow voles. In a somewhat larger Michigan study, the North American deermouse , lead the prey at 34.9% of 321 prey items. In Minnesota , the barred owl was counted as one of the leading causes of mortality of prairie voles . Studies of the barred owl diet in 6 urban metropolitan areas of British Columbia found that the diet was dominated by young rats of the invasive Rattus genus, comprising 52.8% of 688 prey items, well ahead of native Townsend's voles , which were secondary at 19.2% of the diet. The average weight rats taken by owls were clearly juveniles, estimated to average 103 g (3.6 oz) , although several could be anywhere from infant rat to adult rat sizes, i.e. about 25 to 300 g (0.88 to 10.58 oz) . The mean size of black rats taken in Oregon was 250 g (8.8 oz) , indicating that here large adults of this species were selected. Beyond the typical more meadow-dwelling voles and woodland edge-dwelling native mice, larger and more forest dwelling rodents of different varieties can be of variable import. Numerous woodrat species may be taken and may provide a hearty meal to a barred owl, at a mean body mass when taken (in Oregon ) of 285 g (10.1 oz) for unidentified species. In different areas, barred owls may regularly hunt the diverse members of the squirrel family, despite their general penchant for diurnality . Smaller squirrel varieties are usually focused on when hunted as supplement prey, such as chipmunks , averaging about 83 g (2.9 oz) among the different species they prey upon, and pine squirrels , which average about twice as large as chipmunks. Usually juvenile specimens are focused on when taking the larger Sciurus tree squirrels , at least in summer, but presumably a mixture of yearling and adult Sciurus will be taken during winter. The mean weight of western gray squirrels taken during the breeding season in Oregon was 450 g (16 oz) , against a mean adult weight of around 770 g (1.70 lb) . The issue of temporal activities is less pertinent to the predator of flying squirrels , which are nocturnal. All studies of the diet of barred owls in Pacific Northwest show the importance of the northern flying squirrel to their diet. This flying squirrel was found to comprise from about 10.9% to 20% of the diet of barred owls (either as the most or second most important prey species) and, with a mean weight of 134 g (4.7 oz) when taken, they comprised up to 25.6% of the food biomass for this owl species. In Green Ridge State Forest in Maryland , although not numerically the most important prey family compared to unidentified cricetids and shrews, the southern flying squirrel was the most often identified prey species for barred owls. Beyond the aforementioned rodent prey, more infrequently rodent prey can including various other cricetid rodents , pocket gophers , mountain beavers (average weight when taken of up to 550 g (1.21 lb) ) and jumping mice . The largest known rodent prey of barred owls are adult muskrat , which were estimated to weigh 1,169 g (2.577 lb) when taken. The other primary mammalian prey types are the shrews and the moles . At least a dozen species of shrew and most North American species of mole are known as prey of the barred owl. 12.8% of 7077 total prey items from across the range were shrews or moles . A small sample of prey in Michigan was led by the very small masked shrew , which weighs around 4 g (0.14 oz) , at 24% of 34 prey items. A much larger shrew, the northern short-tailed shrew at around 21 g (0.74 oz) , was the leading prey in Glenwood, Minnesota at 36% of 81 prey items. This prey species also is taken quite regularly in several other parts of the range, as well as a closely-related species . Assorted other shrew species and the smallest of the world's moles, the American shrew mole are regular supplement prey elsewhere, especially in the Pacific Northwest. The most frequently taken single prey species through the Pacific Northwest, at 11.8% of 4299 total prey items of barred owls, was the 56 g (2.0 oz) coast mole . Usually, moles are secondary if relatively hearty prey elsewhere in the range. Secondary prey can include several species of cottontail rabbits ( Sylvilagus sp.) and snowshoe hares ( Lepus americanus ). 3.2% of 7077 prey items from across the range for barred owls were rabbits or hares . Among cottontails, small juveniles are largely taken, but rabbits as large as an adult brush rabbits can be taken. The weights of snowshoe hares taken by barred owls in the Pacific Northwest were estimated at ranging from 50 g (0.11 lb) leverets to juveniles and standard-sized adults about 1,200 to 1,400 g (2.6 to 3.1 lb) . Bats are infrequently reported as prey in most of the range but an unusually close association was detected in Valdosta, Georgia , where most of the prey, 65% of pellet contents and 37 total bats, were southeastern myotis ( Myotis austroriparius ). Barred owls are also known predators of small mammalian carnivorans , mainly mustelids such as stoats ( Mustela erminea ) and long-tailed weasels ( Neogale frenata ). Predation on small American mink ( Neogale vison ) have also been reported. As they are seemingly not affected by strong odor, eastern spotted and western spotted skunks ( Spilogale gracilis & S. putorius ) of all ages can be taken. Much larger mammals are sometimes recorded in the foods of barred owls, but there are few details known about the age, condition, or circumstances (i.e. they may have been consumed as carrion or, perhaps more likely, young or infirm specimens were taken). Some such prey species recorded have included the Virginia opossum , the North American porcupine , the striped skunk and the domestic cat . Adults of all these species are known to count amongst the prey of great horned owls which are better suited than barred owls to take particularly large prey given its more robust morphology. Throughout the barred owl's range, other birds are taken as prey, although avian species make up a much smaller proportion of their diets than mammals. The maximum known representation of bird prey in a barred owl food study was 25.1% in Alberta , meaning that they augment their diet less heavily with bird prey than their near equivalent in Europe, the tawny owl . No specific variety of bird is subject to the most frequent predation by barred owls and birds are the most diverse class in these owl's prey spectrum, with more than 100 species of bird known to be hunted. Conspicuous nesting sites of barn swallow and purple martin on manmade structures and objects were revealed via video-monitoring to suffer heavy predation by barred owls. In the case of the barn swallows, all ages of swallow as well as possibly eggs were eaten. 65 of 95 monitoring barn swallow nests were consumed by owls over a 3-year period. The muddy bank nests of cliff swallows are also vulnerable to barred owls, while other swallow species are known to be opportunistically taken. In more enclosed wooded areas, radio-tagging and video-monitoring of various passerines nests as well as examinations of owl pellets has shed light on the relationship of barred owls with these potential prey resources. Not only was the barred owl found to be a surprisingly routine predator at woodland passerine nests, but that an unexpected bulk of the acts of predation in studies from Missouri and Illinois were carried out during the daytime. Many different forest bird species (most frequently acadian flycatchers and indigo buntings in Missouri and Illinois) were hunted. These studies indicated that the barred owl may snatch passerines of any age, but recent fledglings are taken preferentially due to their more conspicuous behavior and limited ability to fly away. In Minnesota, about 62% of studied hermit thrush and ovenbird fledglings were taken per one study, with all thrush that nested in the 50 m (160 ft) radius of the barred owl's nests failing to produce any young. A similarly high rate of local determent by barred owls has been found for other woodland thrushes like the veery , wood thrush and varied thrush , with the additional finding that pre-dawn singing by certain thrushes, when their escape abilities are dulled by the dim light, leaves them vulnerable to barred owl ambushes. Forest birds seem to recognize the barred owl as a threat, with mobbing behavior evoked easily by playing recordings of their calls in the daytime. A wide diversity of bird prey may be occasionally hunted by barred owls in different circumstances. Smaller or mid-sized bird prey species known have including different species, though usually a relatively low species diversity and in low numbers, beyond swallows and thrushes of tyrant flycatchers , vireos , chickadees , wrens , mimids , tanagers , other cardinalids and finches . Somewhat higher diversity of species are known from the sparrow and warbler families. Birds down to the size of the calliope hummingbird , North America's smallest hummingbird at 2.7 g (0.095 oz) , may be taken by barred owls. At the opposite end of passerine prey for barred owls, this species will sometimes take all ages of the American crow , from very young nestlings to adults. Numerous non-passerine birds are also taken, though seldom in great numbers and of low known species diversity. One exceptional family is the woodpeckers , which are probably so widely taken because of their generally overlapping habitat preferences with those of barred owls. Several species of woodpecker are preyed upon almost throughout the range, including at least a half dozen in Oregon alone, from the smallest North American species, the downy woodpecker , to the largest, the pileated woodpecker . Other small-to-medium-sized bird species known as prey for barred owls are: mountain quail , grey partridge , rock dove , band-tailed pigeon , mourning dove , purple gallinule , killdeer , American woodcock , least tern , snowy egret , cattle egret and belted kingfisher . Although they take many chicks of gamebirds, adults of these species are vulnerable as well. In many areas, ruffed grouse are not infrequently taken, comprising up to nearly 6% of prey items in Alberta. In Oregon, the weights estimated for ruffed grouse taken by barred owls varied enormously, from small chicks estimated at 25 g (0.88 oz) , to adults weighing about 576 g (1.270 lb) . Broader study in the Pacific Northwest indicated that adult ruffed grouse were mainly taken. Barred owls are also known to take adult spruce grouse of about the same size as the ruffed grouse, as well as much larger species including the common pheasant and the sooty grouse , the latter estimated to average 1,050 g (2.31 lb) when taken. Barred owls are also known to prey on the young of other, larger birds, such as the American white ibis and wild turkey . Barred owl predation on reptiles is widely reported but they seldom take large numbers in any given area. Most reported instances of such captures are of various small lizards , often of skinks in the genus Plestiodon , most often from the Midwest to the western parts of the range. Several reported instances of barred owls hunting snakes are also known, but they are perhaps even more seldom preyed upon than lizards. More than a half dozen snake species are known to be captured, several of which are colubrids , which are mostly harmless. The estimated body mass of black racer taken in Oregon was only 77 g (2.7 oz) , well under their mean mature size. However, consumption or predation on dangerous pit vipers , such as timber rattlesnakes and copperheads , by barred owls has been reported, although it is not known whether these are taken as adults. Rarer still is barred owl predation on turtles . Predation by this species was reported upon a very young river cooter , which had a carapace width of only 31.4 mm (1.24 in) , as well as on juvenile gopher tortoise and apparently diamondback terrapin . Much more characteristic than any reptilian prey are amphibians , with various types of frogs , salamanders and similar species reported in this owl's foods. Amphibians were considerably more popular in the diet in western part of range, comprising 10.5% of known studies against 4.4% in the east. In total, well over 20 amphibian species have been identified in the foods of barred owls and amphibians collectively can make up to 24.5% of the local diet (as was reported in Alberta). While salamanders and newts are probably often visually discerned while scanning the forest floor, many frogs are probably hunted down by sound during their crepuscular choruses. Amphibians are taken almost entirely during the breeding season, as they become unavailable to barred owls during the winter months. Most reported amphibian prey in Oregon were unidentified "medium-sized salamanders". A diversity of frog sizes may be taken, varying potentially in size from spring peepers , which average around 4 g (0.14 oz) , to American bullfrogs , which average around in mature bullfrogs 430 g (15 oz) . A notable act of successful predation was carried out by a barred owl on a rough-skinned newt , which contains toxins that are often deadly to predators. Apparently, the owl was able to survive after consuming the newt. The rarest variety of vertebrate prey for barred owls is fish. However, there are several accrued accounts of fishing by these owls, including older accounts of barred owls coming to ice holes made by human fishermen and more recent accounts of possibly routine fishing by the owls on the St. Johns River in Florida, in the latter case utilizing a fishing dock as a hunting perch. At least five species of fish have been identified in the foods of barred owls, including fairly large fish like brown bullheads and largemouth bass . The balance of assorted invertebrates in the diet of barred owls can be quite high. Although many of those found in pellets are unidentified to species, nearly 40 species of invertebrates have been found in their foods. Broad studies indicate arthropods (including millipedes and spiders but predominantly insects ) in general comprise up to about 16% of the barred owl's foods. When hunting insects , barred owls most often prefer ground-based beetles . In Oregon, 11.7% of the diet was assorted beetles (14 species were identified), being somewhat more numerous among 3686 prey items than other non-rodent prey orders. However, some insects prey such as luna moth , eastern tiger swallowtail and green darner are presumably hawked on the wing around dawn and dusk. It is known that barred owls will sometimes come hunt near manmade light sources and campfires , flying out from the perch to quickly capture flying insects that were attracted to them. Of 123 prey items found in southern Manitoba, flying Sphinx moths and flightless scarab beetles each comprised 7% (most of the remaining balance being unidentified mammals and birds). Crayfish of at least four identified species are another widely taken type of invertebrate, presumably snatched up by barred owls from shallow waterways. Crayfish seem to be exclusively taken in the east and Midwest, areas where they comprised 3.4% of all known food studies, and none at all were recorded in the western part of the range. In Missouri , annually up to 31.1% (though, in some years, 0%) of the diet was comprised by crayfish. Barred owls occasionally feed on snails and slugs , the latter especially in the Pacific Northwest. Another snail, the Pacific sideband , was surprisingly often present in the foods in Oregon as at least 135 were taken. Beyond slugs, other "soft" invertebrates are sometimes hunted, especially earthworms . Earthworms were most prominent in the foods of barred owls in Nova Scotia , where 27.6% of 186 video-monitored prey deliveries in Nova Scotia were worms, the most regularly delivered of all prey types there. The barred owl's range overlaps with multiple other predators of similar prey species. Due to the time period barred owls are active, the most interaction occurs with other owl species. Of the owls in North America, about three-quarters are reliant on similar small mammal prey, usually rodents, with a mixture of other prey genera as supplements. Other than its ecology where it today co-exists with spotted owls, however, there is some level of niche differentiation from a majority of sympatric owls. In the eastern forest biome, the barred owl is the only large owl species to dwell mainly in continuous forest areas. While many of the owls sympatric with barred owls over majority of their eastern and Midwestern range share a preference for hole-nesting, smaller hole-nesting owls usually prefer different habitats, such as the open country-dwelling barn owl and the screech owls , which usually in North America dwell at the interface of forest and open habitats. Both North American species in the Aegolius owl genus are forest-dwelling cavity nesters but are much smaller and are at entirely different trophic levels . A singular diurnal raptor species that mirrors the barred owl at nearly all ecological levels is the red-shouldered hawk . Both species have similar distributions, habitat preferences and somewhat similar dietary habits and trophic level. They may considered as nearly nocturnal and diurnal ecological equivalents . In multiple parts of the range, including southwestern Ohio, North Carolina and northern Michigan, the paralleling habitat usage and nesting behavior of the barred owl and red-shouldered hawk has been noted. One of the few respects in which their habitat usage differs is that the barred owl is more adaptive to nesting in suburban areas if they have old growth trees that provide plentiful tree hollows . In contrast, red-shouldered hawks tend to avoid suburban areas whilst nesting, but may acclimate to these areas during the winter. Barred owls seldom alter their range throughout the year and remain more or less constrained to the stands they used during nesting. The red-shouldered hawk averages somewhat smaller and has a more limited diet than barred owls, but probably goes after dangerous prey such as snakes more regularly. Multiple occasions are recorded where the barred owl and red-shouldered hawk have nested in the same area, often within the same grove of trees, remarkably with little to no conflict. At least one nest was found including eggs from both species. When nesting near other hawks like red-tailed hawks and Cooper's hawks , the relationship tends to be much more contentious between hawk and owl, despite barred owls sometimes sharing space or using the old nests of these hawks. A wing-clapping display by a pair of barred owls was recorded during antagonistic encounters in Manitoba with a pair of broad-winged hawks . Wing-claps were previously not recorded in this species, and when recorded for other owl species were often for the purposes of courtship displays. One predator that is a major source of conflict for the barred owl is the great horned owl . In every part of their range, barred owls are compelled to share space with the larger owls. There is habitat partitioning between the barred owl and great horned owl that allows them to often co-exist. Great horned owls prefer various more open habitats mixed with trees, often in rather upland areas, which differs from the habitats preferred by the barred owl. If a great horned owl moves into an area, barred owls appear to avoid said areas, based on radio telemetry data. In much of the east, habitat alteration and fragmentation tends to favor the great horned owl at the expense of the barred owl. Where more continuous forest is available, however, the great horned and barred owl can occur surprisingly close to one another. In one case, a barred owl was observed to roost only 400 m (1,300 ft) from a great horned owl. In general the reforestation at the northern sections of the Great Plains have, on the contrary, benefited barred owls (and may have been a part of allowing their westward expansion) and been perhaps slightly detrimental to the great horned owl. However, even where the habitat becomes less ideal, the great horned owl is unlikely to vacate an area, unlike the barred owl which can be entirely displaced if woods become too small and fragmented. Great horned owls and barred owls have similar diets, as both are wide-ranging, large and opportunistic owls. However, the great horned owl is larger in bulk, sometimes averaging nearly twice as heavy, with much heavier, larger feet and talons. The great horned owl has a more powerful grip strength and access to a wider variety of prey than barred owls, which take fewer prey species because they occur in more limited habitats and have a smaller overall distribution. A study utilizing stable isotopes in Alberta appeared to confirm that the great horned owl preys on nearly twice as many prey species as do the barred owls of the area. The great horned owl is indeed likely to be the greatest natural enemy of the barred owl. There are several accounts of the horned owl species preying on nestlings, fledglings and adults of the barred. Other than horned owls, predation of the barred owl seems to be fairly rare outside of the nestling age, both due to the owl's relatively large size and their nesting habits, most often in secluded tree hollows. One more virulent nest predator is likely to be raccoons ( Procyon lotor ), which can nearly decimate both tree hollow and stick nest locations of almost any kind of bird, especially in peri-urban areas where they largely exist without controlling predators. Both the American marten and the fisher are known to be nest predators of barred owls, in turn appearing to cause the owls to switch nest sites. Other birds of prey may be an occasional threat to barred owls. Northern goshawks have reportedly killed both young and adult barred owls. One modern account mentions predation by a goshawk on a nestling barred owl (i.e. weight about 392 g (13.8 oz) ). A well-known instance of a goshawk attack on an adult barred owl concluded with the owl and goshawk killing one another. There are some very rare, singular cases of predation on barred owls (age unknown) by red-tailed hawks , which nonetheless generally appears to be a less menacing co-inhabitant than the goshawk. More surprisingly, a Cooper's hawk , a smaller species of raptor, was observed to apparently prey upon a full-grown barred owl in British Columbia. An American alligator was reported to have preyed on a barred owl in at least one instance. On the other hand, the barred owl is a significant predator of smaller raptor species as well. Most smaller owls that co-exist with barred owls are at occasional risk of predation. A particular cause of concern in intraguild predations [ definition needed ] by the barred has been their encroachment into the areas inhabited by western screech owl ( Megascops kennicotti ). Several instances of predation have been noted on the screech owls and the recent, unprecedented presence of the barred owls appears to have a correlation with the decline of the western screech owl in British Columbia and in Bainbridge Island, Washington . In one instance, a biologist who called in an eastern screech owl ( Megascops asio ) in Ohio observed it to be immediately captured and consumed by a barred owl. The barred owl is a serious predator of eastern screech owls, but is less deadly to them in general than the great horned owl. Various additional owl species known to be preyed upon by barred owls including the flammulated owl ( Psiloscops flammeolus ), northern pygmy owl ( Glaucidium gnoma ), northern saw-whet owl ( Aegolius acadius ) and long-eared owl ( Asio otus ). The interspecific owl trophic chain was perhaps most conspicuous in a case where a barred owl that was shot in New England was found to have a long-eared owl inside its stomach which in turn had an eastern screech-owl in its own stomach. More unexpectedly, barred owls may even prey on other Strix species. As many as four records of circumstantial but likely predation by barred owls on spotted owls have been reported. A likely event of predation by a barred owl on an adult great grey owl was observed. The authors hypothesized that the victim may have been a smaller male great grey owl (which can be about the same body mass as a large female barred) but this is the only known instance to date of a great gray owl being killed by another species of Strix owl. Barred owls have been known to take adults (or full-grown juveniles) of diurnal raptors as well, including snail kites , Cooper's hawks , sharp-shinned hawks and possibly swallow-tailed kites . The predominant small mammals available in forest and woodland edges are generally small rodents , so the barred owl, like other Strix owls, most often relies on rodents as the primary type of food. Preferred rodents to be taken are voles , mice of the genus Peromyscus and assorted rats , including non-native Rattus species as well as unrelated native types like cotton rats , rice rats and woodrats . These all share with barred owls a penchant for nocturnality and crepuscular habits (although many voles are more correctly considered cathemeral ) While during other seasons, the diet of barred owls can be fairly diverse, the winter diet may be almost wholly rodents. This was the case in winter in Montana , where 97.6% of 1153 prey items were montane voles or meadow voles , with a possible slight mixture of other voles. The diet of barred owls in a much smaller study near Urbana, Illinois during winter was less homogeneous but still led by rodents, especially the meadow vole (32.3%) and white-footed mouse (23.5%). A winter food study in Essex County, New Jersey found that among 118 prey items, meadow voles comprised a great majority of the prey, at 91.5% of the balance. An unusual lack of diversity in barred owl pellets was found in several years of possibly an aseasonal study in Ann Arbor, Michigan where of 777 prey items, 83.3% were meadow voles. At Edwin S. George Preserve near the University of Michigan , the summer diet was also heavily rodent based, as among 146 prey items 37.9% were white-footed mice, 22.6% were southern bog lemming and 6.84% were meadow voles. In a somewhat larger Michigan study, the North American deermouse , lead the prey at 34.9% of 321 prey items. In Minnesota , the barred owl was counted as one of the leading causes of mortality of prairie voles . Studies of the barred owl diet in 6 urban metropolitan areas of British Columbia found that the diet was dominated by young rats of the invasive Rattus genus, comprising 52.8% of 688 prey items, well ahead of native Townsend's voles , which were secondary at 19.2% of the diet. The average weight rats taken by owls were clearly juveniles, estimated to average 103 g (3.6 oz) , although several could be anywhere from infant rat to adult rat sizes, i.e. about 25 to 300 g (0.88 to 10.58 oz) . The mean size of black rats taken in Oregon was 250 g (8.8 oz) , indicating that here large adults of this species were selected. Beyond the typical more meadow-dwelling voles and woodland edge-dwelling native mice, larger and more forest dwelling rodents of different varieties can be of variable import. Numerous woodrat species may be taken and may provide a hearty meal to a barred owl, at a mean body mass when taken (in Oregon ) of 285 g (10.1 oz) for unidentified species. In different areas, barred owls may regularly hunt the diverse members of the squirrel family, despite their general penchant for diurnality . Smaller squirrel varieties are usually focused on when hunted as supplement prey, such as chipmunks , averaging about 83 g (2.9 oz) among the different species they prey upon, and pine squirrels , which average about twice as large as chipmunks. Usually juvenile specimens are focused on when taking the larger Sciurus tree squirrels , at least in summer, but presumably a mixture of yearling and adult Sciurus will be taken during winter. The mean weight of western gray squirrels taken during the breeding season in Oregon was 450 g (16 oz) , against a mean adult weight of around 770 g (1.70 lb) . The issue of temporal activities is less pertinent to the predator of flying squirrels , which are nocturnal. All studies of the diet of barred owls in Pacific Northwest show the importance of the northern flying squirrel to their diet. This flying squirrel was found to comprise from about 10.9% to 20% of the diet of barred owls (either as the most or second most important prey species) and, with a mean weight of 134 g (4.7 oz) when taken, they comprised up to 25.6% of the food biomass for this owl species. In Green Ridge State Forest in Maryland , although not numerically the most important prey family compared to unidentified cricetids and shrews, the southern flying squirrel was the most often identified prey species for barred owls. Beyond the aforementioned rodent prey, more infrequently rodent prey can including various other cricetid rodents , pocket gophers , mountain beavers (average weight when taken of up to 550 g (1.21 lb) ) and jumping mice . The largest known rodent prey of barred owls are adult muskrat , which were estimated to weigh 1,169 g (2.577 lb) when taken. The other primary mammalian prey types are the shrews and the moles . At least a dozen species of shrew and most North American species of mole are known as prey of the barred owl. 12.8% of 7077 total prey items from across the range were shrews or moles . A small sample of prey in Michigan was led by the very small masked shrew , which weighs around 4 g (0.14 oz) , at 24% of 34 prey items. A much larger shrew, the northern short-tailed shrew at around 21 g (0.74 oz) , was the leading prey in Glenwood, Minnesota at 36% of 81 prey items. This prey species also is taken quite regularly in several other parts of the range, as well as a closely-related species . Assorted other shrew species and the smallest of the world's moles, the American shrew mole are regular supplement prey elsewhere, especially in the Pacific Northwest. The most frequently taken single prey species through the Pacific Northwest, at 11.8% of 4299 total prey items of barred owls, was the 56 g (2.0 oz) coast mole . Usually, moles are secondary if relatively hearty prey elsewhere in the range. Secondary prey can include several species of cottontail rabbits ( Sylvilagus sp.) and snowshoe hares ( Lepus americanus ). 3.2% of 7077 prey items from across the range for barred owls were rabbits or hares . Among cottontails, small juveniles are largely taken, but rabbits as large as an adult brush rabbits can be taken. The weights of snowshoe hares taken by barred owls in the Pacific Northwest were estimated at ranging from 50 g (0.11 lb) leverets to juveniles and standard-sized adults about 1,200 to 1,400 g (2.6 to 3.1 lb) . Bats are infrequently reported as prey in most of the range but an unusually close association was detected in Valdosta, Georgia , where most of the prey, 65% of pellet contents and 37 total bats, were southeastern myotis ( Myotis austroriparius ). Barred owls are also known predators of small mammalian carnivorans , mainly mustelids such as stoats ( Mustela erminea ) and long-tailed weasels ( Neogale frenata ). Predation on small American mink ( Neogale vison ) have also been reported. As they are seemingly not affected by strong odor, eastern spotted and western spotted skunks ( Spilogale gracilis & S. putorius ) of all ages can be taken. Much larger mammals are sometimes recorded in the foods of barred owls, but there are few details known about the age, condition, or circumstances (i.e. they may have been consumed as carrion or, perhaps more likely, young or infirm specimens were taken). Some such prey species recorded have included the Virginia opossum , the North American porcupine , the striped skunk and the domestic cat . Adults of all these species are known to count amongst the prey of great horned owls which are better suited than barred owls to take particularly large prey given its more robust morphology. Throughout the barred owl's range, other birds are taken as prey, although avian species make up a much smaller proportion of their diets than mammals. The maximum known representation of bird prey in a barred owl food study was 25.1% in Alberta , meaning that they augment their diet less heavily with bird prey than their near equivalent in Europe, the tawny owl . No specific variety of bird is subject to the most frequent predation by barred owls and birds are the most diverse class in these owl's prey spectrum, with more than 100 species of bird known to be hunted. Conspicuous nesting sites of barn swallow and purple martin on manmade structures and objects were revealed via video-monitoring to suffer heavy predation by barred owls. In the case of the barn swallows, all ages of swallow as well as possibly eggs were eaten. 65 of 95 monitoring barn swallow nests were consumed by owls over a 3-year period. The muddy bank nests of cliff swallows are also vulnerable to barred owls, while other swallow species are known to be opportunistically taken. In more enclosed wooded areas, radio-tagging and video-monitoring of various passerines nests as well as examinations of owl pellets has shed light on the relationship of barred owls with these potential prey resources. Not only was the barred owl found to be a surprisingly routine predator at woodland passerine nests, but that an unexpected bulk of the acts of predation in studies from Missouri and Illinois were carried out during the daytime. Many different forest bird species (most frequently acadian flycatchers and indigo buntings in Missouri and Illinois) were hunted. These studies indicated that the barred owl may snatch passerines of any age, but recent fledglings are taken preferentially due to their more conspicuous behavior and limited ability to fly away. In Minnesota, about 62% of studied hermit thrush and ovenbird fledglings were taken per one study, with all thrush that nested in the 50 m (160 ft) radius of the barred owl's nests failing to produce any young. A similarly high rate of local determent by barred owls has been found for other woodland thrushes like the veery , wood thrush and varied thrush , with the additional finding that pre-dawn singing by certain thrushes, when their escape abilities are dulled by the dim light, leaves them vulnerable to barred owl ambushes. Forest birds seem to recognize the barred owl as a threat, with mobbing behavior evoked easily by playing recordings of their calls in the daytime. A wide diversity of bird prey may be occasionally hunted by barred owls in different circumstances. Smaller or mid-sized bird prey species known have including different species, though usually a relatively low species diversity and in low numbers, beyond swallows and thrushes of tyrant flycatchers , vireos , chickadees , wrens , mimids , tanagers , other cardinalids and finches . Somewhat higher diversity of species are known from the sparrow and warbler families. Birds down to the size of the calliope hummingbird , North America's smallest hummingbird at 2.7 g (0.095 oz) , may be taken by barred owls. At the opposite end of passerine prey for barred owls, this species will sometimes take all ages of the American crow , from very young nestlings to adults. Numerous non-passerine birds are also taken, though seldom in great numbers and of low known species diversity. One exceptional family is the woodpeckers , which are probably so widely taken because of their generally overlapping habitat preferences with those of barred owls. Several species of woodpecker are preyed upon almost throughout the range, including at least a half dozen in Oregon alone, from the smallest North American species, the downy woodpecker , to the largest, the pileated woodpecker . Other small-to-medium-sized bird species known as prey for barred owls are: mountain quail , grey partridge , rock dove , band-tailed pigeon , mourning dove , purple gallinule , killdeer , American woodcock , least tern , snowy egret , cattle egret and belted kingfisher . Although they take many chicks of gamebirds, adults of these species are vulnerable as well. In many areas, ruffed grouse are not infrequently taken, comprising up to nearly 6% of prey items in Alberta. In Oregon, the weights estimated for ruffed grouse taken by barred owls varied enormously, from small chicks estimated at 25 g (0.88 oz) , to adults weighing about 576 g (1.270 lb) . Broader study in the Pacific Northwest indicated that adult ruffed grouse were mainly taken. Barred owls are also known to take adult spruce grouse of about the same size as the ruffed grouse, as well as much larger species including the common pheasant and the sooty grouse , the latter estimated to average 1,050 g (2.31 lb) when taken. Barred owls are also known to prey on the young of other, larger birds, such as the American white ibis and wild turkey . Barred owl predation on reptiles is widely reported but they seldom take large numbers in any given area. Most reported instances of such captures are of various small lizards , often of skinks in the genus Plestiodon , most often from the Midwest to the western parts of the range. Several reported instances of barred owls hunting snakes are also known, but they are perhaps even more seldom preyed upon than lizards. More than a half dozen snake species are known to be captured, several of which are colubrids , which are mostly harmless. The estimated body mass of black racer taken in Oregon was only 77 g (2.7 oz) , well under their mean mature size. However, consumption or predation on dangerous pit vipers , such as timber rattlesnakes and copperheads , by barred owls has been reported, although it is not known whether these are taken as adults. Rarer still is barred owl predation on turtles . Predation by this species was reported upon a very young river cooter , which had a carapace width of only 31.4 mm (1.24 in) , as well as on juvenile gopher tortoise and apparently diamondback terrapin . Much more characteristic than any reptilian prey are amphibians , with various types of frogs , salamanders and similar species reported in this owl's foods. Amphibians were considerably more popular in the diet in western part of range, comprising 10.5% of known studies against 4.4% in the east. In total, well over 20 amphibian species have been identified in the foods of barred owls and amphibians collectively can make up to 24.5% of the local diet (as was reported in Alberta). While salamanders and newts are probably often visually discerned while scanning the forest floor, many frogs are probably hunted down by sound during their crepuscular choruses. Amphibians are taken almost entirely during the breeding season, as they become unavailable to barred owls during the winter months. Most reported amphibian prey in Oregon were unidentified "medium-sized salamanders". A diversity of frog sizes may be taken, varying potentially in size from spring peepers , which average around 4 g (0.14 oz) , to American bullfrogs , which average around in mature bullfrogs 430 g (15 oz) . A notable act of successful predation was carried out by a barred owl on a rough-skinned newt , which contains toxins that are often deadly to predators. Apparently, the owl was able to survive after consuming the newt. The rarest variety of vertebrate prey for barred owls is fish. However, there are several accrued accounts of fishing by these owls, including older accounts of barred owls coming to ice holes made by human fishermen and more recent accounts of possibly routine fishing by the owls on the St. Johns River in Florida, in the latter case utilizing a fishing dock as a hunting perch. At least five species of fish have been identified in the foods of barred owls, including fairly large fish like brown bullheads and largemouth bass . The balance of assorted invertebrates in the diet of barred owls can be quite high. Although many of those found in pellets are unidentified to species, nearly 40 species of invertebrates have been found in their foods. Broad studies indicate arthropods (including millipedes and spiders but predominantly insects ) in general comprise up to about 16% of the barred owl's foods. When hunting insects , barred owls most often prefer ground-based beetles . In Oregon, 11.7% of the diet was assorted beetles (14 species were identified), being somewhat more numerous among 3686 prey items than other non-rodent prey orders. However, some insects prey such as luna moth , eastern tiger swallowtail and green darner are presumably hawked on the wing around dawn and dusk. It is known that barred owls will sometimes come hunt near manmade light sources and campfires , flying out from the perch to quickly capture flying insects that were attracted to them. Of 123 prey items found in southern Manitoba, flying Sphinx moths and flightless scarab beetles each comprised 7% (most of the remaining balance being unidentified mammals and birds). Crayfish of at least four identified species are another widely taken type of invertebrate, presumably snatched up by barred owls from shallow waterways. Crayfish seem to be exclusively taken in the east and Midwest, areas where they comprised 3.4% of all known food studies, and none at all were recorded in the western part of the range. In Missouri , annually up to 31.1% (though, in some years, 0%) of the diet was comprised by crayfish. Barred owls occasionally feed on snails and slugs , the latter especially in the Pacific Northwest. Another snail, the Pacific sideband , was surprisingly often present in the foods in Oregon as at least 135 were taken. Beyond slugs, other "soft" invertebrates are sometimes hunted, especially earthworms . Earthworms were most prominent in the foods of barred owls in Nova Scotia , where 27.6% of 186 video-monitored prey deliveries in Nova Scotia were worms, the most regularly delivered of all prey types there. The barred owl's range overlaps with multiple other predators of similar prey species. Due to the time period barred owls are active, the most interaction occurs with other owl species. Of the owls in North America, about three-quarters are reliant on similar small mammal prey, usually rodents, with a mixture of other prey genera as supplements. Other than its ecology where it today co-exists with spotted owls, however, there is some level of niche differentiation from a majority of sympatric owls. In the eastern forest biome, the barred owl is the only large owl species to dwell mainly in continuous forest areas. While many of the owls sympatric with barred owls over majority of their eastern and Midwestern range share a preference for hole-nesting, smaller hole-nesting owls usually prefer different habitats, such as the open country-dwelling barn owl and the screech owls , which usually in North America dwell at the interface of forest and open habitats. Both North American species in the Aegolius owl genus are forest-dwelling cavity nesters but are much smaller and are at entirely different trophic levels . A singular diurnal raptor species that mirrors the barred owl at nearly all ecological levels is the red-shouldered hawk . Both species have similar distributions, habitat preferences and somewhat similar dietary habits and trophic level. They may considered as nearly nocturnal and diurnal ecological equivalents . In multiple parts of the range, including southwestern Ohio, North Carolina and northern Michigan, the paralleling habitat usage and nesting behavior of the barred owl and red-shouldered hawk has been noted. One of the few respects in which their habitat usage differs is that the barred owl is more adaptive to nesting in suburban areas if they have old growth trees that provide plentiful tree hollows . In contrast, red-shouldered hawks tend to avoid suburban areas whilst nesting, but may acclimate to these areas during the winter. Barred owls seldom alter their range throughout the year and remain more or less constrained to the stands they used during nesting. The red-shouldered hawk averages somewhat smaller and has a more limited diet than barred owls, but probably goes after dangerous prey such as snakes more regularly. Multiple occasions are recorded where the barred owl and red-shouldered hawk have nested in the same area, often within the same grove of trees, remarkably with little to no conflict. At least one nest was found including eggs from both species. When nesting near other hawks like red-tailed hawks and Cooper's hawks , the relationship tends to be much more contentious between hawk and owl, despite barred owls sometimes sharing space or using the old nests of these hawks. A wing-clapping display by a pair of barred owls was recorded during antagonistic encounters in Manitoba with a pair of broad-winged hawks . Wing-claps were previously not recorded in this species, and when recorded for other owl species were often for the purposes of courtship displays. One predator that is a major source of conflict for the barred owl is the great horned owl . In every part of their range, barred owls are compelled to share space with the larger owls. There is habitat partitioning between the barred owl and great horned owl that allows them to often co-exist. Great horned owls prefer various more open habitats mixed with trees, often in rather upland areas, which differs from the habitats preferred by the barred owl. If a great horned owl moves into an area, barred owls appear to avoid said areas, based on radio telemetry data. In much of the east, habitat alteration and fragmentation tends to favor the great horned owl at the expense of the barred owl. Where more continuous forest is available, however, the great horned and barred owl can occur surprisingly close to one another. In one case, a barred owl was observed to roost only 400 m (1,300 ft) from a great horned owl. In general the reforestation at the northern sections of the Great Plains have, on the contrary, benefited barred owls (and may have been a part of allowing their westward expansion) and been perhaps slightly detrimental to the great horned owl. However, even where the habitat becomes less ideal, the great horned owl is unlikely to vacate an area, unlike the barred owl which can be entirely displaced if woods become too small and fragmented. Great horned owls and barred owls have similar diets, as both are wide-ranging, large and opportunistic owls. However, the great horned owl is larger in bulk, sometimes averaging nearly twice as heavy, with much heavier, larger feet and talons. The great horned owl has a more powerful grip strength and access to a wider variety of prey than barred owls, which take fewer prey species because they occur in more limited habitats and have a smaller overall distribution. A study utilizing stable isotopes in Alberta appeared to confirm that the great horned owl preys on nearly twice as many prey species as do the barred owls of the area. The great horned owl is indeed likely to be the greatest natural enemy of the barred owl. There are several accounts of the horned owl species preying on nestlings, fledglings and adults of the barred. Other than horned owls, predation of the barred owl seems to be fairly rare outside of the nestling age, both due to the owl's relatively large size and their nesting habits, most often in secluded tree hollows. One more virulent nest predator is likely to be raccoons ( Procyon lotor ), which can nearly decimate both tree hollow and stick nest locations of almost any kind of bird, especially in peri-urban areas where they largely exist without controlling predators. Both the American marten and the fisher are known to be nest predators of barred owls, in turn appearing to cause the owls to switch nest sites. Other birds of prey may be an occasional threat to barred owls. Northern goshawks have reportedly killed both young and adult barred owls. One modern account mentions predation by a goshawk on a nestling barred owl (i.e. weight about 392 g (13.8 oz) ). A well-known instance of a goshawk attack on an adult barred owl concluded with the owl and goshawk killing one another. There are some very rare, singular cases of predation on barred owls (age unknown) by red-tailed hawks , which nonetheless generally appears to be a less menacing co-inhabitant than the goshawk. More surprisingly, a Cooper's hawk , a smaller species of raptor, was observed to apparently prey upon a full-grown barred owl in British Columbia. An American alligator was reported to have preyed on a barred owl in at least one instance. On the other hand, the barred owl is a significant predator of smaller raptor species as well. Most smaller owls that co-exist with barred owls are at occasional risk of predation. A particular cause of concern in intraguild predations [ definition needed ] by the barred has been their encroachment into the areas inhabited by western screech owl ( Megascops kennicotti ). Several instances of predation have been noted on the screech owls and the recent, unprecedented presence of the barred owls appears to have a correlation with the decline of the western screech owl in British Columbia and in Bainbridge Island, Washington . In one instance, a biologist who called in an eastern screech owl ( Megascops asio ) in Ohio observed it to be immediately captured and consumed by a barred owl. The barred owl is a serious predator of eastern screech owls, but is less deadly to them in general than the great horned owl. Various additional owl species known to be preyed upon by barred owls including the flammulated owl ( Psiloscops flammeolus ), northern pygmy owl ( Glaucidium gnoma ), northern saw-whet owl ( Aegolius acadius ) and long-eared owl ( Asio otus ). The interspecific owl trophic chain was perhaps most conspicuous in a case where a barred owl that was shot in New England was found to have a long-eared owl inside its stomach which in turn had an eastern screech-owl in its own stomach. More unexpectedly, barred owls may even prey on other Strix species. As many as four records of circumstantial but likely predation by barred owls on spotted owls have been reported. A likely event of predation by a barred owl on an adult great grey owl was observed. The authors hypothesized that the victim may have been a smaller male great grey owl (which can be about the same body mass as a large female barred) but this is the only known instance to date of a great gray owl being killed by another species of Strix owl. Barred owls have been known to take adults (or full-grown juveniles) of diurnal raptors as well, including snail kites , Cooper's hawks , sharp-shinned hawks and possibly swallow-tailed kites . The barred owl's preferred nest site is usually the hollow trunk of a large tree or the broken-off snag from a large tree branch. Hollows or snags may be made by any variety of sources, often due to a disease or storm, with hollows and snags large enough to accommodate these birds usually only occurring in an old-growth tree. Typically, nest sites are in rather deep and dark wooded areas, often with a well-developed understory but somewhat sparse lower branches, and may be fairly close to water. Average nest heights are between 6.8 and 13.4 m (22 and 44 ft) above the ground. In 25 studies from throughout the range, mean nest tree height was 18.2 m (60 ft) (lowest mean from Florida where it was 5.9 m (19 ft) ; the highest from Oregon where it was 28 m (92 ft) ), mean nest tree diameter was 65.7 cm (25.9 in) (thinnest mean in Saskatchewan at 47.4 cm (18.7 in) ; thickest in Washington at 106 cm (42 in) ), while the mean height of the tree cavity used from these studies was 9.8 m (32 ft) . A big beech with a rotting core, encompassing a large cavity reached through a deep crevice, is an ideal nest site. The most widely reported nesting trees in breeding cards were elms (21%) and beeches (15%), followed by oaks , hickories , yellow birches , sycamores , aspens , maples and poplars . In Washington, the most often used nest trees were balsam poplar , Douglas fir and grand fir . Balsam poplar comprised 62% of known nest sites in Manitoba as well. It was found in Maryland that snags used were significantly higher than the average height of miscellaneous snags available in environment. The mean size of tree holes the owls used in Maryland was 33 cm (13 in) in inside diameter and 54 cm (21 in) in depth. These were slightly larger than the average from Michigan, which hollow used averaged 25 cm (9.8 in) in mean diameter and 35 cm (14 in) in mean depth. Record depth tree cavities used by barred owls was around 2.4 m (7.9 ft) deep from the opening on the tree. One study of cavity nesting birds in Ontario found that the barred owl preferred to nest in the most massive trees of any cavity-nester in the study area. In continuous bottomland forest, nests are often about every 226 ha (560 acres) . Territory lines often remain the same even after the original owls are replaced entirely by a new pair. It was thought in Nova Scotia that some pairs may prospect a potential nest site as much as year before they use it. Despite usually using sickly or dying trees, some nests have found in partially hollow but still living oaks . Usually in areas with few or no natural tree hollows, often within younger secondary forests or overharvested areas, this species will uses other birds' nests and occasionally also the dreys of squirrels. Evidence shows that the preference of barred owls for hollows and snags over bird nests is due to their earlier nest type having a more secure microclimate with better shelter (additionally, owl nests in hollows generally tend to be somewhat less vulnerable to predation than those of owls using old bird nests). Nest built by other birds that are most widely used are probably red-shouldered hawk and Cooper's hawks , while those of red-tailed hawks , usually being in more open areas, are used secondarily outside of a local basis. In the south, nests have been found between fronds of palmetto palm leaves, in holes of broken palm stems and rotten snags of the palms. One unconventional nest was on the ground at the base of a lookout tower in Everglades National Park . Another was on the roof of a shed in Saskatchewan. Yet another was in an earthen bank in Texas. Locally, barred owls can take to nest boxes but, in general, barred owls take to these less readily than their cousin Strix owls in Europe. Suitable nesting hollows may be used quite often in subsequent years, with records of a single hollow seeing up to 25 years of barred owl use (presumably not by the same owls however). Other long-used nests were one reused in New England for 10 years by the same pair until it rotted out and while a nest box in Nova Scotia was reused 10 times over 16 years. Over 6 years in Minnesota, 14 nest boxes were reused; 7 were used once, 6 were twice and one was used three times. Like all owls, barred owls never construct their owl nest but they may press or dig slightly if soil is present or remove the top leaves from a squirrel drey . In normal circumstances, barred owls tend to pair bond for life. Courting pairs are usually newly mature birds but also possibly widowed owls or those re-establishing existing pair bonds after the winter. During courtship, barred owl males especially may engage in nodding, bowing with half-spread wings and may wobble and twist their head from side to side. Courting pairs will often engage in duets. Copulation between pairs usually occurs in late winter, February to March, and occurs several times, probably to ensure implantation. The female enters a pre-breeding lethargy stage wherein she is fed by the male. In barred owls, egg laying occurs at two to three day intervals. Egg laying typically begins in March and runs throughout April. In more tropical locales like Florida, egg laying may occur as early as late December, though 22 were laid in between early January and early March. At similar latitudes in Texas, 22 first eggs were laid between as early as mid-February to as late as early June (although the latter may have been a replacement clutch). 23 clutches in Iowa and Illinois were initiated in between late February and late April, with roughly corresponding initial egg dates in New Jersey and probably western Maryland as well. 63 initial eggs in New England were laid between mid-March and mid-May. Further north, 38 clutches in Nova Scotia were initiated in between late March and late May, with initial clutches dates about a week later in Ontario. Normally the female lays 2 to 3 eggs, although as many as 5 is possible, directly on the base of the nest site. The mean clutch size in three broad samples from several parts of the range was between 2.22 and 2.46. In Minnesota, the mean clutch size was 2.68. The eggs are pure white, slightly rough and not glossy, and oval in shape. In 157 eggs, the length of the egg could measure from 42.5 to 55.5 mm (1.67 to 2.19 in) while the diameter could range from 37.5 to 45.3 mm (1.48 to 1.78 in) , with a mean of 50.6 mm × 43.3 mm (1.99 in × 1.70 in) . 25 eggs in Nova Scotia averaged slightly smaller, at 49 mm × 41 mm (1.9 in × 1.6 in) . The mean weight of the egg is around 45.5 g (1.60 oz) . The female alone incubates, doing so for about 28 days, while the male gathers food for her. The female tends to closely brood the young for three weeks. Then after, she begins to hunt for the young. Both parents normally continue hunt for the young until they are about 6 weeks old and can fly well. During the first three weeks, the male does all prey deliveries, either bringing prey directly into the nest or leaves for the female at the nest entrance or on a nearby branch. The mean number of prey deliveries when the young are 6–10 days old is 2.4 per night, 1.4 when they are 11–15 days old, 3.6 when they are 16–20 days old and 2.2 when they are 21–25 days old. He will continue hunting until the young disperse. The female's prey deliveries are much more frequent when she resumes hunting, ranging from a mean of 4.8 to 8 deliveries nightly. Male prey deliveries are often sporadically at any point through the night while female deliveries tend to be clustered immediately after sunset or just before sunrise. Barred owls have a variable reaction to human disturbance. Some parent owls remain sitting, while some leave the nest upon a person's approach and some attack people climbing to the nest, as well as those approaching young on or near the ground. There are several accounts of barred owls engaging in fierce nest defense against humans, sometimes reportedly knocking people out of trees. However, their aggression is variable and, based on studies of similar owls like tawny and Ural owls from Europe, attacks tend to only occur when intrusions and disturbance by humans are frequent. A distraction display was recorded by a female barred owl when humans approached. In it, she spread and quivered her wings and engaged in chittering and squealing, somewhat similar to the sounds made by begging young. The average hatchling weighs about 46 g (1.6 oz) . Like most birds, the young are initially altricial . The white down feathers that the barred owls are hatched with is replaced by white-tipped barred-buff second down at two to three weeks of age, correspondingly with growth of the wing primaries. The earlier chicks are bigger and stronger, while the latter ones may not survive if food is scarce. Size differences between barred owl nestlings may be less pronounced if the female does not begin incubation until the laying of the second egg. The larger young may fight with the younger siblings for food. The young barred owls first start moving about the nest at around this 3 week point and may start to perform threat displays if scared. Adult-like feathers begin to appear at six weeks of age, starting at the scapulars, then radiating down across the abdomen and flanks up through the upper breast, with the last wisps of down remaining for up to 4 months. The young often start exploring around the nest tree, often falling to ground, which makes them quite vulnerable to predation despite the parents' continued protection. However, the fledglings can usually clamber back up the tree using their feet and bills, constantly wing-flapping. Fledging occurs at about 36–39 days. After that, both parents continue to hunt for the young but prey deliveries taper off as the young begin to make their first flights and practice hunting. Short flights are typical when the young barred owls are up to around 10 weeks old with longer flights commencing at about 14 weeks. By the time they are flying and hunting somewhat assuredly in early to mid-autumn, the young move away and gain independence. Dispersal of 5 young from Nova Scotia was 0.8 to 64 km (0.50 to 39.77 mi) away from their nests of origin. Furthermore, a recovered 6 month old was 8 km (5.0 mi) away from its nest of origin, while five encountered as adults were found at a distance of 16 and 43 km (9.9 and 26.7 mi) from the nests where they hatched. An exceptional dispersal distance from Nova Scotia was 1,600 km (990 mi) away to Stoney Creek, Ontario . The post-dispersal stage is one of great mortality among young owls. Usually juvenile owls are considered "floaters", often hovering around the perimeter of fiercely defended territories for some time. In some areas, floaters may make use of nest boxes more readily than mature birds. Yearlings have been known to breed only very rarely, otherwise barred owl usually first breed when they are around two (sometimes three) years old. Therefore, around two years old is considered the age of maturity. The percentages of successful nests (i.e. at least 1 fledgling produced per attempt), per study were found to be: 86% of 22 clutches in Minnesota (with a mean of 2.42 fledglings per successful attempt), 66% of 114 clutches in Michigan (with a mean of 1.97 fledglings per successful attempt), 25% of 6 clutches in Maryland (with a mean of 1 fledgling per all attempts and 1.48 per successful attempts), 69% of 48 clutches in Nova Scotia (with a mean of 0.25 fledgling per all attempts and 2 per successful attempts) and 50% of 12 nests in Washington state. Little is known about the specific factors that dictate breeding success, but are likely to include the quality of the nesting site, the food supply in the area, the levels of disturbance from outside actors (usually humans) and the maturity of the pair.The barred owl is a naturally long-living bird. Some record lifespans recorded per banding studies in the wild are 18 years 2 months (initial banding Kentucky , died in Ohio ) and 24 years and 1 month in Minnesota. There are several records of breeding barred owls nesting successfully for a decade or more. The record lifespan for a barred owl in captivity, where many animals can live longer without the stresses of surviving in wild conditions, was 34 years and 1 month, with six records of captive barred owls living over 30 years. Known causes of mortality are diverse, some due to predation (largely great horned owls, for nestlings to adults, and probably raccoons, for eggs, nestlings and fledglings). Some mortality is known to occur during hunting accidents. There are cases of barred owls being inadvertently killed in furbearer traps . Sometimes deaths occurs due to the defenses of prey. One barred owl was killed by the bite of an unknown rodent that was likely defending itself. Some cases of cannibalism between adult barred owls have been reported as well. This species, like other forest owls, is vulnerable to the respiratory disease aspergillosis . Spontaneous infections of West Nile fever are also known to kill wild barred owls. Barred owls were the most regularly infected with West Nile Virus of owl species in Georgia, as about 15% of studied barred tested positive (still at a lower rate than some hawks). Cases of Avipoxvirus are also known in barred owls but, as with West Nile virus, the rate of mortality to viral infection is not well-known. A case of follicular thyroid cancer was found in a wild barred owl that was unable to continue to fly. Fatty liver diseases have been recorded for barred owls in captivity. Eye lesions are fairly common in barred owls, but can be survived and possibly surgically corrected. Parasitism is frequent in barred owls as expected for many different kinds of wild birds. The parasite load of helminths was determined to be higher in larger owls in Florida like the barred and great horned owl and lower in smaller owl species, like eastern screech owl . While parasitic infestations are not typically detected as direct mortality causes, in some severe cases complications or direct death can occur. These cases of mortality are most widely recorded in cases of toxoplasmosis , although generally owls have lower rates of dangerous Toxoplasma parasites than some other species of birds of prey. Of barred owls in one study, 26.7% had Toxoplasma gondii , the cause of toxoplasmosis, upon necropsy study, with adults having it more often than immature birds. Lethal cases of trichomoniasis are also known. The effect of other parasites are more poorly known beyond generally compromising their hosts' condition, but in one case Sarcocystis strixi may have caused paralysis in a barred owl. Other parasites recorded in barred owls include Eimeria varia , Novyella , Neodiplostomum as well as apparently rare species of Centrorhynchus and Tetrameres that were first found within barred owls. Trematode flatworms such as strigeids as well as Tylodelphys and Brachylaima are found in intermediate volume in barred owls relative to other owls. Invertebrates such as hippoboscid flies and Mallophaga are known to infect barred owls as ectoparasites but seldom at severe levels. Concern was expressed that barred owls may compromise spotted owl populations with novel parasites. However, studies of Haemoproteus in barred and spotted owls in northwestern California found that native parasites were finding a new host in barred owls and may have been transmitted from spotted to barred owls but that the barred owl acted as a poor parasite host and may have diluted the parasite levels in owl populations. Furthermore, there was no evidence found that barred owls were spreading parasites to spotted owls. The barred owl is one of the most common owls in North America. Partners in Flight estimates that the barred owl may number up to 3 million individuals globally, making it, perhaps, the second most numerous North American owl behind the great horned owl and perhaps slightly ahead of other commoner species like barn owls and northern saw-whet owls . It estimated that Canada in total holds about 10,000–50,000 pairs. Canadian Maritimes had highest densities known, with 3600 pairs, being found in 80% of 10 km 2 (3.9 sq mi) blocks totaling 377; this was a conspicuously higher density than that recorded in Ontario, where they were in 28% of 1824 study blocks. Iowa, Tennessee and Maryland had the highest densities of pairs apparently in the United States, being present from 39 to 47% of blocks. Throughout the year, the mean number of sightings per route is 0.12 sightings while during Christmas Bird Counts (CBC), the mean in 0.25 per route. Barred owls are thought to be partly responsible for the recent decline of the northern spotted owl , native to British Columbia, Washington , Oregon , and California . The 2011 Revised Recovery Plan for the Northern Spotted Owl states "Based on the best available scientific information, competition from the barred owl ( S. varia ) poses a significant and complex threat to the spotted owl." Northern spotted owls were thought to be already declining considerably before barred owls moved into their range, mostly in sync with large-scale logging operations and land development carried out by humans, with their problems now further exacerbated by the barred species's presence. There are ecological discrepancies between the species in areas of sympatry. While both species prefer old-growth forest areas, the spotted owls tend to live in significantly higher elevation areas in Washington's Cascade mountains, with nest sites averaging 966.2 m (3,170 ft) meters above sea level against a mean of 54.1 m (177 ft) for barred owls, in areas with more steep slopes. The barred owls of the area additionally prefer wetter, more variable forest areas, down to riparian zones with limited forested land, while the spotted tended to cluster in more homogeneous upland and ancient coniferous forests . However, little is known on the feasibility or benefits of habitat maintenance that favors spotted over barred owls. Habitat management measures are hypothesized to be insufficient to mitigate the negative effect the barred owls are having. In areas where barred owls moved in within 0.8 km (0.50 mi) of a spotted owl nest area, 39% of spotted owls disappeared and were not seen again, while in areas still free of barred owls (so spared from this interspecific pressure), 11% of spotted owls disappeared and were not found again. Since the 1960s, barred owls have been expanding their range westward from the eastern US and Canada. While some authors have described the expansion of barred owls into the west as "natural", others state that this is a mischaracterization, as there is little to suggest that the barred owls could have reached the spotted's range without the inadvertent aid of humans — increasing temperatures, wildlife suppression, and tree planting likely facilitated the range increase. When spotted owls and barred owls share the same area, the barred owls generally are more aggressive and out-compete the spotted owls, leading to decreased populations of the native owls. The more aggressive response of barred owls to interspecific stimuli has been verified with experiments incorporating vocalization and owl dummies. Additionally, the adult survival rates appear higher for barred owls (an estimated 91%) than for spotted owls (an estimated 82%). Therefore, the barred owl is considered "demographically superior". In December 2023, the U.S. Fish and Wildlife Service issued a draft of a management plan indicating that hunters in the Pacific Northwest would be encouraged to shoot more than a half million barred owls. The rationale was to cull the numbers of this invasive species, to help protect native species, particularly the spotted owl which had been listed as threatened under the Endangered Species Act. Another potential threat is that barred owls and spotted owls occasionally interbreed, creating hybrids ("sparred owl" or "botted owl"). Only 47 hybrids with barred owls (all between female barred owls and male spotted owls) were found in an analysis of more than 9,000 banded spotted owls; consequently, hybridization between these two species is considered to be "an interesting biological phenomenon that is probably inconsequential compared with the real threat—direct competition between the two species for food and space". Most hybrids favor their barred owl heritage with similar and more pale overall coloring than spotted owls, though the back tends to be intermediate in color between the two and the beak coloring is variable. However, there has been much variation described. Due to variances in appearance, previously hybrids between the species were overestimated from field identification, only being certainly identified by genetic loci . Moreover, no recent hybrids could be detected in a survey of the Cascade Mountains . John James Audubon illustrated the barred owl in Birds of America (published in London, 1827–1838) as Plate 46, where it is shown threatening a grey squirrel . The image was engraved and colored by Robert Havell 's London workshops. The original aquatint by Audubon is owned by the Brooklyn Museum.

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West Nile

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West African crocodile

C. niloticus suchus The West African crocodile , desert crocodile , or sacred crocodile ( Crocodylus suchus ) is a species of crocodile related to — and often confused with — the larger and more aggressive Nile crocodile ( C. niloticus ). The species was named by Étienne Geoffroy Saint-Hilaire in 1807, who discovered differences between the skulls of a mummified crocodile and those of Nile crocodile ( C. niloticus ). This new species was, however, long afterwards regarded as a synonym of the Nile crocodile. In 2003, a study resurrected C. suchus as a valid species, and this was confirmed by several other studies in 2011–2015. Despite the long history of confusion, genetic testing has revealed that the two are not particularly close. The closest relatives of the Nile crocodile are the Crocodylus species from the Americas, while the West African crocodile is basal to the clade of Nile and American crocodiles. Below is a cladogram based on a 2018 tip dating study by Lee & Yates simultaneously using morphological , molecular ( DNA sequencing ), and stratigraphic ( fossil age) data, as revised by the 2021 Hekkala et al. paleogenomics study using DNA extracted from the extinct Voay . Voay †Crocodylus anthropophagus †Crocodylus thorbjarnarsoni †Crocodylus palaeindicus †Crocodylus Tirari Desert †Crocodylus johnstoni , freshwater crocodile Crocodylus novaeguineae , New Guinea crocodile Crocodylus mindorensis , Philippine crocodile Crocodylus porosus , saltwater crocodile Crocodylus siamensis , Siamese crocodile Crocodylus palustris , mugger crocodile Crocodylus checchiai †Crocodylus falconensis †Crocodylus suchus , West African crocodile Crocodylus niloticus , Nile crocodile Crocodylus moreletii , Morelet's crocodile Crocodylus rhombifer , Cuban crocodile Crocodylus intermedius , Orinoco crocodile Crocodylus acutus , American crocodileThe muzzle is short and thick. The distance between the eyes and the tip of the muzzle is 1.5 to 2 times longer than the width of the muzzle at the level of the front edge of the eyes (1.2 to 1.5 times in case of juveniles). The coloration is generally brown to olive . Juveniles are paler, with black bandings , especially on the tail. Like all other species of crocodiles , the West African crocodile's eyes reflect light at night allowing it to be spotted easily through a flashlight. It is found to be active day and night. It can stay submerged underwater for more than 30 minutes, and can reach speeds of up to 30 km/h (19 mph) in short bursts. On land, it is often observed basking motionless in the sun , often with its mouth agape. Compared to the Nile crocodile , which can grow over 5 m (16 ft 5 in) in length, the West African crocodile is smaller. It typically grows between 2 and 3 m (6 ft 7 in and 9 ft 10 in) in length, with an occasional male growing over 4 m (13 ft 1 in) in rare cases. Adults weigh between 90 and 250 kg (200 and 550 lb) , with particularly large male specimens exceeding 300 kg (660 lb) in weight. The West African crocodile inhabits much of West and Central Africa , ranging east to South Sudan and Uganda , and south to Democratic Republic of the Congo (in all three countries it may come into contact with Nile crocodiles). Other countries where it is found include Mauritania , Benin , Liberia , Guinea-Bissau , Nigeria , Niger , Cameroon , Chad , Sierra Leone , the Central African Republic , Equatorial Guinea , Senegal , Mali , Guinea , Gambia , Burkina Faso , Ghana , Gabon , Togo , Ivory Coast and the Republic of Congo . As late as the 1920s, museums continued to obtain West African crocodile specimens from the White Nile , but today the species has disappeared from this river. In Mauritania the species has adapted to the arid desert environment of the Sahara – Sahel by staying in caves or burrows in a state of aestivation during the driest periods, leading to the alternative common name desert crocodile. When it rains, these desert crocodiles gather at gueltas . In much of its range, the West African crocodile may come into contact with other crocodile species and there appears to be a level of habitat segregation between them. The Nile crocodile typically prefers large seasonal rivers in savannah or grassland, while the West African crocodile generally prefers lagoons and wetlands in forested regions, at least where the two species may come into contact. The details of this probable segregations remains to be confirmed for certain. In a study of habitat use by the three crocodile species in Liberia (West African, slender-snouted and dwarf ), it was found that the West African crocodile typically occupied larger, more open waterways consisting of river basins and mangrove swamps, and was the species most tolerant of brackish waters. In comparison, the slender-snouted crocodile typically occupies rivers within forest interiors, while dwarf crocodiles are distributed in smaller rivers (mainly tributaries), streams and brooks also within forested areas. The West African crocodile is less aggressive than the Nile crocodile, but several attacks on humans have been recorded, including fatal ones. Mauritanian traditional peoples who live in close proximity to West African crocodiles revere them and protect them from harm. This is due to their belief that, just as water is essential to crocodiles, so crocodiles are essential to the water, which would permanently disappear if they were not there to inhabit it. Here the crocodiles live in apparent peace with the humans, and are not known to attack swimmers. The people of ancient Egypt worshiped Sobek , a crocodile-god associated with fertility , protection, and the power of the pharaoh . They had an ambivalent relationship with Sobek, as they did (and do) with C. suchus : sometimes they hunted crocodiles and reviled Sobek, and sometimes they saw him as a protector and source of pharaonic power. C. suchus was known to be more docile than the Nile crocodile and was chosen by the ancient Egyptians for spiritual rites , including mummification. DNA testing found that all sampled mummified crocodiles from the grotto of Thebes , grotto of Samoun, and Upper Egypt belonged to this species whereas the ones from a burial pit at Qubbet el-Hawa are believed on the basis of anatomy to consist of a mix of the two species. Sobek was depicted as a crocodile, as a mummified crocodile, or as a man with the head of a crocodile. The center of his worship was in the Middle Kingdom city of Arsinoe in the Faiyum , known as " Crocodilopolis " by the Greeks . Another major temple to Sobek is in Kom Ombo ; other temples were scattered across the country. Historically, C. suchus inhabited the Nile in Lower Egypt along with the Nile crocodile. Herodotus wrote that the Egyptian priests were selective when picking crocodiles. Priests were aware of the difference between the two species, C. suchus being smaller and more docile, making it easier to catch and tame. Herodotus also indicated that some Egyptians kept crocodiles as pampered pets. In Sobek's temple in Arsinoe, a crocodile was kept in the pool of the temple, where it was fed, covered with jewelry, and worshipped. When the crocodiles died, they were embalmed, mummified, placed in sarcophagi , and then buried in a sacred tomb. Many mummified C. suchus specimens and even crocodile eggs have been found in Egyptian tombs. Spells were used to appease crocodiles in ancient Egypt, and even in modern times Nubian fishermen stuff and mount crocodiles over their doorsteps to ward against evil. The West African crocodile only received wider recognition as a valid species in 2011. Consequently, captives have typically been confused with other species, especially the Nile crocodile. In Europe, breeding pairs of West African crocodiles live in Copenhagen Zoo , Lyon Zoo and Vivarium de Lausanne , and offspring of the first pair are in Dublin Zoo and Kristiansand Zoo . A study in 2015 that included 16 captive "Nile crocodiles" in 6 US zoos (almost a quarter of the "Nile crocodiles" in AZA zoos) found that all but one were actually West African crocodiles. The people of ancient Egypt worshiped Sobek , a crocodile-god associated with fertility , protection, and the power of the pharaoh . They had an ambivalent relationship with Sobek, as they did (and do) with C. suchus : sometimes they hunted crocodiles and reviled Sobek, and sometimes they saw him as a protector and source of pharaonic power. C. suchus was known to be more docile than the Nile crocodile and was chosen by the ancient Egyptians for spiritual rites , including mummification. DNA testing found that all sampled mummified crocodiles from the grotto of Thebes , grotto of Samoun, and Upper Egypt belonged to this species whereas the ones from a burial pit at Qubbet el-Hawa are believed on the basis of anatomy to consist of a mix of the two species. Sobek was depicted as a crocodile, as a mummified crocodile, or as a man with the head of a crocodile. The center of his worship was in the Middle Kingdom city of Arsinoe in the Faiyum , known as " Crocodilopolis " by the Greeks . Another major temple to Sobek is in Kom Ombo ; other temples were scattered across the country. Historically, C. suchus inhabited the Nile in Lower Egypt along with the Nile crocodile. Herodotus wrote that the Egyptian priests were selective when picking crocodiles. Priests were aware of the difference between the two species, C. suchus being smaller and more docile, making it easier to catch and tame. Herodotus also indicated that some Egyptians kept crocodiles as pampered pets. In Sobek's temple in Arsinoe, a crocodile was kept in the pool of the temple, where it was fed, covered with jewelry, and worshipped. When the crocodiles died, they were embalmed, mummified, placed in sarcophagi , and then buried in a sacred tomb. Many mummified C. suchus specimens and even crocodile eggs have been found in Egyptian tombs. Spells were used to appease crocodiles in ancient Egypt, and even in modern times Nubian fishermen stuff and mount crocodiles over their doorsteps to ward against evil.The West African crocodile only received wider recognition as a valid species in 2011. Consequently, captives have typically been confused with other species, especially the Nile crocodile. In Europe, breeding pairs of West African crocodiles live in Copenhagen Zoo , Lyon Zoo and Vivarium de Lausanne , and offspring of the first pair are in Dublin Zoo and Kristiansand Zoo . A study in 2015 that included 16 captive "Nile crocodiles" in 6 US zoos (almost a quarter of the "Nile crocodiles" in AZA zoos) found that all but one were actually West African crocodiles.

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West Nile

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West Nile Rural Electrification Company

West Nile Rural Electrification Company Limited (WENRECO) is an electric energy generating and distribution company in the West Nile sub-region of the Northern Region of Uganda . WENRECO is a wholly owned subsidiary of Industrial Promotion Services (IPS), the industrial development arm of the Aga Khan Fund for Economic Development (AKFED). AKFED is a member of the Aga Khan Development Network .In 2003, WENRECO, through competitive bidding, won a concession to generate, distribute, and sell electricity in the West Nile sub-region, consisting of eight districts and home to an estimated 2.3 million people. The company owns a 1.5 megawatt heavy fuel electric generator and is part-owner and operator of the Nyagak I Power Station . WENRECO is the implementer and co-funder of the West Nile Rural Electrification Project, which was initiated in 2013. The project targeted electrification of 30 health centers, 60 schools, 250 businesses, and 6,000 households between 2013 and 2015. Funding for the project was provided by the government of Uganda , KfW , WENRECO, and the Energy Facility Pooling Mechanism. In 2013, WENRECO began switching the 4,000 customers that it had at that time to pre-paid metering service. WENRECO operates two power stations: WENRECO heavy fuel thermal plant with a capacity of 1.5 megawatts, located in Ewuata, Arua District ; and the Nyagak I Power Station, a 3.5 megawatt mini-hydropower station, located in Paidha , Zombo District . These facilities are the main public electric power sources available to the West Nile sub-region, which is not yet connected to the national grid. Connection to the national grid is expected following the completion of the Karuma Hydroelectric Power Station around 2020.

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West Nile

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Crocodile farm

A crocodile farm or alligator farm is an establishment for breeding and raising of crocodilians in order to produce crocodile and alligator meat , leather from crocodile and alligator skin, and other goods. Many species of both alligators and crocodiles are farmed internationally. In Louisiana alone, alligator farming is a $60 to $70 million industry. Most crocodile farms are located in Thailand .Alligators and crocodiles are not truly domesticated and their being bred in farms probably began as late as the early 20th century. Most of the early businesses, such as St. Augustine Alligator Farm Zoological Park , established in 1893, were farms in name only, primarily keeping alligators and crocodiles as a tourist attraction . Only in the 1960s did commercial operations that either harvested eggs from the wild or bred alligators on-site begin to appear. This was largely driven by diminishing stocks of wild alligators, which had been hunted nearly to extinction by that time. As the American alligator was placed under official protection in 1967 (under a law preceding the 1973 Endangered Species Act ), farming alligators for skins became the most viable option for producing leather. Mostly concentrated in the Southern U.S. states of Louisiana , Florida , and Georgia , the practice quickly spread to other nations. Both the American and Chinese alligator are farmed intensively today, mostly within each species' respective native region. The Nile crocodile is found in ranches all over Africa, and the saltwater crocodile is farmed in Australia and other areas. The smaller caimans are generally not of enough market value to farm, though captive breeding of the spectacled caiman does take place in South America. Farming alligators and crocodiles first grew out of the demand for skins, which can fetch hundreds of dollars each. But alligator and crocodile meat, long a part of Southern cooking (especially Cajun cuisine ) and some Asian and African cuisines , began to be sold and shipped to markets unfamiliar with crocodilian meat. Chinese cuisine based on traditional Chinese medicine considers the meat to be a curative food for colds and cancer prevention, although there is no scientific evidence to support this. Crocodile meat was eaten, albeit rarely and as an exotic dish, in Vietnamese cuisine , but it was taboo and off limits for Chinese. In Vietnam, skinning is performed on still living crocodiles. A common misconception [ among whom? ] is that crocodilians are an easy source of revenue and not difficult to care for in captivity; however, few crocodilian businesses are successful in the developing world. To offset overhead costs and have a regular source of income, crocodilian facilities can add tourism; in this way alligator farming can assist native species and provide people with work. Alligator farming has minimal adverse effects on the environment, and has at least two positive direct effects on alligator conservation. Because the luxury goods industry has a reliable stream of product, illegal poaching is reduced. Juvenile crocodilians can also be released into the wild to support a steady population. Wild alligator conservation has also benefited indirectly from farming. Ranching businesses protect alligator habitats to take care of nesting sites. The fiscal incentive to keep a healthy environment for breeding alligators means that the environment and its wildlife are seen as an economic resource. This can augment the government's willingness to take care of crocodilian populations. Animals other than crocodilians may benefit from a similar application of sustainable and ethical farming. Ranching, wild harvesting, and captive breeding are the three ways to obtain crocodilians recognized by the Convention on International Trade in Endangered Species (CITES) and the Crocodile Specialist Group (CSG). Alligators can be raised in captivity on farms or on ranches. Alligator farms breed alligators, whereas ranches incubate and rear hatchlings collected from the wild. Farms do collect eggs from the wild but they also keep breeding adults in their facilities to produce their own eggs whereas ranches do not. Farming and ranching operations typically return a certain percentage of juveniles to the wild at a size associated with a high survival rate, an approach that increases overall alligator survival rates from the low numbers of successful eggs and juveniles usually observed in the wild. Crocodiles can be housed in a number of ways depending on the goals of the rearing facility. Large areas of a lake or marsh can be enclosed for many individuals or a smaller area can be created for fewer individuals. Due to the size and lifespan of the animals, adult crocodiles need a substantial amount of space. Tourism can bring additional revenue to crocodile rearing facilities, but they must be made safe for the public and the crocodiles, while maintaining an aesthetically pleasing environment. This frequently depends on enclosures that can be easily cleaned without harming the animals. If closed to public viewing, facilities have fewer requirements and can have a more practical design. Alligators and crocodiles can be raised in captivity with "open cycle" or "closed cycle" methods. Open cycle refers to programs that are concerned with the health of the wild population and are using captive rearing as a means to supplement the wild populations. Closed-cycle operations are primarily concerned with harvest. In closed cycle operations, adult females are kept in captivity, and the eggs they lay are collected, incubated artificially, hatched, and the juveniles are grown to a certain size and harvested. Closed cycle operations provide no incentive for conservation and are often unsuccessful because the cost of starting and managing the operation often outweighs the profits gained from products. Although the cost of operating an open cycle operation is comparable to closed cycle, the goal of an open cycle operation is the overall health of the species, rather than economic profit. Captive breeding and ranching operations provide more incentive to protect natural populations and are important contributors to the success of crocodilian populations. Welfare concerns include the threat of crocodilian diseases such as caiman pox, adenoviral Hepatitis , mycoplasmosis , and chlamydiosis . Crocodiles suffer from stress in confined spaces such as farms, leading to disease outbreaks. Most crocodilians keep a body temperature within 28 and 33 degrees Celsius. On farms, body temperatures can reach 36 degrees Celsius, which affects the animals' immune system, and puts them at risk of various illnesses. Another concern is for the cleanliness of the water in enclosures. Many alligator farms in the United States have experienced property damage from Sus scrofa (feral swine). Between 2001 and 2003, West Nile virus (WNV) infected and caused deaths resulting in economic loss in American alligators in Georgia , Florida , Louisiana , and Idaho . The disease is transmitted by mosquitoes. WNV has been found in Mexico at a crocodile farm in Ciudad del Carmen . The skin, most notably the underside, of alligators and crocodiles is of commercial value, so diseases of the skin need to be treated properly and effectively. Crocodilian diseases vary between species. Salmonellosis is common on some farms, and is acquired from infected food; it may also be spread by poor hygiene practices. Chlamydia , (specifically Chlamydophila psittaci ) can persist for years if not treated, for example with tetracycline . Crocodilians may acquire mycobacteria from infected meat. Illnesses affecting crocodilians include crocodile pox, which is caused by Parapoxvirus, affecting hatchlings and juveniles. It causes a brown residue to form around the eyes, oral cavity, and tail. Caiman pox similarly causes white lesions around the eyes, oral cavity, and tail. Adenoviral hepatitis causes organ failure and death. Mycoplasmosis causes polyarthritis and pneumonia in crocodilians under the age of three. Infected animals have swollen jaws and are unable to move. Chlamydiosis has two forms that affects juveniles under one year of age. The first causes acute hepatitis, usually resulting in death. The other causes chronic bilateral conjunctivitis, usually resulting in blindness. Parasitic infections include tapeworm cysts, Trichinella spiralis nelsoni in the meat of Nile crocodiles in Zimbabwe, and Coccidia. There have been reports of crocodiles escaping from farms during flooding. In 2013, approximately 15,000 crocodiles were released into the Limpopo River from flood gates at the nearby Rakwena Crocodile Farm. Welfare concerns include the threat of crocodilian diseases such as caiman pox, adenoviral Hepatitis , mycoplasmosis , and chlamydiosis . Crocodiles suffer from stress in confined spaces such as farms, leading to disease outbreaks. Most crocodilians keep a body temperature within 28 and 33 degrees Celsius. On farms, body temperatures can reach 36 degrees Celsius, which affects the animals' immune system, and puts them at risk of various illnesses. Another concern is for the cleanliness of the water in enclosures. Many alligator farms in the United States have experienced property damage from Sus scrofa (feral swine). Between 2001 and 2003, West Nile virus (WNV) infected and caused deaths resulting in economic loss in American alligators in Georgia , Florida , Louisiana , and Idaho . The disease is transmitted by mosquitoes. WNV has been found in Mexico at a crocodile farm in Ciudad del Carmen . The skin, most notably the underside, of alligators and crocodiles is of commercial value, so diseases of the skin need to be treated properly and effectively. Crocodilian diseases vary between species. Salmonellosis is common on some farms, and is acquired from infected food; it may also be spread by poor hygiene practices. Chlamydia , (specifically Chlamydophila psittaci ) can persist for years if not treated, for example with tetracycline . Crocodilians may acquire mycobacteria from infected meat. Illnesses affecting crocodilians include crocodile pox, which is caused by Parapoxvirus, affecting hatchlings and juveniles. It causes a brown residue to form around the eyes, oral cavity, and tail. Caiman pox similarly causes white lesions around the eyes, oral cavity, and tail. Adenoviral hepatitis causes organ failure and death. Mycoplasmosis causes polyarthritis and pneumonia in crocodilians under the age of three. Infected animals have swollen jaws and are unable to move. Chlamydiosis has two forms that affects juveniles under one year of age. The first causes acute hepatitis, usually resulting in death. The other causes chronic bilateral conjunctivitis, usually resulting in blindness. Parasitic infections include tapeworm cysts, Trichinella spiralis nelsoni in the meat of Nile crocodiles in Zimbabwe, and Coccidia.There have been reports of crocodiles escaping from farms during flooding. In 2013, approximately 15,000 crocodiles were released into the Limpopo River from flood gates at the nearby Rakwena Crocodile Farm. A crocodilian farm in Louisiana (in reality, Jamaica) is featured in the 1973 James Bond film Live and Let Die . Tee Hee Johnson, one of the villain's henchman, attempts to feed James Bond to the alligators and crocodiles. In the second season of The Amazing Race Australia , teams had to visit a Cuban alligator farm and feed a wheelbarrow full of chum to a pen of alligators along with capturing an alligator with a stick and rope in order to receive their next clue.Source:

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West Nile

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CCR5

2L87 , 2RLL , 2RRS , 2MZX , 4MBS parietal pleura visceral pleura palpebral conjunctiva germinal epithelium mucosa of urinary bladder appendix superficial temporal artery jejunal mucosa lymph node monocyte morula blood lymph node submandibular gland superior frontal gyrus spleen blastocyst thymus uterus white adipose tissue 1234 12774 ENSG00000160791 ENSMUSG00000079227 P51681 P51682 NM_001100168 NM_000579 NM_001394783 NM_009917 NP_000570 NP_001093638 NP_034047 C-C chemokine receptor type 5 , also known as CCR5 or CD195 , is a protein on the surface of white blood cells that is involved in the immune system as it acts as a receptor for chemokines . In humans, the CCR5 gene that encodes the CCR5 protein is located on the short (p) arm at position 21 on chromosome 3 . Certain populations have inherited the Delta 32 mutation, resulting in the genetic deletion of a portion of the CCR5 gene. Homozygous carriers of this mutation are resistant to infection by macrophage-tropic (M-tropic) strains of HIV-1 . The CCR5 protein belongs to the beta chemokine receptors family of integral membrane proteins . It is a G protein–coupled receptor which functions as a chemokine receptor in the CC chemokine group . CCR5's cognate ligands include CCL3 , CCL4 (also known as MIP 1 α and 1 β , respectively), and CCL3L1 . CCR5 furthermore interacts with CCL5 (a chemotactic cytokine protein also known as RANTES). CCR5 is predominantly expressed on T cells , macrophages , dendritic cells , eosinophils , microglia and a subpopulation of either breast or prostate cancer cells. The expression of CCR5 is selectively induced during the cancer transformation process and is not expressed in normal breast or prostate epithelial cells. Approximately 50% of human breast cancer expressed CCR5, primarily in triple negative breast cancer . CCR5 inhibitors blocked the migration and metastasis of breast and prostate cancer cells that expressed CCR5, suggesting that CCR5 may function as a new therapeutic target. Recent studies suggest that CCR5 is expressed in a subset of cancer cells with characteristics of cancer stem cells, which are known to drive therapy resistance, and that CCR5 inhibitors enhanced the number of cells killed by current chemotherapy. It is likely that CCR5 plays a role in inflammatory responses to infection, though its exact role in normal immune function is unclear. Regions of this protein are also crucial for chemokine ligand binding, the functional response of the receptor, and HIV co-receptor activity. Modulation of CCR5 activity contributes to a non-pathogenic course of infection with simian immunodeficiency virus (SIV) in several African non-human primate species that are long-term natural hosts of SIV and avoid immunodeficiency upon the infection. These regulatory mechanisms include: genetic deletions that abrogate cell surface expression of CCR5, downregulation of CCR5 on the surface of CD4+ T cells, in particular on memory cells, and delayed onset of CCR5 expression on the CD4+ T cells during development. HIV-1 most commonly uses the chemokine receptors CCR5 and/or CXCR4 as co-receptors to enter target immunological cells. These receptors are located on the surface of host immune cells whereby they provide a method of entry for the HIV-1 virus to infect the cell. The HIV-1 envelope glycoprotein structure is essential in enabling the viral entry of HIV-1 into a target host cell. The envelope glycoprotein structure consists of two protein subunits cleaved from a Gp160 protein precursor encoded for by the HIV-1 env gene: the Gp120 external subunit and the Gp41 transmembrane subunit. This envelope glycoprotein structure is arranged into a spike-like structure located on the surface of the virion and consists of a trimer of Gp120-Gp41 hetero-dimers. The Gp120 envelope protein is a chemokine mimic. Though it lacks the unique structure of a chemokine, it is still capable of binding to the CCR5 and CXCR4 chemokine receptors. During HIV-1 infection, the Gp120 envelope glycoprotein subunit binds to a CD4 glycoprotein and a HIV-1 co-receptor expressed on a target cell, forming a heterotrimeric complex. The formation of this complex stimulates the release of a fusogenic peptide, causing the viral membrane to fuse with the membrane of the target host cell. Because binding to CD4 alone can sometimes result in gp120 shedding, gp120 must next bind to co-receptor CCR5 in order for fusion to proceed. The tyrosine-sulfated amino terminus of this co-receptor is the "essential determinant" of binding to the gp120 glycoprotein. The co-receptor also recognizes the V1-V2 region of gp120 and the bridging sheet (an antiparallel, 4-stranded β sheet that connects the inner and outer domains of gp120). The V1-V2 stem can influence "co-receptor usage through its peptide composition as well as by the degree of N-linked glycosylation." Unlike V1-V2 however, the V3 loop is highly variable and thus is the most important determinant of co-receptor specificity. The normal ligands for this receptor, RANTES , MIP-1β , and MIP-1α , are able to suppress HIV-1 infection in vitro . In individuals infected with HIV, CCR5-using viruses are the predominant species isolated during the early stages of viral infection, suggesting that these viruses may have a selective advantage during transmission or the acute phase of disease. Moreover, at least half of all infected individuals harbor only CCR5-using viruses throughout the course of infection. CCR5 is the primary co-receptor used by gp120 sequentially with CD4. This bind results in gp41, the other protein product of gp160, released from its metastable conformation and inserted into the membrane of the host cell. Although it has not been confirmed, binding of gp120-CCR5 involves two crucial steps: 1) The tyrosine-sulfated amino terminus of this co-receptor is an "essential determinant" of binding to gp120 (as stated previously) 2) Following step 1., there must be reciprocal action (synergy, intercommunication) between gp120 and the CCR5 transmembrane domains. CCR5 is essential for the spread of the R5-strain of the HIV-1 virus. Knowledge of the mechanism by which this strain of HIV-1 mediates infection has prompted research into the development of therapeutic interventions to block CCR5 function. A number of new experimental HIV drugs, called CCR5 receptor antagonists , have been designed to interfere with binding between the Gp120 envelope protein and the HIV co-receptor CCR5. These experimental drugs include PRO140 ( CytoDyn ), Vicriviroc (Phase III trials were cancelled in July 2010) ( Schering Plough ), Aplaviroc (GW-873140) ( GlaxoSmithKline ) and Maraviroc (UK-427857) ( Pfizer ). Maraviroc was approved for use by the FDA in August 2007. It is the only one thus far approved by the FDA for clinical use, thus becoming the first CCR5 inhibitor. A problem of this approach is that, while CCR5 is the major co-receptor by which HIV infects cells, it is not the only such co-receptor. It is possible that under selective pressure HIV will evolve to use another co-receptor. However, examination of viral resistance to AD101, molecular antagonist of CCR5, indicated that resistant viruses did not switch to another co-receptor (CXCR4), but persisted in using CCR5: they either bound to alternative domains of CCR5 or to the receptor at a higher affinity. However, because there is still another co-receptor available, it is probable that lacking the CCR5 gene does not make one immune to the virus; it would simply be more challenging for the individual to contract it. Also, the virus still has access to CD4. Unlike CCR5, which is not required (as evidenced by those living healthy lives even when lacking the gene as a result of the delta32 mutation), CD4 is critical in the body's immune defense system. Even without the availability of either co-receptor (even CCR5), the virus can still invade cells if gp41 were to go through an alteration (including its cytoplasmic tail) that resulted in the independence of CD4 without the need of CCR5 and/or CXCR4 as a doorway. Expression of CCR5 is induced in breast and prostate epithelial cells upon transformation. The induction of CCR5 expression promotes cellular invasion, migration, and metastasis. The induction of metastasis involves homing to the metastatic site. CCR5 inhibitors including maraviroc and leronlimab have been shown to block lung metastasis of human breast cancer cell lines. In preclinical studies of immune competent mice CCR5 inhibitors blocked metastasis to the bones and brain. CCR5 inhibitors also reduce the infiltration of tumor associated macrophages. A Phase 1 clinical study of a CCR5 inhibitor in heavily pretreated patients with metastatic colon cancer demonstrated an objective clinical response and reduction in metastatic tumor burden. Increased levels of CCR5 are part of the inflammatory response to stroke and death. Blocking CCR5 with Maraviroc (a drug approved for HIV) may enhance recovery after stroke. In the developing brain, chemokine receptors such as CCR5 influence neuronal migration and connection. After stroke, they seem to decrease the number of connection sites on neurons near the damage. CCR5-Δ32 (or CCR5-D32 or CCR5 delta 32) is an allele of CCR5. CCR5 Δ32 is a 32-base-pair deletion that introduces a premature stop codon into the CCR5 receptor locus, resulting in a nonfunctional receptor. CCR5 is required for M-tropic HIV-1 virus entry. Individuals homozygous (denoted Δ32/Δ32) for CCR5 Δ32 do not express functional CCR5 receptors on their cell surfaces and are resistant to HIV-1 infection, despite multiple high-risk exposures. Individuals heterozygous (+/Δ32) for the mutant allele have a greater than 50% reduction in functional CCR5 receptors on their cell surfaces due to dimerization between mutant and wild-type receptors that interferes with transport of CCR5 to the cell surface. Heterozygote carriers are resistant to HIV-1 infection relative to wild types and when infected, heterozygotes exhibit reduced viral loads and a 2-3-year-slower progression to AIDS relative to wild types. Heterozygosity for this mutant allele also has shown to improve one's virological response to anti-retroviral treatment. CCR5 Δ32 has an (heterozygote) allele frequency of 9% in Europe, and a homozygote frequency of 1%. Recent research indicates that CCR5 Δ32 enhances cognition and memory. In 2016, researchers showed that removing the CCR5 gene from mice significantly improved their memory. CCR5 is a powerful suppressor for neuronal plasticity, learning, and memory; CCR5 over-activation by viral proteins may contribute to HIV-associated cognitive deficits. The CCR5 Δ32 allele is notable for its recent origin, unexpectedly high frequency, and distinct geographic distribution, which together suggest that (a) it arose from a single mutation, and (b) it was historically subject to positive selection. Two studies have used linkage analysis to estimate the age of the CCR5 Δ32 deletion, assuming that the amount of recombination and mutation observed on genomic regions surrounding the CCR5 Δ32 deletion would be proportional to the age of the deletion. Using a sample of 4000 individuals from 38 ethnic populations, Stephens et al. estimated that the CCR5-Δ32 deletion occurred 700 years ago (275-1875, 95% confidence interval). Another group, Libert et al. (1998), used microsatellite mutations to estimate the age of the CCR5 Δ32 mutation to be 2100 years (700-4800, 95% confidence interval). On the basis of observed recombination events, they estimated the age of the mutation to be 2250 years (900-4700, 95% confidence interval). A third hypothesis relies on the north-to-south gradient of allele frequency in Europe, which shows that the highest allele frequency occurred in the Nordic countries and lowest allele frequency in southern Europe. Because the Vikings historically occupied these countries, it may be possible that the allele spread throughout Europe due to the Viking dispersal in the 8th to 10th centuries. Vikings were later replaced by the Varangians in Russia, which may have contributed to the observed east-to-west cline of allele frequency. HIV-1 was initially transmitted from chimpanzees ( Pan troglodytes ) to humans in the early 1900s in Southeast Cameroon, Africa, through exposure to infected blood and body fluids while butchering bushmeat. However, HIV-1 was effectively absent from Europe until the 1980s. Therefore, given the average age of roughly 1000 years for the CCR5-Δ32 allele, it can be established that HIV-1 did not exert selection pressure on the human population for long enough to achieve the current frequencies. Hence, other pathogens have been suggested as agents of positive selection for CCR5 Δ32, including bubonic plague ( Yersinia pestis ) and smallpox ( Variola major ). Other data suggest that the allele frequency experienced negative selection pressure as a result of pathogens that became more widespread during Roman expansion. The idea that negative selection played a role in the allele's low frequency is also supported by experiments using knockout mice and Influenza A, which demonstrated that the presence of the CCR5 receptor is important for efficient response to a pathogen. Several lines of evidence suggest that the CCR5 Δ32 allele evolved only once. First, CCR5 Δ32 has a relatively high frequency in several different European populations but is comparatively absent in Asian, Middle Eastern and American Indian populations, suggesting that a single mutation occurred after divergence of Europeans from their African ancestor. Second, genetic linkage analysis indicates that the mutation occurs on a homogeneous genetic background, implying that inheritance of the mutation occurred from a common ancestor. This was demonstrated by showing that the CCR5 Δ32 allele is in strong linkage disequilibrium with highly polymorphic microsatellites. More than 95% of CCR5 Δ32 chromosomes also carried the IRI3.1-0 allele, while 88% carried the IRI3.2 allele. By contrast, the microsatellite markers IRI3.1-0 and IRI3.2-0 were found in only 2 or 1.5% of chromosomes carrying a wild-type CCR5 allele. This evidence of linkage disequilibrium supports the hypothesis that most, if not all, CCR5 Δ32 alleles arose from a single mutational event. Finally, the CCR5 Δ32 allele has a unique geographical distribution indicating a single Northern origin followed by migration. A study measuring allele frequencies in 18 European populations found a North-to-South gradient, with the highest allele frequencies in Finnish and Mordvinian populations (16%), and the lowest in Sardinia (4%). In the absence of selection, a single mutation would take an estimated 127,500 years to rise to a population frequency of 10%. Estimates based on genetic recombination and mutation rates place the age of the allele between 1000 and 2000 years. This discrepancy is a signature of positive selection. It is estimated that HIV-1 entered the human population in Africa in the early 1900s, but symptomatic infections were not reported until the 1980s. The HIV-1 epidemic is therefore far too young to be the source of positive selection that drove the frequency of CCR5 Δ32 from zero to 10% in 2000 years. Protection from bubonic plague . Stephens, et al. (1998), suggest that bubonic plague ( Yersinia pestis ) had exerted positive selective pressure on CCR5 Δ32. This hypothesis was based on the timing and severity of the Black Death pandemic, which killed 30% of the European population of all ages between 1346 and 1352. After the Black Death, there were less severe, intermittent epidemics. Individual cities experienced high mortality, but overall mortality in Europe was only a few percent. In 1655-1656 a second pandemic called the "Great Plague" killed 15-20% of London's population. [ dubious – discuss ] Importantly, the plague epidemics were intermittent. Bubonic plague is a zoonotic disease, primarily infecting rodents, spread by fleas, and only occasionally infecting humans. Human-to-human infection of bubonic plague does not occur, though it can occur in pneumonic plague, which infects the lungs. Only when the density of rodents is low are infected fleas forced to feed on alternative hosts such as humans, and under these circumstances a human epidemic may occur. Based on population genetic models, Galvani and Slatkin (2003) argue that the intermittent nature of plague epidemics did not generate a sufficiently strong selective force to drive the allele frequency of CCR5 Δ32 to 10% in Europe. To test this hypothesis, Galvani and Slatkin (2003) modeled the historical selection pressures produced by plague and smallpox. Protection from smallpox . Plague was modeled according to historical accounts, while age-specific smallpox mortality was gleaned from the age distribution of smallpox burials in York (England) between 1770 and 1812. Smallpox preferentially infects young, pre-reproductive members of the population since they are the only individuals who are not immunized or dead from past infection. Because smallpox preferentially kills pre-reproductive members of a population, it generates stronger selective pressure than plague. Unlike plague, smallpox does not have an animal reservoir and is only transmitted from human to human. The authors calculated that if plague were selecting for CCR5 Δ32, the frequency of the allele would still be less than 1%, while smallpox has exerted a selective force sufficient to reach 10%. The hypothesis that smallpox exerted positive selection for CCR5 Δ32 is also biologically plausible, since poxviruses, like HIV, enter white blood cells using chemokine receptors. By contrast, Yersinia pestis is a bacterium with a very different biology. Although Europeans are the only group to have subpopulations with a high frequency of CCR5 Δ32, they are not the only population that has been subject to selection by smallpox, which had a worldwide distribution before it was declared eradicated in 1980. The earliest unmistakable descriptions of smallpox appear in the 5th century A.D. in China, the 7th century A.D. in India and the Mediterranean, and the 10th century A.D. in southwestern Asia. By contrast, the CCR5 Δ 32 mutation is found only in European, West Asian, and North African populations. The anomalously high frequency of CCR5 Δ32 in these populations appears to require both a unique origin in Northern Europe and subsequent selection by smallpox. CCR5 Δ32 can be beneficial to the host in some infections (e.g., HIV-1, possibly smallpox), but detrimental in others (e.g., tick-borne encephalitis , West Nile virus ). Whether CCR5 function is helpful or harmful in the context of a given infection depends on a complex interplay between the immune system and the pathogen. In general, research suggests that the CCR5 Δ32 mutation may play a deleterious role in post-infection inflammatory processes, which can injure tissue and create further pathology. The best evidence for this proposed antagonistic pleiotropy is found in flavivirus infections. In general many viral infections are asymptomatic or produce only mild symptoms in the vast majority of the population. However, certain unlucky individuals experience a particularly destructive clinical course, which is otherwise unexplained but appears to be genetically mediated. Patients homozygous for CCR5 Δ32 were found to be at higher risk for a neuroinvasive form of tick-borne encephalitis (caused by a flavivirus ). In addition, functional CCR5 may be required to prevent symptomatic disease after infection with West Nile virus, another flavivirus; CCR5 Δ32 was associated with early symptom development and more pronounced clinical manifestations after infection with West Nile virus. This finding in humans confirmed a previously observed experiment in an animal model of CCR5 Δ32 homozygosity. After infection with West Nile virus, CCR5 Δ32 mice had markedly increased viral titers in the central nervous system and had increased mortality compared with that of wild-type mice, thus suggesting that CCR5 expression was necessary to mount a strong host defense against West Nile virus. A genetic approach involving intrabodies that block CCR5 expression has been proposed as a treatment for HIV-1 infected individuals. When T-cells modified so they no longer express CCR5 were mixed with unmodified T-cells expressing CCR5 and then challenged by infection with HIV-1, the modified T-cells that do not express CCR5 eventually take over the culture, as HIV-1 kills the non-modified T-cells. This same method might be used in vivo to establish a virus-resistant cell pool in infected individuals. This hypothesis was tested in an AIDS patient who had also developed myeloid leukemia , and was treated with chemotherapy to suppress the cancer. A bone marrow transplant containing stem cells from a matched donor was then used to restore the immune system. However, the transplant was performed from a donor with 2 copies of CCR5-Δ32 mutation gene. After 600 days, the patient was healthy and had undetectable levels of HIV in the blood and in examined brain and rectal tissues. Before the transplant, low levels of HIV X4 , which does not use the CCR5 receptor, were also detected. Following the transplant, however, this type of HIV was not detected either. However, this outcome is consistent with the observation that cells expressing the CCR5-Δ32 variant protein lack both the CCR5 and CXCR4 receptors on their surfaces, thereby conferring resistance to a broad range of HIV variants including HIVX4. After over six years, the patient has maintained the resistance to HIV and has been pronounced cured of the HIV infection. Enrollment of HIV-positive patients in a clinical trial was started in 2009 in which the patients' cells were genetically modified with a zinc finger nuclease to carry the CCR5-Δ32 trait and then reintroduced into the body as a potential HIV treatment. Results reported in 2014 were promising. Inspired by the first person ever to be cured of HIV, The Berlin Patient , StemCyte began collaborations with cord blood banks worldwide to systematically screen umbilical cord blood samples for the CCR5 mutation beginning in 2011. In November 2018, Jiankui He announced that he had edited two human embryos, to attempt to disable the gene for CCR5, which codes for a receptor that HIV uses to enter cells. He said that twin girls, Lulu and Nana , had been born a few weeks earlier, and that the girls still carried functional copies of CCR5 along with disabled CCR5 ( mosaicism ), hence being still vulnerable to HIV. The work was widely condemned as unethical, dangerous, and premature. The CCR5 Δ32 allele is notable for its recent origin, unexpectedly high frequency, and distinct geographic distribution, which together suggest that (a) it arose from a single mutation, and (b) it was historically subject to positive selection. Two studies have used linkage analysis to estimate the age of the CCR5 Δ32 deletion, assuming that the amount of recombination and mutation observed on genomic regions surrounding the CCR5 Δ32 deletion would be proportional to the age of the deletion. Using a sample of 4000 individuals from 38 ethnic populations, Stephens et al. estimated that the CCR5-Δ32 deletion occurred 700 years ago (275-1875, 95% confidence interval). Another group, Libert et al. (1998), used microsatellite mutations to estimate the age of the CCR5 Δ32 mutation to be 2100 years (700-4800, 95% confidence interval). On the basis of observed recombination events, they estimated the age of the mutation to be 2250 years (900-4700, 95% confidence interval). A third hypothesis relies on the north-to-south gradient of allele frequency in Europe, which shows that the highest allele frequency occurred in the Nordic countries and lowest allele frequency in southern Europe. Because the Vikings historically occupied these countries, it may be possible that the allele spread throughout Europe due to the Viking dispersal in the 8th to 10th centuries. Vikings were later replaced by the Varangians in Russia, which may have contributed to the observed east-to-west cline of allele frequency. HIV-1 was initially transmitted from chimpanzees ( Pan troglodytes ) to humans in the early 1900s in Southeast Cameroon, Africa, through exposure to infected blood and body fluids while butchering bushmeat. However, HIV-1 was effectively absent from Europe until the 1980s. Therefore, given the average age of roughly 1000 years for the CCR5-Δ32 allele, it can be established that HIV-1 did not exert selection pressure on the human population for long enough to achieve the current frequencies. Hence, other pathogens have been suggested as agents of positive selection for CCR5 Δ32, including bubonic plague ( Yersinia pestis ) and smallpox ( Variola major ). Other data suggest that the allele frequency experienced negative selection pressure as a result of pathogens that became more widespread during Roman expansion. The idea that negative selection played a role in the allele's low frequency is also supported by experiments using knockout mice and Influenza A, which demonstrated that the presence of the CCR5 receptor is important for efficient response to a pathogen. Several lines of evidence suggest that the CCR5 Δ32 allele evolved only once. First, CCR5 Δ32 has a relatively high frequency in several different European populations but is comparatively absent in Asian, Middle Eastern and American Indian populations, suggesting that a single mutation occurred after divergence of Europeans from their African ancestor. Second, genetic linkage analysis indicates that the mutation occurs on a homogeneous genetic background, implying that inheritance of the mutation occurred from a common ancestor. This was demonstrated by showing that the CCR5 Δ32 allele is in strong linkage disequilibrium with highly polymorphic microsatellites. More than 95% of CCR5 Δ32 chromosomes also carried the IRI3.1-0 allele, while 88% carried the IRI3.2 allele. By contrast, the microsatellite markers IRI3.1-0 and IRI3.2-0 were found in only 2 or 1.5% of chromosomes carrying a wild-type CCR5 allele. This evidence of linkage disequilibrium supports the hypothesis that most, if not all, CCR5 Δ32 alleles arose from a single mutational event. Finally, the CCR5 Δ32 allele has a unique geographical distribution indicating a single Northern origin followed by migration. A study measuring allele frequencies in 18 European populations found a North-to-South gradient, with the highest allele frequencies in Finnish and Mordvinian populations (16%), and the lowest in Sardinia (4%). In the absence of selection, a single mutation would take an estimated 127,500 years to rise to a population frequency of 10%. Estimates based on genetic recombination and mutation rates place the age of the allele between 1000 and 2000 years. This discrepancy is a signature of positive selection. It is estimated that HIV-1 entered the human population in Africa in the early 1900s, but symptomatic infections were not reported until the 1980s. The HIV-1 epidemic is therefore far too young to be the source of positive selection that drove the frequency of CCR5 Δ32 from zero to 10% in 2000 years. Protection from bubonic plague . Stephens, et al. (1998), suggest that bubonic plague ( Yersinia pestis ) had exerted positive selective pressure on CCR5 Δ32. This hypothesis was based on the timing and severity of the Black Death pandemic, which killed 30% of the European population of all ages between 1346 and 1352. After the Black Death, there were less severe, intermittent epidemics. Individual cities experienced high mortality, but overall mortality in Europe was only a few percent. In 1655-1656 a second pandemic called the "Great Plague" killed 15-20% of London's population. [ dubious – discuss ] Importantly, the plague epidemics were intermittent. Bubonic plague is a zoonotic disease, primarily infecting rodents, spread by fleas, and only occasionally infecting humans. Human-to-human infection of bubonic plague does not occur, though it can occur in pneumonic plague, which infects the lungs. Only when the density of rodents is low are infected fleas forced to feed on alternative hosts such as humans, and under these circumstances a human epidemic may occur. Based on population genetic models, Galvani and Slatkin (2003) argue that the intermittent nature of plague epidemics did not generate a sufficiently strong selective force to drive the allele frequency of CCR5 Δ32 to 10% in Europe. To test this hypothesis, Galvani and Slatkin (2003) modeled the historical selection pressures produced by plague and smallpox. Protection from smallpox . Plague was modeled according to historical accounts, while age-specific smallpox mortality was gleaned from the age distribution of smallpox burials in York (England) between 1770 and 1812. Smallpox preferentially infects young, pre-reproductive members of the population since they are the only individuals who are not immunized or dead from past infection. Because smallpox preferentially kills pre-reproductive members of a population, it generates stronger selective pressure than plague. Unlike plague, smallpox does not have an animal reservoir and is only transmitted from human to human. The authors calculated that if plague were selecting for CCR5 Δ32, the frequency of the allele would still be less than 1%, while smallpox has exerted a selective force sufficient to reach 10%. The hypothesis that smallpox exerted positive selection for CCR5 Δ32 is also biologically plausible, since poxviruses, like HIV, enter white blood cells using chemokine receptors. By contrast, Yersinia pestis is a bacterium with a very different biology. Although Europeans are the only group to have subpopulations with a high frequency of CCR5 Δ32, they are not the only population that has been subject to selection by smallpox, which had a worldwide distribution before it was declared eradicated in 1980. The earliest unmistakable descriptions of smallpox appear in the 5th century A.D. in China, the 7th century A.D. in India and the Mediterranean, and the 10th century A.D. in southwestern Asia. By contrast, the CCR5 Δ 32 mutation is found only in European, West Asian, and North African populations. The anomalously high frequency of CCR5 Δ32 in these populations appears to require both a unique origin in Northern Europe and subsequent selection by smallpox.CCR5 Δ32 can be beneficial to the host in some infections (e.g., HIV-1, possibly smallpox), but detrimental in others (e.g., tick-borne encephalitis , West Nile virus ). Whether CCR5 function is helpful or harmful in the context of a given infection depends on a complex interplay between the immune system and the pathogen. In general, research suggests that the CCR5 Δ32 mutation may play a deleterious role in post-infection inflammatory processes, which can injure tissue and create further pathology. The best evidence for this proposed antagonistic pleiotropy is found in flavivirus infections. In general many viral infections are asymptomatic or produce only mild symptoms in the vast majority of the population. However, certain unlucky individuals experience a particularly destructive clinical course, which is otherwise unexplained but appears to be genetically mediated. Patients homozygous for CCR5 Δ32 were found to be at higher risk for a neuroinvasive form of tick-borne encephalitis (caused by a flavivirus ). In addition, functional CCR5 may be required to prevent symptomatic disease after infection with West Nile virus, another flavivirus; CCR5 Δ32 was associated with early symptom development and more pronounced clinical manifestations after infection with West Nile virus. This finding in humans confirmed a previously observed experiment in an animal model of CCR5 Δ32 homozygosity. After infection with West Nile virus, CCR5 Δ32 mice had markedly increased viral titers in the central nervous system and had increased mortality compared with that of wild-type mice, thus suggesting that CCR5 expression was necessary to mount a strong host defense against West Nile virus.A genetic approach involving intrabodies that block CCR5 expression has been proposed as a treatment for HIV-1 infected individuals. When T-cells modified so they no longer express CCR5 were mixed with unmodified T-cells expressing CCR5 and then challenged by infection with HIV-1, the modified T-cells that do not express CCR5 eventually take over the culture, as HIV-1 kills the non-modified T-cells. This same method might be used in vivo to establish a virus-resistant cell pool in infected individuals. This hypothesis was tested in an AIDS patient who had also developed myeloid leukemia , and was treated with chemotherapy to suppress the cancer. A bone marrow transplant containing stem cells from a matched donor was then used to restore the immune system. However, the transplant was performed from a donor with 2 copies of CCR5-Δ32 mutation gene. After 600 days, the patient was healthy and had undetectable levels of HIV in the blood and in examined brain and rectal tissues. Before the transplant, low levels of HIV X4 , which does not use the CCR5 receptor, were also detected. Following the transplant, however, this type of HIV was not detected either. However, this outcome is consistent with the observation that cells expressing the CCR5-Δ32 variant protein lack both the CCR5 and CXCR4 receptors on their surfaces, thereby conferring resistance to a broad range of HIV variants including HIVX4. After over six years, the patient has maintained the resistance to HIV and has been pronounced cured of the HIV infection. Enrollment of HIV-positive patients in a clinical trial was started in 2009 in which the patients' cells were genetically modified with a zinc finger nuclease to carry the CCR5-Δ32 trait and then reintroduced into the body as a potential HIV treatment. Results reported in 2014 were promising. Inspired by the first person ever to be cured of HIV, The Berlin Patient , StemCyte began collaborations with cord blood banks worldwide to systematically screen umbilical cord blood samples for the CCR5 mutation beginning in 2011. In November 2018, Jiankui He announced that he had edited two human embryos, to attempt to disable the gene for CCR5, which codes for a receptor that HIV uses to enter cells. He said that twin girls, Lulu and Nana , had been born a few weeks earlier, and that the girls still carried functional copies of CCR5 along with disabled CCR5 ( mosaicism ), hence being still vulnerable to HIV. The work was widely condemned as unethical, dangerous, and premature.

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West Nile

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Equatoria

Equatoria is the southernmost region of South Sudan , along the upper reaches of the White Nile and the border between South Sudan and Uganda. Juba , the national capital and the largest city in South Sudan, is located in Equatoria. Originally a province of Anglo-Egyptian Sudan , it also contained most of northern parts of present-day Uganda , including Lake Albert and West Nile . It was an idealistic effort to create a model state in the interior of Africa that never consisted of more than a handful of adventurers and soldiers in isolated outposts. Equatoria was established by Samuel Baker in 1870. Charles George Gordon took over as governor in 1874, followed by Emin Pasha in 1878. The Mahdist Revolt put an end to Equatoria as an Egyptian outpost in 1889. Later British Governors included Martin Willoughby Parr . Important towns in Equatoria included Lado , Gondokoro , Dufile and Wadelai . The last two former areas of Equatoria, Lake Albert and West Nile are now situated in Uganda. Under Anglo-Egyptian rule , most of Equatoria became one of the eight original provinces of Sudan. The region of Bahr el Ghazal was split from Equatoria in 1948. In 1976, Equatoria was further split into the provinces of East and West Equatoria . The region has been troubled with violence during both the First and Second Sudanese Civil Wars , as well as the anti-Ugandan insurgencies based in Sudan such as the Lord's Resistance Army and West Nile Bank Front .Equatoria consists of the following states : Between October 2015 and February 2020, Equatoria consisted of the following states:Equatoria consists of the following states : Between October 2015 and February 2020, Equatoria consisted of the following states:The people of Equatoria are traditionally peasants or nomads belonging to numerous ethnic groups. They live in the counties of Budi , Ezo, Juba , Kajo-keji, Kapoeta , Magwi , Maridi , Lainya , Mundri, Terekeka , Tombura, Torit , Yambio , and Yei . Equatoria is inhabited by the ethnolinguistic groups listed below. The following tribes occupy the three states of Greater Equatoria: Acholi , Avukaya , Baka , Balanda , Bari , Didinga , Kakwa , Keliko , Kuku , Lango , Lokoya , Narim, Lopit , Lugbwara , Lulubo, Madi , Makaraka or Adio, Moru , Mundari , Mundu , Nyangwara , Otuho , Pari , Pojulu , Tenet , Toposa and Azande . Some of these tribes like Bari, Pojulu, Kuku, Kakwa, Mundari and Nyangwara share a common language, but their accents, and some adjectives and nouns do vary; the same applies to Keliko, Moru and Madi.Other than Arabic or (Arabi Juba) and English, the following languages are spoken in Equatoria according to Ethnologue . Due to the many years of the civil war , the Equatorian culture is heavily influenced by the countries neighboring Equatoria and hosting Equatorians. Many Equatorians fled to Ethiopia , Kenya , Uganda , the Democratic Republic of the Congo , the Central African Republic , Sudan , the United States , Canada , the United Kingdom , Australia and Europe , where they interacted with the nationals and learnt their languages and culture. For most of those who remained in the country, or went North to Sudan and Egypt , they greatly assimilated Arabic culture. Most Equatorians kept the core of their culture even while in exile and diaspora . Traditionally, culture is highly upheld and a great focus is given to knowing one's origin and dialect . Although the common languages spoken in Equatoria are Juba Arabic/Arabi Juba and English , Lingala and Kiswahili are being introduced to the population to improve the country's relations with its East African neighbors. Many musicians from Equatoria use English, Lingala, Kiswahili, Arabi Juba (Arabic Creole), their language or dialect or a mix of all. Popular artists sing Afro-beat , R&B , and zouk . Dynamiq is popular for his reggae .In the 19th century, Egypt controlled Sudan and established the Equatoria province to further control its interests over the Nile . The Egyptian authorities selected British explorer Sir Samuel Baker to establish Equatoria for them, which he did in 1870. Baker was instructed to establish trading posts along the White Nile and Gondokoro ( Gondu kuru , means "difficult to dig", in Bari ), a trading center located on the east bank of the White Nile in Southern Sudan. Gondokoro was an important center since it was located within a few kilometres from the cutoff point of navigability of the Nile from Khartoum . It is presently located near the city of Juba in Equatoria. Baker's attempt to create additional trading posts and control Equatoria was unsuccessful because villages surrounding Gondokoro were frequently bypassed by Arab invaders who wanted to impose their culture and way of life on the people. King Gbudwe who ruled the western part of Equatoria at the time as The King of Azande Kingdom despised the Arab culture and way of life and encouraged the tribes to resist the invaders and protect their African culture and their way of life. The invaders were met with stiff resistance from Equatorian tribes such as the Azande, Bari , Lokoya , Otuho , and Pari . At the end of Baker's service as governor, British general Charles George Gordon was appointed governor of Sudan. Gordon took over in 1874 and administered the region until 1876. He was more successful in creating additional trading posts in the area. In 1876, Gordon's views clashed with those of the Egyptian governor of Khartoum forcing him to go back to London. In 1878 Gordon was succeeded by the Chief Medical Officer of the Equatoria province, Mehemet Emin , popularly known as Emin Pasha. Emin made his headquarters at Lado (now in South Sudan). Emin Pasha had little influence over the area because the Khartoum governor was uninterested in his development proposals for the Equatoria region. In 1881, Muhammad Ahmad Abdullah, a Muslim religious leader, proclaimed himself the Mahdi ("expected one") and began a holy war to unify the tribes of Western and Central Sudan, including Equatoria. By 1883 the Mahdists had cut off outside communications. However, Emin Pasha managed to request assistance from Britain via Buganda . The British sent the explorer Henry Morton Stanley and who led a relief expedition , called the "Advance," in February 1887 to rescue Emin. The Advance navigated up the Congo River and then through the Ituri Forest , one of the most difficult forest routes in Africa, resulting in the loss of two-thirds of the expedition's personnel. While the Advance succeeded in reaching Emin Pasha by February of the following year, the Mahdists had already overrun the bulk of the province, and Emin had already been deposed as governor by his officers in August 1887. The Advance reached the coast, with Emin, by the end of the year, by which point the Mahdists were firmly in control of Equatoria. In 1898, the Mahdist State was overthrown by the Anglo-Egyptian force led by British Field Marshal Lord Kitchener . Sudan was proclaimed a condominium under British-Egyptian administration with Equatoria being administered by the British. Equatoria received little attention from the British prior to World War I . Equatoria was closed to outside influences and developed along indigenous lines. As a result, the region remained isolated and underdeveloped. Limited social services to the region were provided by Christian missionaries who opened schools and medical clinics. The education provided by the missionaries was mainly limited to learning English language and arithmetic. In February 1953, the United Kingdom and Egypt reached an agreement providing for Sudanese self-government and self-determination . On January 1, 1956 Sudan gained independence from the British and Egyptian governments. The new state was under the control of the Arab led Khartoum government. The Arab Khartoum government had promised Southerners full participation in the political system, however, after independence the Khartoum government reneged on its promises. Southerners were denied participation in free elections and marginalized from political power. The government actions created resentment in the south that led to a mutiny by a group of Equatorians sparking the 21 year civil war (1955–1972 and 1983–2004). Equatorians played an instrumental role in the struggle for autonomy in South Sudan. The origins of Sudan's civil war dates back to 1955, a year before independence, when it became clear the Arabs were going to take over the national government in Khartoum. Equatoria gave its name to the southernmost unit of the British Sudan Defence Force , formed during the Anglo-Egyptian administration . This was the Equatoria or Southern Corps. On August 18, 1955, No. 2 Company of the Equatoria Corps mutinied at Torit , Eastern Equatoria. No. 2 Company had been ordered to make ready to move to the north, but instead of obeying, the troops mutinied, along with other Southern soldiers across the south in Juba , Yei , Yambio, and Maridi . The Khartoum government sent other Sudan Defence Force units to quell the rebellion and many mutineers of the Equatoria Corps went into hiding rather than surrender. This marked the beginning of the first civil war in southern Sudan. The rebellion that emerged from the Equatoria Corps was later called Anya Nya and the leaders were separatists, who demanded the creation of a separate South Sudanese nation, free from Arab domination. The Equatorian leaders of the Anya Nya and founders of the struggle were Rev. Fr Saturnino Ohure who was of Lotuho origin and was said to have been the first man to have fired a bullet, and launched the start of the first civil war, in Torit; Fr. Saturnino Lohure from Otuho; Aggrey Jaden from Pojulu Joseph Ohide, from Otuho Marko Rume, from Kuku Ezboni Mondiri , from Moru Albino Tombe, from Lokoya Tafeng Lodongi, from Otuho Lazaru Mutek, from Otuho Benjamin Loki , from Pojulu Elia Lupe, from Kakwa Elia Kuzee, from ZandeTimon Boro, from Moru Dominic Dabi Manango, from Zande Alison Monani Magaya, from Zande Isaiah Paul, from Zande Dominic Kassiano Dombo, from Zande and many others. The Khartoum government sent its forces to arrest the rebels and capture anyone who supported their cause. By the early 1960s civilians believed to be Anya Nya sympathizers were arrested and shipped to Kodok concentration camp where they were tortured and killed. Some of the first detainees and survivors of the horrific torture at Kodok include Emmanuel Lukudu and Philip Lomodong Lako. [ citation needed ] By 1969 the Equatorian rebels found support among foreign governments and were able to obtained weapons and supplies. Anya Nya recruits were trained in Israel where they also got some of their weapons. The Anya Nya rebels received financial assistance from Southern Sudanese and Southern exiles from the Middle East, Western Europe, and North America. By the late 1960s, the war had resulted in the deaths of half a million people and several hundred thousand southerners escaped to hide in the forests or to refugee camps in neighboring countries. Anya Nya controlled the southern countryside while the government forces controlled the major towns in the region. The Anya Nya rebels were small in number and scattered all over the region making their operations ineffective. It is estimated that there were between 5,000 and 10,000 Anya Nya rebels. On May 25, 1969, Colonel Gaafar Muhammed Nimeiri led a military coup and overthrew General Ibrahim Abboud's regime. In 1971 Joseph Lagu , from the Madi ethnic group, became the leader of the southern forces opposed to Khartoum government and founded the South Sudan Liberation Movement (SSLM). Anya Nya leaders united and rallied behind Lagu. Lagu was also supported by exiled southern politicians. With Lagu's leadership the SSLM created a governing infrastructure throughout many areas in southern Sudan. In 1972 Nimeri held negotiations with the Anya Nya at Addis Ababa, Ethiopia. At the talks the Anya Nya demanded a separate southern government and an army to defend the south. Ethiopia's Emperor Haile Selassie moderated the talks and helped the two sides reach an agreement. The result was the Addis Ababa Agreement . The agreement granted autonomy for the South with three provinces: Equatoria, Bar al Ghazal and Upper Nile. The south would have a regional president appointed by the national president to oversee all aspects of government in the region. The national government would maintain authority over defense, foreign affairs, currency, and finance, and economic and social planning, and interregional concerns. The members of the Anya Nya would be incorporated into the Sudanese army and have equal status with the northern forces. The agreement declared Arabic as Sudan's official language and English as the south's principal language for administration and schooling. Despite opposition from SSLM leaders on the terms of the Agreement, Joseph Lagu approved the agreement and both sides agreed to a cease-fire. The Addis Ababa Accords were signed on March 27, 1972 and the Sudanese celebrated that day as National Unity Day. This agreement resulted in a hiatus in the Sudanese civil war from 1972 to 1983. In 1983, President Gaafar Nimeiry abolished the parliament and embarked on a campaign to Islamize all of Sudan. He outlawed political parties and enacted Sharia law in the penal code. Non-Muslim southerners were now forced to obey Islamic laws and traditions. The policies revived southern opposition and military insurgency in the South. In 1985 Abdel Rahman Swar al-Dahab led a coup and overthrew the regime. In 1986, Sadiq al-Mahdi was elected president of Sudan. The new regime began negotiations led by Colonel John Garang de Mabior , the leader of the Sala, but failed to reach an agreement to end the southern insurgency. Civil war has continued since then, but international pressure led SPLA and the Khartoum government to reach an agreement to end the 21-year civil war. In January 2020, the National Alliance for Democracy and Freedom Action (NADAFA) sought to join talks in Rome seeking to resolve political rifts within South Sudan. The group is a coalition of holdout political groups including the People's Democratic Movement (PDM), which was not signatory to the peace agreement signed by President Salva Kiir's South Sudanese government in 2018. NADAFA sought a power-sharing arrangement in the new national government, with "People's Constitutional Conventions" held in Equatoria, Upper Nile and Bahr al Ghazal. In September 2020, Sudans Post published a message from Dr. Hakim Dario, the leader of NADAFA, expressing concern that the new nation had been named "South Sudan" and proposed that the nation should be called "Equatoria Federal Republic". On February 9, 2022, the Azande community in Yambio held a coronation ceremony for King Atoroba Peni Rikito Gbudue. The traditional royal title was last held by King Rikito's great-grandfather King Gbudue, who died in 1905. Some neighboring cultural groups such as the Maridi and Balanda people wrote letters to the new king, warning him that they would not be subjects to the restored kingdom, with the Maridi letter specifically rejecting any ethnic political divisions, saying "We stand to promote the Republic of South Sudan, not the culture of a specific group." However, Badagbu Daniel Rimbasa, the king's brother, stated that the new king will not participate in politics. "It's purely promotion of our culture and its preservation and heritage, not political." In the 19th century, Egypt controlled Sudan and established the Equatoria province to further control its interests over the Nile . The Egyptian authorities selected British explorer Sir Samuel Baker to establish Equatoria for them, which he did in 1870. Baker was instructed to establish trading posts along the White Nile and Gondokoro ( Gondu kuru , means "difficult to dig", in Bari ), a trading center located on the east bank of the White Nile in Southern Sudan. Gondokoro was an important center since it was located within a few kilometres from the cutoff point of navigability of the Nile from Khartoum . It is presently located near the city of Juba in Equatoria. Baker's attempt to create additional trading posts and control Equatoria was unsuccessful because villages surrounding Gondokoro were frequently bypassed by Arab invaders who wanted to impose their culture and way of life on the people. King Gbudwe who ruled the western part of Equatoria at the time as The King of Azande Kingdom despised the Arab culture and way of life and encouraged the tribes to resist the invaders and protect their African culture and their way of life. The invaders were met with stiff resistance from Equatorian tribes such as the Azande, Bari , Lokoya , Otuho , and Pari . At the end of Baker's service as governor, British general Charles George Gordon was appointed governor of Sudan. Gordon took over in 1874 and administered the region until 1876. He was more successful in creating additional trading posts in the area. In 1876, Gordon's views clashed with those of the Egyptian governor of Khartoum forcing him to go back to London. In 1878 Gordon was succeeded by the Chief Medical Officer of the Equatoria province, Mehemet Emin , popularly known as Emin Pasha. Emin made his headquarters at Lado (now in South Sudan). Emin Pasha had little influence over the area because the Khartoum governor was uninterested in his development proposals for the Equatoria region. In 1881, Muhammad Ahmad Abdullah, a Muslim religious leader, proclaimed himself the Mahdi ("expected one") and began a holy war to unify the tribes of Western and Central Sudan, including Equatoria. By 1883 the Mahdists had cut off outside communications. However, Emin Pasha managed to request assistance from Britain via Buganda . The British sent the explorer Henry Morton Stanley and who led a relief expedition , called the "Advance," in February 1887 to rescue Emin. The Advance navigated up the Congo River and then through the Ituri Forest , one of the most difficult forest routes in Africa, resulting in the loss of two-thirds of the expedition's personnel. While the Advance succeeded in reaching Emin Pasha by February of the following year, the Mahdists had already overrun the bulk of the province, and Emin had already been deposed as governor by his officers in August 1887. The Advance reached the coast, with Emin, by the end of the year, by which point the Mahdists were firmly in control of Equatoria. In 1898, the Mahdist State was overthrown by the Anglo-Egyptian force led by British Field Marshal Lord Kitchener . Sudan was proclaimed a condominium under British-Egyptian administration with Equatoria being administered by the British.Equatoria received little attention from the British prior to World War I . Equatoria was closed to outside influences and developed along indigenous lines. As a result, the region remained isolated and underdeveloped. Limited social services to the region were provided by Christian missionaries who opened schools and medical clinics. The education provided by the missionaries was mainly limited to learning English language and arithmetic.In February 1953, the United Kingdom and Egypt reached an agreement providing for Sudanese self-government and self-determination . On January 1, 1956 Sudan gained independence from the British and Egyptian governments. The new state was under the control of the Arab led Khartoum government. The Arab Khartoum government had promised Southerners full participation in the political system, however, after independence the Khartoum government reneged on its promises. Southerners were denied participation in free elections and marginalized from political power. The government actions created resentment in the south that led to a mutiny by a group of Equatorians sparking the 21 year civil war (1955–1972 and 1983–2004).Equatorians played an instrumental role in the struggle for autonomy in South Sudan. The origins of Sudan's civil war dates back to 1955, a year before independence, when it became clear the Arabs were going to take over the national government in Khartoum. Equatoria gave its name to the southernmost unit of the British Sudan Defence Force , formed during the Anglo-Egyptian administration . This was the Equatoria or Southern Corps. On August 18, 1955, No. 2 Company of the Equatoria Corps mutinied at Torit , Eastern Equatoria. No. 2 Company had been ordered to make ready to move to the north, but instead of obeying, the troops mutinied, along with other Southern soldiers across the south in Juba , Yei , Yambio, and Maridi . The Khartoum government sent other Sudan Defence Force units to quell the rebellion and many mutineers of the Equatoria Corps went into hiding rather than surrender. This marked the beginning of the first civil war in southern Sudan. The rebellion that emerged from the Equatoria Corps was later called Anya Nya and the leaders were separatists, who demanded the creation of a separate South Sudanese nation, free from Arab domination. The Equatorian leaders of the Anya Nya and founders of the struggle were Rev. Fr Saturnino Ohure who was of Lotuho origin and was said to have been the first man to have fired a bullet, and launched the start of the first civil war, in Torit; Fr. Saturnino Lohure from Otuho; Aggrey Jaden from Pojulu Joseph Ohide, from Otuho Marko Rume, from Kuku Ezboni Mondiri , from Moru Albino Tombe, from Lokoya Tafeng Lodongi, from Otuho Lazaru Mutek, from Otuho Benjamin Loki , from Pojulu Elia Lupe, from Kakwa Elia Kuzee, from ZandeTimon Boro, from Moru Dominic Dabi Manango, from Zande Alison Monani Magaya, from Zande Isaiah Paul, from Zande Dominic Kassiano Dombo, from Zande and many others. The Khartoum government sent its forces to arrest the rebels and capture anyone who supported their cause. By the early 1960s civilians believed to be Anya Nya sympathizers were arrested and shipped to Kodok concentration camp where they were tortured and killed. Some of the first detainees and survivors of the horrific torture at Kodok include Emmanuel Lukudu and Philip Lomodong Lako. [ citation needed ] By 1969 the Equatorian rebels found support among foreign governments and were able to obtained weapons and supplies. Anya Nya recruits were trained in Israel where they also got some of their weapons. The Anya Nya rebels received financial assistance from Southern Sudanese and Southern exiles from the Middle East, Western Europe, and North America. By the late 1960s, the war had resulted in the deaths of half a million people and several hundred thousand southerners escaped to hide in the forests or to refugee camps in neighboring countries. Anya Nya controlled the southern countryside while the government forces controlled the major towns in the region. The Anya Nya rebels were small in number and scattered all over the region making their operations ineffective. It is estimated that there were between 5,000 and 10,000 Anya Nya rebels. On May 25, 1969, Colonel Gaafar Muhammed Nimeiri led a military coup and overthrew General Ibrahim Abboud's regime. In 1971 Joseph Lagu , from the Madi ethnic group, became the leader of the southern forces opposed to Khartoum government and founded the South Sudan Liberation Movement (SSLM). Anya Nya leaders united and rallied behind Lagu. Lagu was also supported by exiled southern politicians. With Lagu's leadership the SSLM created a governing infrastructure throughout many areas in southern Sudan. In 1972 Nimeri held negotiations with the Anya Nya at Addis Ababa, Ethiopia. At the talks the Anya Nya demanded a separate southern government and an army to defend the south. Ethiopia's Emperor Haile Selassie moderated the talks and helped the two sides reach an agreement. The result was the Addis Ababa Agreement . The agreement granted autonomy for the South with three provinces: Equatoria, Bar al Ghazal and Upper Nile. The south would have a regional president appointed by the national president to oversee all aspects of government in the region. The national government would maintain authority over defense, foreign affairs, currency, and finance, and economic and social planning, and interregional concerns. The members of the Anya Nya would be incorporated into the Sudanese army and have equal status with the northern forces. The agreement declared Arabic as Sudan's official language and English as the south's principal language for administration and schooling. Despite opposition from SSLM leaders on the terms of the Agreement, Joseph Lagu approved the agreement and both sides agreed to a cease-fire. The Addis Ababa Accords were signed on March 27, 1972 and the Sudanese celebrated that day as National Unity Day. This agreement resulted in a hiatus in the Sudanese civil war from 1972 to 1983.In 1983, President Gaafar Nimeiry abolished the parliament and embarked on a campaign to Islamize all of Sudan. He outlawed political parties and enacted Sharia law in the penal code. Non-Muslim southerners were now forced to obey Islamic laws and traditions. The policies revived southern opposition and military insurgency in the South. In 1985 Abdel Rahman Swar al-Dahab led a coup and overthrew the regime. In 1986, Sadiq al-Mahdi was elected president of Sudan. The new regime began negotiations led by Colonel John Garang de Mabior , the leader of the Sala, but failed to reach an agreement to end the southern insurgency. Civil war has continued since then, but international pressure led SPLA and the Khartoum government to reach an agreement to end the 21-year civil war. In January 2020, the National Alliance for Democracy and Freedom Action (NADAFA) sought to join talks in Rome seeking to resolve political rifts within South Sudan. The group is a coalition of holdout political groups including the People's Democratic Movement (PDM), which was not signatory to the peace agreement signed by President Salva Kiir's South Sudanese government in 2018. NADAFA sought a power-sharing arrangement in the new national government, with "People's Constitutional Conventions" held in Equatoria, Upper Nile and Bahr al Ghazal. In September 2020, Sudans Post published a message from Dr. Hakim Dario, the leader of NADAFA, expressing concern that the new nation had been named "South Sudan" and proposed that the nation should be called "Equatoria Federal Republic". On February 9, 2022, the Azande community in Yambio held a coronation ceremony for King Atoroba Peni Rikito Gbudue. The traditional royal title was last held by King Rikito's great-grandfather King Gbudue, who died in 1905. Some neighboring cultural groups such as the Maridi and Balanda people wrote letters to the new king, warning him that they would not be subjects to the restored kingdom, with the Maridi letter specifically rejecting any ethnic political divisions, saying "We stand to promote the Republic of South Sudan, not the culture of a specific group." However, Badagbu Daniel Rimbasa, the king's brother, stated that the new king will not participate in politics. "It's purely promotion of our culture and its preservation and heritage, not political."

Wiki

West Nile

https://api.wikimedia.org/core/v1/wikipedia/en/page/Nile_tilapia/html

Nile tilapia

Tilapia crassispina Arambourg , 1948 Perca nilotica Linnaeus, 1758 Chromis nilotica (Linnaeus, 1758) Chromis niloticus (Linnaeus, 1758) Oreochromis nilotica (Linnaeus, 1758) Oreochromis niloticus niloticus (Linnaeus, 1758) Sarotherodon niloticus (Linnaeus, 1758) Tilapia nilotica (Linnaeus, 1758) Tilapia nilotica nilotica (Linnaeus, 1758) Chromis guentheri Steindachner , 1864 Tilapia eduardiana Boulenger , 1912 Oreochromis niloticus eduardianus (Boulenger, 1912) Tilapia nilotica eduardiana Boulenger, 1912 Tilapia cancellata Nichols , 1923 Oreochromis cancellatus cancellatus (Nichols, 1923) Oreochromis niloticus cancellatus (Nichols, 1923) Tilapia nilotica cancellata Nichols, 1923 Tilapia calciati Gianferrari , 1924 Tilapia regani Poll , 1932 Tilapia nilotica regani Poll, 1932 Tilapia inducta Trewavas , 1933 Tilapia vulcani Trewavas, 1933 Oreochromis niloticus vulcani (Trewavas, 1933) Oreochromis vulcani (Trewavas, 1933) Oreochromis niloticus baringoensis Trewavas, 1983 Oreochromis niloticus filoa Trewavas, 1983 Oreochromis cancellatus filoa Trewavas, 1983 Oreochromis niloticus sugutae Trewavas, 1983 Oreochromis niloticus tana Seyoum & Kornfield, 1992 The Nile tilapia ( Oreochromis niloticus ) is a species of tilapia , a cichlid fish native to parts of Africa and the Levant , particularly Israel and Lebanon . Numerous introduced populations exist outside its natural range. It is also commercially known as mango fish (not to be confused with mango tilapia , or Sarotherodon galilaeus ), nilotica , or boulti . The Nile tilapia reaches up to 60 cm (24 in) in length, and can exceed 5 kg (11 lb) . As typical of tilapia, males reach a larger size and grow faster than females. Wild, natural-type Nile tilapias are brownish or grayish overall, often with indistinct banding on their body, and the tail is vertically striped. When breeding, males become reddish, especially on their fins. It is commonly confused with the blue tilapita ( O. aureus ); that species lacks the striped tail pattern, has a red edge to the dorsal fin (this edge is gray or black in Nile tilapia), and males are bluish overall when breeding. The two species can also be separated by meristics . Because many tilapia in aquaculture and introduced around the world are selectively bred variants and/or hybrids , identifying them using the standard features that can be used in the wild, natural types is often not possible. The virtually unknown O. ismailiaensis has a plain tail, but otherwise closely resembles (and may only be a variant of) the Nile tilapia. Regardless, O. ismailiaensis might be extinct, as its only known habitat in northeastern Egypt has disappeared, although similar-looking individuals (perhaps the same) are known from the vicinity. Nile tilapia can live for more than 10 years. The Nile tilapia is native to larger parts of Africa , except Maghreb and almost all of Southern Africa . It is native to tropical West Africa , the Lake Chad basin, and much of the Nile system, including lakes Tana , Albert and Edward – George , as well as lakes Kivu , Tanganyika , and Turkana , and the Awash and Omo Rivers . In Israel , it is native to coastal river basins. It has been widely introduced elsewhere, both in Africa and other continents , including tens of countries in Asia , Europe , North America , and South America . In these places, it often becomes highly invasive , threatening the native ecosystems and species. However, some introduced populations historically labelled as Nile tilapia either are hybrids or another species; the Nile tilapia and blue tilapia especially often have been confused. In India , especially in the southern state of Tamil Nadu , the Nile Tilapia was introduced by K. Kamaraj , the then Chief Minister and has become a threat to the native fish species hence. The Nile tilapia can be found in most types of freshwater habitats , such as rivers , streams , canals , lakes , and ponds , and ranging from sea level to an altitude of 1,830 m (6,000 ft) . It also occurs in brackish water, but is unable to survive long-term in full salt water. The species has been recorded at water temperatures between 8 and 42 °C (46 and 108 °F) , although typically above 13.5 °C (56.5 °F) , and the upper lethal limit usually is at 39–40 °C (102–104 °F) . Also, some variations occur depending on the population. For example, those in the northern part of its range survive down to the coldest temperatures, while isolated populations in hot springs in the Awash basin and at Suguta River generally live in waters that are at least 32–33 °C (90–91 °F) . Although Nile tilapia can survive down to relatively cold temperatures, breeding generally only occurs when the water reaches 24 °C (75 °F) . Although FishBase considers the species as monotypic , several distinctive populations often are recognized as valid subspecies : O. n. niloticus (Linnaeus, 1758) – most of species' range O. n. baringoensis Trewavas, 1983 – Lake Baringo in Kenya O. n. cancellatus (Nichols, 1923) – Awash basin in Ethiopia O. n. eduardianus (Boulenger, 1912) – Albertine Rift Valley lakes O. n. filoa Trewavas, 1983 – hot springs in Awash basin in Ethiopia O. n. sugutae Trewavas, 1983 – Karpeddo soda springs at Suguta River in Kenya O. n. tana Seyoum & Kornfield, 1992 – Lake Tana in Ethiopia O. n. vulcani Trewavas, 1933 – Lake Turkana in Ethiopia and Kenya While the species is overall very widespread and common, the IUCN considers O. n. baringoensis as endangered , O. n. sugutae as vulnerable , and O. n. filoa as data deficient . A population found in Lake Bogoria appears to be an undescribed subspecies. The forms referred to as Oreochromis (or Tilapia ) nyabikere and kabagole seem to belong to this species, too. An undescribed population found at, for example, Wami River , Lake Manyara , and Tingaylanda seems to be a close relative. Although FishBase considers the species as monotypic , several distinctive populations often are recognized as valid subspecies : O. n. niloticus (Linnaeus, 1758) – most of species' range O. n. baringoensis Trewavas, 1983 – Lake Baringo in Kenya O. n. cancellatus (Nichols, 1923) – Awash basin in Ethiopia O. n. eduardianus (Boulenger, 1912) – Albertine Rift Valley lakes O. n. filoa Trewavas, 1983 – hot springs in Awash basin in Ethiopia O. n. sugutae Trewavas, 1983 – Karpeddo soda springs at Suguta River in Kenya O. n. tana Seyoum & Kornfield, 1992 – Lake Tana in Ethiopia O. n. vulcani Trewavas, 1933 – Lake Turkana in Ethiopia and Kenya While the species is overall very widespread and common, the IUCN considers O. n. baringoensis as endangered , O. n. sugutae as vulnerable , and O. n. filoa as data deficient . A population found in Lake Bogoria appears to be an undescribed subspecies. The forms referred to as Oreochromis (or Tilapia ) nyabikere and kabagole seem to belong to this species, too. An undescribed population found at, for example, Wami River , Lake Manyara , and Tingaylanda seems to be a close relative. The Nile tilapia is mostly a herbivore , but with omnivorous tendencies, especially when young. They mostly feed on phytoplankton and algae , and in some populations other macrophytes also are important. Other recorded food items are detritus and aquatic insect larvae , including those of mosquitoes , making it a possible tool in the fight against malaria in Africa . However, when introduced outside its native range, it often becomes invasive , threatening more localized species. The Nile tilapia typically feeds during daytime, which suggests that, similar to trout and salmon , it exhibits a behavioral response to light as a main factor contributing to feeding activity. Due to its fast reproductive rate, however, overpopulation often results within groups of Nile tilapia. To obtain the necessary nutrients, night feeding may also occur due to competition for food during daylight. A recent study found evidence that, contrary to popular belief, size dimorphism between the sexes results from differential food conversion efficiency rather than different amounts of food consumed. Hence, although males and females eat equal amounts of food, males tend to grow larger due to a higher efficiency of converting food to body weight . Groups of Nile tilapia establish social hierarchies in which the dominant males have priority for both food and mating . Circular nests are built predominantly by males through mouth digging to become future spawning sites . These nests often become sites of intense courtship rituals and parental care . Like other fish, Nile tilapia travel almost exclusively in schools . Although males settle down in their crafted nesting zones, females travel between zones to find mates, resulting in competition between the males for females. [ citation needed ] Like other tilapias, such as Mozambique tilapia , dominance between the males is established first through noncontact displays such as lateral display and tail beats. Unsuccessful attempts to reconcile the hierarchy results in contact fighting to inflict injuries. Nile tilapia have been observed to modify their fighting behavior based upon experiences during development. Thus, experience in a certain form of agonistic behavior results in differential aggressiveness among individuals. Once the social hierarchy is established within a group, the dominant males enjoy the benefits of both increased access to food and an increased number of mates. However, social interactions between males in the presence of females results in higher energy expenditures as a consequence of courtship displays and sexual competition. Typical of most fish, Nile tilapia reproduce through mass spawning of a brood within a nest made by the male. In such an arrangement, territoriality and sexual competition amongst the males lead to large variations in reproductive success for individuals in a group. The genetic consequence of such behavior is reduced genetic variability in the long run, as inbreeding is likely to occur among different generations due to differential male reproductive success. Perhaps driven by reproductive competition, tilapias reproduce within a few months after birth. The relatively young age of sexual maturation within Nile tilapia leads to high birth and turnover rates. Consequently, the rapid reproductive rate of individuals can actually have a negative impact on growth rate, leading to the appearance of stunted tilapia as a result of a reduction in somatic growth in favor of sexual maturation. Female Nile tilapia, in the presence of other females either visually or chemically, exhibit shortened interspawning intervals. Although parental investment by a female extends the interspawning period, female tilapia that abandon their young to the care of a male gain this advantage of increased interspawning periods. One of the possible purposes behind this mechanism is to increase the reproductive advantage of females that do not have to care for young, allowing them more opportunities to spawn. For males, reproductive advantage goes to the more dominant males. Males have differential levels of gonadotropic hormones responsible for spermatogenesis , with dominant males having higher levels of the hormone. Thus, selection has favored larger sperm production with more successful males. Similarly, dominant males have both the best territory in terms of resources and the greatest access to mates. Furthermore, visual communication between Nile tilapia mates both stimulates and modulates reproductive behavior between partners such as courtship , spawning frequency, and nest building. Species belonging to the genus Oreochromis typically care for their young through mouthbrooding , oral incubation of the eggs and larvae. Similar to other tilapia, Nile tilapia are maternal mouthbrooders and extensive care is, therefore, provided almost exclusively by the female. After spawning in a nest made by a male, the young fry or eggs are carried in the mouth of the mother for a period of 12 days. Sometimes, the mother pushes the young back into her mouth if she believes they are not ready for the outside. Nile tilapias also demonstrate parental care in times of danger. When approached by a danger, the young often swim back into the protection of their mother's mouth. However, mouthbrooding leads to significant metabolic modifications for the parents, usually the mother, as reflected by fluctuations in body weight and low fitness . Thus, parental-offspring conflict can be observed through the costs and benefits of mouthbrooding. Protection of the young ensures passage of an individual's genes into the future generations, but caring for the young also reduces an individual's own reproductive fitness. Since female Nile tilapia exhibiting parental care show extended interspawning periods, one of the benefits is slowing down vitellogenesis (yolk deposition) to increase the survival rate of one's own young. The size of spawned eggs correlates directly with advantages concerning hatching time, growth, survival, and onset of feeding, since increased egg size means increased nutrients for the developing young. Thus, one of the reasons behind a delayed interspawning period by female Nile tilapia may be for the benefit of offspring survival. The Nile tilapia is mostly a herbivore , but with omnivorous tendencies, especially when young. They mostly feed on phytoplankton and algae , and in some populations other macrophytes also are important. Other recorded food items are detritus and aquatic insect larvae , including those of mosquitoes , making it a possible tool in the fight against malaria in Africa . However, when introduced outside its native range, it often becomes invasive , threatening more localized species. The Nile tilapia typically feeds during daytime, which suggests that, similar to trout and salmon , it exhibits a behavioral response to light as a main factor contributing to feeding activity. Due to its fast reproductive rate, however, overpopulation often results within groups of Nile tilapia. To obtain the necessary nutrients, night feeding may also occur due to competition for food during daylight. A recent study found evidence that, contrary to popular belief, size dimorphism between the sexes results from differential food conversion efficiency rather than different amounts of food consumed. Hence, although males and females eat equal amounts of food, males tend to grow larger due to a higher efficiency of converting food to body weight . Groups of Nile tilapia establish social hierarchies in which the dominant males have priority for both food and mating . Circular nests are built predominantly by males through mouth digging to become future spawning sites . These nests often become sites of intense courtship rituals and parental care . Like other fish, Nile tilapia travel almost exclusively in schools . Although males settle down in their crafted nesting zones, females travel between zones to find mates, resulting in competition between the males for females. [ citation needed ] Like other tilapias, such as Mozambique tilapia , dominance between the males is established first through noncontact displays such as lateral display and tail beats. Unsuccessful attempts to reconcile the hierarchy results in contact fighting to inflict injuries. Nile tilapia have been observed to modify their fighting behavior based upon experiences during development. Thus, experience in a certain form of agonistic behavior results in differential aggressiveness among individuals. Once the social hierarchy is established within a group, the dominant males enjoy the benefits of both increased access to food and an increased number of mates. However, social interactions between males in the presence of females results in higher energy expenditures as a consequence of courtship displays and sexual competition. Typical of most fish, Nile tilapia reproduce through mass spawning of a brood within a nest made by the male. In such an arrangement, territoriality and sexual competition amongst the males lead to large variations in reproductive success for individuals in a group. The genetic consequence of such behavior is reduced genetic variability in the long run, as inbreeding is likely to occur among different generations due to differential male reproductive success. Perhaps driven by reproductive competition, tilapias reproduce within a few months after birth. The relatively young age of sexual maturation within Nile tilapia leads to high birth and turnover rates. Consequently, the rapid reproductive rate of individuals can actually have a negative impact on growth rate, leading to the appearance of stunted tilapia as a result of a reduction in somatic growth in favor of sexual maturation. Female Nile tilapia, in the presence of other females either visually or chemically, exhibit shortened interspawning intervals. Although parental investment by a female extends the interspawning period, female tilapia that abandon their young to the care of a male gain this advantage of increased interspawning periods. One of the possible purposes behind this mechanism is to increase the reproductive advantage of females that do not have to care for young, allowing them more opportunities to spawn. For males, reproductive advantage goes to the more dominant males. Males have differential levels of gonadotropic hormones responsible for spermatogenesis , with dominant males having higher levels of the hormone. Thus, selection has favored larger sperm production with more successful males. Similarly, dominant males have both the best territory in terms of resources and the greatest access to mates. Furthermore, visual communication between Nile tilapia mates both stimulates and modulates reproductive behavior between partners such as courtship , spawning frequency, and nest building. Species belonging to the genus Oreochromis typically care for their young through mouthbrooding , oral incubation of the eggs and larvae. Similar to other tilapia, Nile tilapia are maternal mouthbrooders and extensive care is, therefore, provided almost exclusively by the female. After spawning in a nest made by a male, the young fry or eggs are carried in the mouth of the mother for a period of 12 days. Sometimes, the mother pushes the young back into her mouth if she believes they are not ready for the outside. Nile tilapias also demonstrate parental care in times of danger. When approached by a danger, the young often swim back into the protection of their mother's mouth. However, mouthbrooding leads to significant metabolic modifications for the parents, usually the mother, as reflected by fluctuations in body weight and low fitness . Thus, parental-offspring conflict can be observed through the costs and benefits of mouthbrooding. Protection of the young ensures passage of an individual's genes into the future generations, but caring for the young also reduces an individual's own reproductive fitness. Since female Nile tilapia exhibiting parental care show extended interspawning periods, one of the benefits is slowing down vitellogenesis (yolk deposition) to increase the survival rate of one's own young. The size of spawned eggs correlates directly with advantages concerning hatching time, growth, survival, and onset of feeding, since increased egg size means increased nutrients for the developing young. Thus, one of the reasons behind a delayed interspawning period by female Nile tilapia may be for the benefit of offspring survival. Tilapia, likely the Nile tilapia, was well known as food fish in Ancient Egypt and commonly featured in their art (paintings and sculptures). This includes a 4000-year-old tomb illustration that shows them in man-made ponds, likely an early form of aquaculture . In modern aquaculture, wild-type Nile tilapia are not farmed very often because the dark color of their flesh is undesirable for many customers, and because of the reputation the fish has as being a trash fish . However, they are fast-growing and produce good fillets ; leucistic ("red") breeds which have lighter meat have been developed to counter the consumer distaste for darker meat. [ citation needed ] Hybrid stock is also used in aquaculture; Nile × blue tilapia hybrids are usually rather dark, but a light-colored hybrid breed known as "Rocky Mountain White" tilapia is often grown due to its very light flesh and tolerance of low temperatures. The red-hybrid Nile tilapia is known in the Thai language as pla thapthim ( Thai : ปลาทับทิม ), meaning " pomegranate fish" or " ruby fish". This type of tilapia is very popular in Thai cuisine , where it is prepared in a variety of ways. The black-and-white-striped tilapia pla nin ( Thai : ปลานิล ), has darker flesh and is commonly either salted and grilled or deep-fried, and it can also be steamed with lime ( pla nin nueng manao ). Nile tilapia, called بلطي bulṭī in Arabic , is (being native to Egypt) among the most common fish in Egyptian cuisine , and probably the most common in regions far from the coast. It is generally either battered and pan-fried whole ( بلطي ٠قلي bulṭī maqlī [bʊltˤiː maʔliː] ) or grilled whole ( بلطي ٠شوي bulṭī mashwī [bʊltˤiː maʃwiː] ). Like other fish in Egypt, is generally served with rice cooked with onions and other seasonings to turn it red. [ citation needed ] In Israel , Nile tilapia is commonly fried, grilled or baked with vegetables herbs and spices and eaten with rice or bulgur pilafs. It is also baked in the oven with tahini sauce drizzled over it with potatoes , onions , asparagus , sweet peppers or tomatoes and flavored with sumac and dried mint. [ citation needed ] Tilapia, often farmed, is a popular and common supermarket fish in the United States. [ citation needed ] In India, Nile tilapia is the most dominant fish in some of the South Indian reservoirs and available throughout the year. O. niloticus grows faster and reaches bigger sizes in a given time. The littoral areas of Kelavarappalli Reservoir are full of nests of Nile tilapia and they breed during south-west monsoon (July–September). The fish mainly feed on detritus. Zooplankton, phytoplankton, and macrophytes also were recorded occasionally from the gut of Nile tilapia. The demand is heavy, especially from local poor people, as this fish is affordable to the lowest income group in this area.

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West Nile

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Encephalitis

Encephalitis is inflammation of the brain . The severity can be variable with symptoms including reduction or alteration in consciousness, headache , fever , confusion , a stiff neck , and vomiting . Complications may include seizures , hallucinations , trouble speaking, memory problems , and problems with hearing . Causes of encephalitis include viruses such as herpes simplex virus and rabies virus as well as bacteria , fungi , or parasites . Other causes include autoimmune diseases and certain medications. In many cases the cause remains unknown. Risk factors include a weak immune system . Diagnosis is typically based on symptoms and supported by blood tests , medical imaging , and analysis of cerebrospinal fluid . Certain types are preventable with vaccines . Treatment may include antiviral medications (such as acyclovir ), anticonvulsants , and corticosteroids . Treatment generally takes place in hospital. Some people require artificial respiration . Once the immediate problem is under control, rehabilitation may be required. In 2015, encephalitis was estimated to have affected 4.3 million people and resulted in 150,000 deaths worldwide. Adults with encephalitis present with acute onset of fever , headache , confusion , and sometimes seizures. Younger children or infants may present with irritability, poor appetite and fever. Neurological examinations usually reveal a drowsy or confused person. Stiff neck , due to the irritation of the meninges covering the brain, indicates that the patient has either meningitis or meningoencephalitis . In 30%-40% of encephalitis cases, the etiology remains unknown. Viral infections are the usual cause of infectious encephalitis. Viral encephalitis can occur either as a direct effect of an acute infection , or as one of the sequelae of a latent infection . The majority of viral cases of encephalitis have an unknown cause; however, the most common identifiable cause of viral encephalitis is from herpes simplex infection. Other causes of acute viral encephalitis are rabies virus , poliovirus , and measles virus . Additional possible viral causes are arboviral flavivirus ( St. Louis encephalitis , West Nile virus ), bunyavirus (La Crosse strain), arenavirus (lymphocytic choriomeningitis virus), reovirus (Colorado tick virus), and henipavirus infections. The Powassan virus is a rare cause of encephalitis. It can be caused by a bacterial infection, such as bacterial meningitis , or may be a complication of a current infectious disease such as syphilis (secondary encephalitis). Certain parasitic or protozoal infestations, such as toxoplasmosis , malaria , or primary amoebic meningoencephalitis , can also cause encephalitis in people with compromised immune systems . Lyme disease or Bartonella henselae may also cause encephalitis. [ citation needed ] Other bacterial pathogens, like Mycoplasma and those causing rickettsial disease , cause inflammation of the meninges and consequently encephalitis. A non-infectious cause includes acute disseminated encephalitis which is demyelinated. Limbic encephalitis refers to inflammatory disease confined to the limbic system of the brain. The clinical presentation often includes disorientation , disinhibition , memory loss , seizures , and behavioral anomalies. MRI imaging reveals T2 hyperintensity in the structures of the medial temporal lobes, and in some cases, other limbic structures. Some cases of limbic encephalitis are of autoimmune origin. Autoimmune encephalitis signs can include catatonia , psychosis , abnormal movements, and autonomic dysregulation . Antibody-mediated anti-N-methyl-D-aspartate-receptor encephalitis and Rasmussen encephalitis are examples of autoimmune encephalitis. Anti-NMDA receptor encephalitis is the most common autoimmune form, and is accompanied by ovarian teratoma in 58 percent of affected women 18–45 years of age. Encephalitis lethargica is identified by high fever, headache , delayed physical response, and lethargy . Individuals can exhibit upper body weakness , muscular pains , and tremors , though the cause of encephalitis lethargica is not currently known. From 1917 to 1928, an epidemic of encephalitis lethargica occurred worldwide. Viral infections are the usual cause of infectious encephalitis. Viral encephalitis can occur either as a direct effect of an acute infection , or as one of the sequelae of a latent infection . The majority of viral cases of encephalitis have an unknown cause; however, the most common identifiable cause of viral encephalitis is from herpes simplex infection. Other causes of acute viral encephalitis are rabies virus , poliovirus , and measles virus . Additional possible viral causes are arboviral flavivirus ( St. Louis encephalitis , West Nile virus ), bunyavirus (La Crosse strain), arenavirus (lymphocytic choriomeningitis virus), reovirus (Colorado tick virus), and henipavirus infections. The Powassan virus is a rare cause of encephalitis. It can be caused by a bacterial infection, such as bacterial meningitis , or may be a complication of a current infectious disease such as syphilis (secondary encephalitis). Certain parasitic or protozoal infestations, such as toxoplasmosis , malaria , or primary amoebic meningoencephalitis , can also cause encephalitis in people with compromised immune systems . Lyme disease or Bartonella henselae may also cause encephalitis. [ citation needed ] Other bacterial pathogens, like Mycoplasma and those causing rickettsial disease , cause inflammation of the meninges and consequently encephalitis. A non-infectious cause includes acute disseminated encephalitis which is demyelinated. Limbic encephalitis refers to inflammatory disease confined to the limbic system of the brain. The clinical presentation often includes disorientation , disinhibition , memory loss , seizures , and behavioral anomalies. MRI imaging reveals T2 hyperintensity in the structures of the medial temporal lobes, and in some cases, other limbic structures. Some cases of limbic encephalitis are of autoimmune origin. Autoimmune encephalitis signs can include catatonia , psychosis , abnormal movements, and autonomic dysregulation . Antibody-mediated anti-N-methyl-D-aspartate-receptor encephalitis and Rasmussen encephalitis are examples of autoimmune encephalitis. Anti-NMDA receptor encephalitis is the most common autoimmune form, and is accompanied by ovarian teratoma in 58 percent of affected women 18–45 years of age. Encephalitis lethargica is identified by high fever, headache , delayed physical response, and lethargy . Individuals can exhibit upper body weakness , muscular pains , and tremors , though the cause of encephalitis lethargica is not currently known. From 1917 to 1928, an epidemic of encephalitis lethargica occurred worldwide. People should only be diagnosed with encephalitis if they have a decreased or altered level of consciousness, lethargy, or personality change for at least twenty-four hours without any other explainable cause. Diagnosing encephalitis is done via a variety of tests: Vaccination is available against tick-borne and Japanese encephalitis and should be considered for at-risk individuals. Post-infectious encephalomyelitis complicating smallpox vaccination is avoidable, for all intents and purposes, as smallpox is nearly eradicated. Contraindication to Pertussis immunization should be observed in patients with encephalitis. An ideal drug to treat brain infection should be small, moderately lipophilic at pH of 7.4, low level of plasma protein binding, volume of distribution of litre per kg, does not have strong affinity towards binding with P-glycoprotein , or other efflux pumps on the surface of blood–brain barrier . Some drugs such as isoniazid, pyrazinamide, linezolid, metronidazole, fluconazole, and some fluoroquinolones have good penetration to blood brain barrier. Treatment (which is based on supportive care) is as follows: Pyrimethamine -based maintenance therapy is often used to treat toxoplasmic encephalitis (TE), which is caused by Toxoplasma gondii and can be life-threatening for people with weak immune systems. The use of highly active antiretroviral therapy (HAART), in conjunction with the established pyrimethamine-based maintenance therapy, decreases the chance of relapse in patients with HIV and TE from approximately 18% to 11%. This is a significant difference as relapse may impact the severity and prognosis of disease and result in an increase in healthcare expenditure. The effectiveness of intravenous immunoglobulin for the management of childhood encephalitis is unclear. Systematic reviews have been unable to draw firm conclusions because of a lack of randomised double-blind studies with sufficient numbers of patients and sufficient follow-up. There is the possibility of a benefit of intravenous immunoglobulin for some forms of childhood encephalitis on some indicators such as length of hospital stay, time to stop spasms, time to regain consciousness, and time to resolution of neuropathic symptoms and fever. Intravenous immunoglobulin for Japanese encephalitis appeared to have no benefit when compared with placebo (pretend) treatment. Identification of poor prognostic factors include cerebral edema , status epilepticus , and thrombocytopenia . In contrast, a normal encephalogram at the early stages of diagnosis is associated with high rates of survival. The number of new cases a year of acute encephalitis in Western countries is 7.4 cases per 100,000 people per year. In tropical countries, the incidence is 6.34 per 100,000 people per year. The number of cases of encephalitis has not changed much over time, with about 250,000 cases a year from 2005 to 2015 in the US. Approximately seven per 100,000 people were hospitalized for encephalitis in the US during this time. In 2015, encephalitis was estimated to have affected 4.3 million people and resulted in 150,000 deaths worldwide. Herpes simplex encephalitis has an incidence of 2–4 per million of the population per year. Encephalitis with meningitis is known as meningoencephalitis , while encephalitis with involvement of the spinal cord is known as encephalomyelitis . The word is from Ancient Greek ἐγκέφαλος , enképhalos 'brain', composed of ἐν , en , 'in' and κεφαλή , kephalé , 'head', and the medical suffix -itis 'inflammation'.

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West Nile

https://api.wikimedia.org/core/v1/wikipedia/en/page/Fly/html

Fly

Housefly (Muscidae) (top left) Haematopota pluvialis (Tabanidae) (top right) Ctenophora pectinicornis (Tipulidae) (mid left) Ochlerotatus notoscriptus (Culicidae) (mid right) Milesia crabroniformis (Syrphidae) (bottom left) Holcocephala fusca (Asilidae) (bottom right) Nematocera (includes Eudiptera ) Brachycera Flies are insects of the order Diptera , the name being derived from the Greek δι- di- "two", and πτερόν pteron "wing". Insects of this order use only a single pair of wings to fly, the hindwings having evolved into advanced mechanosensory organs known as halteres , which act as high-speed sensors of rotational movement and allow dipterans to perform advanced aerobatics. Diptera is a large order containing an estimated 1,000,000 species including horse-flies , [lower-alpha 1] crane flies , hoverflies , mosquitoes and others, although only about 125,000 species have been described . Flies have a mobile head, with a pair of large compound eyes , and mouthparts designed for piercing and sucking (mosquitoes, black flies and robber flies), or for lapping and sucking in the other groups. Their wing arrangement gives them great maneuverability in flight, and claws and pads on their feet enable them to cling to smooth surfaces. Flies undergo complete metamorphosis ; the eggs are often laid on the larval food-source and the larvae, which lack true limbs, develop in a protected environment, often inside their food source. Other species like Metopia argyrocephala are ovoviviparous , opportunistically depositing hatched or hatching maggots instead of eggs on carrion , dung, decaying material, or open wounds of mammals. The pupa is a tough capsule from which the adult emerges when ready to do so; flies mostly have short lives as adults. Diptera is one of the major insect orders and of considerable ecological and human importance. Flies are important pollinators, second only to the bees and their Hymenopteran relatives. Flies may have been among the evolutionarily earliest pollinators responsible for early plant pollination . Fruit flies are used as model organisms in research, but less benignly, mosquitoes are vectors for malaria , dengue , West Nile fever , yellow fever , encephalitis , and other infectious diseases ; and houseflies , commensal with humans all over the world, spread foodborne illnesses . Flies can be annoyances especially in some parts of the world where they can occur in large numbers, buzzing and settling on the skin or eyes to bite or seek fluids. Larger flies such as tsetse flies and screwworms cause significant economic harm to cattle. Blowfly larvae, known as gentles , and other dipteran larvae, known more generally as maggots , are used as fishing bait and as food for carnivorous animals. They are also used in medicine in debridement to clean wounds .Dipterans are holometabolans , insects that undergo radical metamorphosis. They belong to the Mecopterida, alongside the Mecoptera , Siphonaptera , Lepidoptera and Trichoptera . The possession of a single pair of wings distinguishes most true flies from other insects with "fly" in their names. However, some true flies such as Hippoboscidae (louse flies) have become secondarily wingless. The cladogram represents the current consensus view. Diptera Mecoptera (scorpionflies, hangingflies, 400 spp .) (exc. Boreidae) Boreidae (snow scorpionflies, 30 spp.) Siphonaptera (fleas, 2500 spp.) Trichoptera (caddisflies) Lepidoptera (butterflies and moths) Hymenoptera (sawflies, wasps, ants, bees) The first true dipterans known are from the Middle Triassic (around 240 million years ago), and they became widespread during the Middle and Late Triassic . Modern flowering plants did not appear until the Cretaceous (around 140 million years ago), so the original dipterans must have had a different source of nutrition other than nectar . Based on the attraction of many modern fly groups to shiny droplets, it has been suggested that they may have fed on honeydew produced by sap-sucking bugs which were abundant at the time, and dipteran mouthparts are well-adapted to softening and lapping up the crusted residues. The basal clades in the Diptera include the Deuterophlebiidae and the enigmatic Nymphomyiidae . Three episodes of evolutionary radiation are thought to have occurred based on the fossil record. Many new species of lower Diptera developed in the Triassic , about 220 million years ago. Many lower Brachycera appeared in the Jurassic , some 180 million years ago. A third radiation took place among the Schizophora at the start of the Paleogene , 66 million years ago. The phylogenetic position of Diptera has been controversial. The monophyly of holometabolous insects has long been accepted, with the main orders being established as Lepidoptera, Coleoptera, Hymenoptera and Diptera, and it is the relationships between these groups which has caused difficulties. Diptera is widely thought to be a member of Mecopterida , along with Lepidoptera (butterflies and moths), Trichoptera (caddisflies), Siphonaptera (fleas), Mecoptera (scorpionflies) and possibly Strepsiptera (twisted-wing flies). Diptera has been grouped with Siphonaptera and Mecoptera in the Antliophora, but this has not been confirmed by molecular studies. Diptera were traditionally broken down into two suborders, Nematocera and Brachycera , distinguished by the differences in antennae. The Nematocera are identified by their elongated bodies and many-segmented, often feathery antennae as represented by mosquitoes and crane flies. The Brachycera have rounder bodies and much shorter antennae. Subsequent studies have identified the Nematocera as being non-monophyletic with modern phylogenies placing the Brachycera within grades of groups formerly placed in the Nematocera. The construction of a phylogenetic tree has been the subject of ongoing research. The following cladogram is based on the FLYTREE project. Ptychopteromorpha (phantom and primitive crane-flies) Culicomorpha (mosquitoes, blackflies and midges) Blephariceromorpha (net-winged midges, etc) Bibionomorpha (gnats) Psychodomorpha (drain flies, sand flies, etc) Tipuloidea (crane flies) Stratiomyomorpha (soldier flies, etc) Xylophagomorpha (stink flies, etc) Tabanomorpha (horse flies, snipe flies, etc) Nemestrinoidea Asiloidea (robber flies, bee flies, etc) Empidoidea (dance flies, etc) Aschiza (in part) Phoroidea (flat-footed flies, etc) Syrphoidea (hoverflies) Hippoboscoidea (louse flies, etc) Muscoidea (house flies, dung flies, etc) Oestroidea (blow flies, flesh flies, etc) Acalyptratae (marsh flies, etc) Flies are often abundant and are found in almost all terrestrial habitats in the world apart from Antarctica. They include many familiar insects such as house flies, blow flies, mosquitoes, gnats, black flies, midges and fruit flies. More than 150,000 have been formally described and the actual species diversity is much greater, with the flies from many parts of the world yet to be studied intensively. The suborder Nematocera include generally small, slender insects with long antennae such as mosquitoes, gnats, midges and crane-flies, while the Brachycera includes broader, more robust flies with short antennae. Many nematoceran larvae are aquatic. There are estimated to be a total of about 19,000 species of Diptera in Europe, 22,000 in the Nearctic region, 20,000 in the Afrotropical region, 23,000 in the Oriental region and 19,000 in the Australasian region. While most species have restricted distributions, a few like the housefly ( Musca domestica ) are cosmopolitan. Gauromydas heros ( Asiloidea ), with a length of up to 7 cm (2.8 in) , is generally considered to be the largest fly in the world, while the smallest is Euryplatea nanaknihali , which at 0.4 mm (0.016 in) is smaller than a grain of salt. Brachycera are ecologically very diverse, with many being predatory at the larval stage and some being parasitic. Animals parasitised include molluscs , woodlice , millipedes , insects, mammals , and amphibians . Flies are the second largest group of pollinators after the Hymenoptera (bees, wasps and relatives). In wet and colder environments flies are significantly more important as pollinators. Compared to bees, they need less food as they do not need to provision their young. Many flowers that bear low nectar and those that have evolved trap pollination depend on flies. It is thought that some of the earliest pollinators of plants may have been flies. The greatest diversity of gall forming insects are found among the flies, principally in the family Cecidomyiidae (gall midges). Many flies (most importantly in the family Agromyzidae) lay their eggs in the mesophyll tissue of leaves with larvae feeding between the surfaces forming blisters and mines. Some families are mycophagous or fungus feeding. These include the cave dwelling Mycetophilidae (fungus gnats) whose larvae are the only diptera with bioluminescence. The Sciaridae are also fungus feeders. Some plants are pollinated by fungus feeding flies that visit fungus infected male flowers. The larvae of Megaselia scalaris (Phoridae) are almost omnivorous and consume such substances as paint and shoe polish. The Exorista mella (Walker) fly are considered generalists and parasitoids of a variety of hosts. The larvae of the shore flies (Ephydridae) and some Chironomidae survive in extreme environments including glaciers ( Diamesa sp., Chironomidae ), hot springs, geysers, saline pools, sulphur pools, septic tanks and even crude oil ( Helaeomyia petrolei ). Adult hoverflies (Syrphidae) are well known for their mimicry and the larvae adopt diverse lifestyles including being inquiline scavengers inside the nests of social insects. Some brachycerans are agricultural pests, some bite animals and humans and suck their blood, and some transmit diseases. Dipterans are holometabolans , insects that undergo radical metamorphosis. They belong to the Mecopterida, alongside the Mecoptera , Siphonaptera , Lepidoptera and Trichoptera . The possession of a single pair of wings distinguishes most true flies from other insects with "fly" in their names. However, some true flies such as Hippoboscidae (louse flies) have become secondarily wingless. The cladogram represents the current consensus view. Diptera Mecoptera (scorpionflies, hangingflies, 400 spp .) (exc. Boreidae) Boreidae (snow scorpionflies, 30 spp.) Siphonaptera (fleas, 2500 spp.) Trichoptera (caddisflies) Lepidoptera (butterflies and moths) Hymenoptera (sawflies, wasps, ants, bees)The first true dipterans known are from the Middle Triassic (around 240 million years ago), and they became widespread during the Middle and Late Triassic . Modern flowering plants did not appear until the Cretaceous (around 140 million years ago), so the original dipterans must have had a different source of nutrition other than nectar . Based on the attraction of many modern fly groups to shiny droplets, it has been suggested that they may have fed on honeydew produced by sap-sucking bugs which were abundant at the time, and dipteran mouthparts are well-adapted to softening and lapping up the crusted residues. The basal clades in the Diptera include the Deuterophlebiidae and the enigmatic Nymphomyiidae . Three episodes of evolutionary radiation are thought to have occurred based on the fossil record. Many new species of lower Diptera developed in the Triassic , about 220 million years ago. Many lower Brachycera appeared in the Jurassic , some 180 million years ago. A third radiation took place among the Schizophora at the start of the Paleogene , 66 million years ago. The phylogenetic position of Diptera has been controversial. The monophyly of holometabolous insects has long been accepted, with the main orders being established as Lepidoptera, Coleoptera, Hymenoptera and Diptera, and it is the relationships between these groups which has caused difficulties. Diptera is widely thought to be a member of Mecopterida , along with Lepidoptera (butterflies and moths), Trichoptera (caddisflies), Siphonaptera (fleas), Mecoptera (scorpionflies) and possibly Strepsiptera (twisted-wing flies). Diptera has been grouped with Siphonaptera and Mecoptera in the Antliophora, but this has not been confirmed by molecular studies. Diptera were traditionally broken down into two suborders, Nematocera and Brachycera , distinguished by the differences in antennae. The Nematocera are identified by their elongated bodies and many-segmented, often feathery antennae as represented by mosquitoes and crane flies. The Brachycera have rounder bodies and much shorter antennae. Subsequent studies have identified the Nematocera as being non-monophyletic with modern phylogenies placing the Brachycera within grades of groups formerly placed in the Nematocera. The construction of a phylogenetic tree has been the subject of ongoing research. The following cladogram is based on the FLYTREE project. Ptychopteromorpha (phantom and primitive crane-flies) Culicomorpha (mosquitoes, blackflies and midges) Blephariceromorpha (net-winged midges, etc) Bibionomorpha (gnats) Psychodomorpha (drain flies, sand flies, etc) Tipuloidea (crane flies) Stratiomyomorpha (soldier flies, etc) Xylophagomorpha (stink flies, etc) Tabanomorpha (horse flies, snipe flies, etc) Nemestrinoidea Asiloidea (robber flies, bee flies, etc) Empidoidea (dance flies, etc) Aschiza (in part) Phoroidea (flat-footed flies, etc) Syrphoidea (hoverflies) Hippoboscoidea (louse flies, etc) Muscoidea (house flies, dung flies, etc) Oestroidea (blow flies, flesh flies, etc) Acalyptratae (marsh flies, etc)Flies are often abundant and are found in almost all terrestrial habitats in the world apart from Antarctica. They include many familiar insects such as house flies, blow flies, mosquitoes, gnats, black flies, midges and fruit flies. More than 150,000 have been formally described and the actual species diversity is much greater, with the flies from many parts of the world yet to be studied intensively. The suborder Nematocera include generally small, slender insects with long antennae such as mosquitoes, gnats, midges and crane-flies, while the Brachycera includes broader, more robust flies with short antennae. Many nematoceran larvae are aquatic. There are estimated to be a total of about 19,000 species of Diptera in Europe, 22,000 in the Nearctic region, 20,000 in the Afrotropical region, 23,000 in the Oriental region and 19,000 in the Australasian region. While most species have restricted distributions, a few like the housefly ( Musca domestica ) are cosmopolitan. Gauromydas heros ( Asiloidea ), with a length of up to 7 cm (2.8 in) , is generally considered to be the largest fly in the world, while the smallest is Euryplatea nanaknihali , which at 0.4 mm (0.016 in) is smaller than a grain of salt. Brachycera are ecologically very diverse, with many being predatory at the larval stage and some being parasitic. Animals parasitised include molluscs , woodlice , millipedes , insects, mammals , and amphibians . Flies are the second largest group of pollinators after the Hymenoptera (bees, wasps and relatives). In wet and colder environments flies are significantly more important as pollinators. Compared to bees, they need less food as they do not need to provision their young. Many flowers that bear low nectar and those that have evolved trap pollination depend on flies. It is thought that some of the earliest pollinators of plants may have been flies. The greatest diversity of gall forming insects are found among the flies, principally in the family Cecidomyiidae (gall midges). Many flies (most importantly in the family Agromyzidae) lay their eggs in the mesophyll tissue of leaves with larvae feeding between the surfaces forming blisters and mines. Some families are mycophagous or fungus feeding. These include the cave dwelling Mycetophilidae (fungus gnats) whose larvae are the only diptera with bioluminescence. The Sciaridae are also fungus feeders. Some plants are pollinated by fungus feeding flies that visit fungus infected male flowers. The larvae of Megaselia scalaris (Phoridae) are almost omnivorous and consume such substances as paint and shoe polish. The Exorista mella (Walker) fly are considered generalists and parasitoids of a variety of hosts. The larvae of the shore flies (Ephydridae) and some Chironomidae survive in extreme environments including glaciers ( Diamesa sp., Chironomidae ), hot springs, geysers, saline pools, sulphur pools, septic tanks and even crude oil ( Helaeomyia petrolei ). Adult hoverflies (Syrphidae) are well known for their mimicry and the larvae adopt diverse lifestyles including being inquiline scavengers inside the nests of social insects. Some brachycerans are agricultural pests, some bite animals and humans and suck their blood, and some transmit diseases. Flies are adapted for aerial movement and typically have short and streamlined bodies. The first tagma of the fly, the head, bears the eyes, the antennae , and the mouthparts (the labrum, labium, mandible, and maxilla make up the mouthparts). The second tagma, the thorax , bears the wings and contains the flight muscles on the second segment, which is greatly enlarged; the first and third segments have been reduced to collar-like structures, and the third segment bears the halteres , which help to balance the insect during flight. The third tagma is the abdomen consisting of 11 segments, some of which may be fused, and with the 3 hindmost segments modified for reproduction. Some Dipterans are mimics and can only be distinguished from their models by very careful inspection. An example of this is Spilomyia longicornis , which is a fly but mimics a vespid wasp. Flies have a mobile head with a pair of large compound eyes on the sides of the head, and in most species, three small ocelli on the top. The compound eyes may be close together or widely separated, and in some instances are divided into a dorsal region and a ventral region, perhaps to assist in swarming behaviour. The antennae are well-developed but variable, being thread-like, feathery or comb-like in the different families. The mouthparts are adapted for piercing and sucking, as in the black flies, mosquitoes and robber flies, and for lapping and sucking as in many other groups. Female horse-flies use knife-like mandibles and maxillae to make a cross-shaped incision in the host's skin and then lap up the blood that flows. The gut includes large diverticulae , allowing the insect to store small quantities of liquid after a meal. For visual course control, flies' optic flow field is analyzed by a set of motion-sensitive neurons. A subset of these neurons is thought to be involved in using the optic flow to estimate the parameters of self-motion, such as yaw, roll, and sideward translation. Other neurons are thought to be involved in analyzing the content of the visual scene itself, such as separating figures from the ground using motion parallax. The H1 neuron is responsible for detecting horizontal motion across the entire visual field of the fly, allowing the fly to generate and guide stabilizing motor corrections midflight with respect to yaw. The ocelli are concerned in the detection of changes in light intensity, enabling the fly to react swiftly to the approach of an object. Like other insects, flies have chemoreceptors that detect smell and taste, and mechanoreceptors that respond to touch. The third segments of the antennae and the maxillary palps bear the main olfactory receptors, while the gustatory receptors are in the labium, pharynx, feet, wing margins and female genitalia, enabling flies to taste their food by walking on it. The taste receptors in females at the tip of the abdomen receive information on the suitability of a site for ovipositing. Flies that feed on blood have special sensory structures that can detect infrared emissions, and use them to home in on their hosts, and many blood-sucking flies can detect the raised concentration of carbon dioxide that occurs near large animals. Some tachinid flies (Ormiinae) which are parasitoids of bush crickets , have sound receptors to help them locate their singing hosts. Diptera have one pair of fore wings on the mesothorax and a pair of halteres , or reduced hind wings, on the metathorax . A further adaptation for flight is the reduction in number of the neural ganglia , and concentration of nerve tissue in the thorax, a feature that is most extreme in the highly derived Muscomorpha infraorder. Some flies such as the ectoparasitic Nycteribiidae and Streblidae are exceptional in having lost their wings and become flightless. The only other order of insects bearing a single pair of true, functional wings, in addition to any form of halteres, are the Strepsiptera . In contrast to the flies, the Strepsiptera bear their halteres on the mesothorax and their flight wings on the metathorax. Each of the fly's six legs has a typical insect structure of coxa, trochanter, femur, tibia and tarsus, with the tarsus in most instances being subdivided into five tarsomeres . At the tip of the limb is a pair of claws, and between these are cushion-like structures known as pulvilli which provide adhesion. The abdomen shows considerable variability among members of the order. It consists of eleven segments in primitive groups and ten segments in more derived groups, the tenth and eleventh segments having fused. The last two or three segments are adapted for reproduction. Each segment is made up of a dorsal and a ventral sclerite , connected by an elastic membrane. In some females, the sclerites are rolled into a flexible, telescopic ovipositor . Flies are capable of great manoeuvrability during flight due to the presence of the halteres. These act as gyroscopic organs and are rapidly oscillated in time with the wings; they act as a balance and guidance system by providing rapid feedback to the wing-steering muscles, and flies deprived of their halteres are unable to fly. The wings and halteres move in synchrony but the amplitude of each wing beat is independent, allowing the fly to turn sideways. The wings of the fly are attached to two kinds of muscles, those used to power it and another set used for fine control. Flies tend to fly in a straight line then make a rapid change in direction before continuing on a different straight path. The directional changes are called saccades and typically involve an angle of 90°, being achieved in 50 milliseconds. They are initiated by visual stimuli as the fly observes an object, nerves then activate steering muscles in the thorax that cause a small change in wing stroke which generate sufficient torque to turn. Detecting this within four or five wingbeats, the halteres trigger a counter-turn and the fly heads off in a new direction. Flies have rapid reflexes that aid their escape from predators but their sustained flight speeds are low. Dolichopodid flies in the genus Condylostylus respond in less than 5 milliseconds to camera flashes by taking flight. In the past, the deer bot fly, Cephenemyia , was claimed to be one of the fastest insects on the basis of an estimate made visually by Charles Townsend in 1927. This claim, of speeds of 600 to 800 miles per hour, was regularly repeated until it was shown to be physically impossible as well as incorrect by Irving Langmuir. Langmuir suggested an estimated speed of 25 miles per hour. Although most flies live and fly close to the ground, a few are known to fly at heights and a few like Oscinella (Chloropidae) are known to be dispersed by winds at altitudes of up to 2000 ft and over long distances. Some hover flies like Metasyrphus corollae have been known to undertake long flights in response to aphid population spurts. Males of fly species such as Cuterebra , many hover flies, bee flies (Bombyliidae) and fruit flies (Tephritidae) maintain territories within which they engage in aerial pursuit to drive away intruding males and other species. While these territories may be held by individual males, some species, such as A. freeborni , form leks with many males aggregating in displays. Some flies maintain an airspace and still others form dense swarms that maintain a stationary location with respect to landmarks. Many flies mate in flight while swarming. Flies are capable of great manoeuvrability during flight due to the presence of the halteres. These act as gyroscopic organs and are rapidly oscillated in time with the wings; they act as a balance and guidance system by providing rapid feedback to the wing-steering muscles, and flies deprived of their halteres are unable to fly. The wings and halteres move in synchrony but the amplitude of each wing beat is independent, allowing the fly to turn sideways. The wings of the fly are attached to two kinds of muscles, those used to power it and another set used for fine control. Flies tend to fly in a straight line then make a rapid change in direction before continuing on a different straight path. The directional changes are called saccades and typically involve an angle of 90°, being achieved in 50 milliseconds. They are initiated by visual stimuli as the fly observes an object, nerves then activate steering muscles in the thorax that cause a small change in wing stroke which generate sufficient torque to turn. Detecting this within four or five wingbeats, the halteres trigger a counter-turn and the fly heads off in a new direction. Flies have rapid reflexes that aid their escape from predators but their sustained flight speeds are low. Dolichopodid flies in the genus Condylostylus respond in less than 5 milliseconds to camera flashes by taking flight. In the past, the deer bot fly, Cephenemyia , was claimed to be one of the fastest insects on the basis of an estimate made visually by Charles Townsend in 1927. This claim, of speeds of 600 to 800 miles per hour, was regularly repeated until it was shown to be physically impossible as well as incorrect by Irving Langmuir. Langmuir suggested an estimated speed of 25 miles per hour. Although most flies live and fly close to the ground, a few are known to fly at heights and a few like Oscinella (Chloropidae) are known to be dispersed by winds at altitudes of up to 2000 ft and over long distances. Some hover flies like Metasyrphus corollae have been known to undertake long flights in response to aphid population spurts. Males of fly species such as Cuterebra , many hover flies, bee flies (Bombyliidae) and fruit flies (Tephritidae) maintain territories within which they engage in aerial pursuit to drive away intruding males and other species. While these territories may be held by individual males, some species, such as A. freeborni , form leks with many males aggregating in displays. Some flies maintain an airspace and still others form dense swarms that maintain a stationary location with respect to landmarks. Many flies mate in flight while swarming. Diptera go through a complete metamorphosis with four distinct life stages – egg, larva, pupa and adult. In many flies, the larval stage is long and adults may have a short life. Most dipteran larvae develop in protected environments; many are aquatic and others are found in moist places such as carrion, fruit, vegetable matter, fungi and, in the case of parasitic species, inside their hosts. They tend to have thin cuticles and become desiccated if exposed to the air. Apart from the Brachycera , most dipteran larvae have sclerotised head capsules, which may be reduced to remnant mouth hooks; the Brachycera, however, have soft, gelatinized head capsules from which the sclerites are reduced or missing. Many of these larvae retract their heads into their thorax. The spiracles in the larva and pupa do not have any internal mechanical closing device. Some other anatomical distinction exists between the larvae of the Nematocera and the Brachycera . Especially in the Brachycera, little demarcation is seen between the thorax and abdomen, though the demarcation may be visible in many Nematocera, such as mosquitoes; in the Brachycera, the head of the larva is not clearly distinguishable from the rest of the body, and few, if any, sclerites are present. Informally, such brachyceran larvae are called maggots, but the term is not technical and often applied indifferently to fly larvae or insect larvae in general. The eyes and antennae of brachyceran larvae are reduced or absent, and the abdomen also lacks appendages such as cerci . This lack of features is an adaptation to food such as carrion, decaying detritus, or host tissues surrounding endoparasites . Nematoceran larvae generally have well-developed eyes and antennae, while those of Brachyceran larvae are reduced or modified. Dipteran larvae have no jointed, "true legs", but some dipteran larvae, such as species of Simuliidae , Tabanidae and Vermileonidae , have prolegs adapted to hold onto a substrate in flowing water, host tissues or prey. The majority of dipterans are oviparous and lay batches of eggs, but some species are ovoviviparous , where the larvae starting development inside the eggs before they hatch or viviparous, the larvae hatching and maturing in the body of the mother before being externally deposited. These are found especially in groups that have larvae dependent on food sources that are short-lived or are accessible for brief periods. This is widespread in some families such as the Sarcophagidae. In Hylemya strigosa (Anthomyiidae) the larva moults to the second instar before hatching, and in Termitoxenia (Phoridae) females have incubation pouches, and a full developed third instar larva is deposited by the adult and it almost immediately pupates with no freely feeding larval stage. The tsetse fly (as well as other Glossinidae, Hippoboscidae, Nycteribidae and Streblidae) exhibits adenotrophic viviparity ; a single fertilised egg is retained in the oviduct and the developing larva feeds on glandular secretions. When fully grown, the female finds a spot with soft soil and the larva works its way out of the oviduct, buries itself and pupates. Some flies like Lundstroemia parthenogenetica (Chironomidae) reproduce by thelytokous parthenogenesis , and some gall midges have larvae that can produce eggs ( paedogenesis ). The pupae take various forms. In some groups, particularly the Nematocera, the pupa is intermediate between the larval and adult form; these pupae are described as "obtect", having the future appendages visible as structures that adhere to the pupal body. The outer surface of the pupa may be leathery and bear spines, respiratory features or locomotory paddles. In other groups, described as "coarctate", the appendages are not visible. In these, the outer surface is a puparium , formed from the last larval skin, and the actual pupa is concealed within. When the adult insect is ready to emerge from this tough, desiccation-resistant capsule, it inflates a balloon-like structure on its head, and forces its way out. The adult stage is usually short, its function is only to mate and lay eggs. The genitalia of male flies are rotated to a varying degree from the position found in other insects. In some flies, this is a temporary rotation during mating, but in others, it is a permanent torsion of the organs that occurs during the pupal stage. This torsion may lead to the anus being below the genitals, or, in the case of 360° torsion, to the sperm duct being wrapped around the gut and the external organs being in their usual position. When flies mate, the male initially flies on top of the female, facing in the same direction, but then turns around to face in the opposite direction. This forces the male to lie on his back for his genitalia to remain engaged with those of the female, or the torsion of the male genitals allows the male to mate while remaining upright. This leads to flies having more reproduction abilities than most insects, and much quicker. Flies occur in large populations due to their ability to mate effectively and quickly during the mating season. More primitive groups mates in the air during swarming, but most of the more advanced species with a 360° torsion mate on a substrate. In many flies, the larval stage is long and adults may have a short life. Most dipteran larvae develop in protected environments; many are aquatic and others are found in moist places such as carrion, fruit, vegetable matter, fungi and, in the case of parasitic species, inside their hosts. They tend to have thin cuticles and become desiccated if exposed to the air. Apart from the Brachycera , most dipteran larvae have sclerotised head capsules, which may be reduced to remnant mouth hooks; the Brachycera, however, have soft, gelatinized head capsules from which the sclerites are reduced or missing. Many of these larvae retract their heads into their thorax. The spiracles in the larva and pupa do not have any internal mechanical closing device. Some other anatomical distinction exists between the larvae of the Nematocera and the Brachycera . Especially in the Brachycera, little demarcation is seen between the thorax and abdomen, though the demarcation may be visible in many Nematocera, such as mosquitoes; in the Brachycera, the head of the larva is not clearly distinguishable from the rest of the body, and few, if any, sclerites are present. Informally, such brachyceran larvae are called maggots, but the term is not technical and often applied indifferently to fly larvae or insect larvae in general. The eyes and antennae of brachyceran larvae are reduced or absent, and the abdomen also lacks appendages such as cerci . This lack of features is an adaptation to food such as carrion, decaying detritus, or host tissues surrounding endoparasites . Nematoceran larvae generally have well-developed eyes and antennae, while those of Brachyceran larvae are reduced or modified. Dipteran larvae have no jointed, "true legs", but some dipteran larvae, such as species of Simuliidae , Tabanidae and Vermileonidae , have prolegs adapted to hold onto a substrate in flowing water, host tissues or prey. The majority of dipterans are oviparous and lay batches of eggs, but some species are ovoviviparous , where the larvae starting development inside the eggs before they hatch or viviparous, the larvae hatching and maturing in the body of the mother before being externally deposited. These are found especially in groups that have larvae dependent on food sources that are short-lived or are accessible for brief periods. This is widespread in some families such as the Sarcophagidae. In Hylemya strigosa (Anthomyiidae) the larva moults to the second instar before hatching, and in Termitoxenia (Phoridae) females have incubation pouches, and a full developed third instar larva is deposited by the adult and it almost immediately pupates with no freely feeding larval stage. The tsetse fly (as well as other Glossinidae, Hippoboscidae, Nycteribidae and Streblidae) exhibits adenotrophic viviparity ; a single fertilised egg is retained in the oviduct and the developing larva feeds on glandular secretions. When fully grown, the female finds a spot with soft soil and the larva works its way out of the oviduct, buries itself and pupates. Some flies like Lundstroemia parthenogenetica (Chironomidae) reproduce by thelytokous parthenogenesis , and some gall midges have larvae that can produce eggs ( paedogenesis ). The pupae take various forms. In some groups, particularly the Nematocera, the pupa is intermediate between the larval and adult form; these pupae are described as "obtect", having the future appendages visible as structures that adhere to the pupal body. The outer surface of the pupa may be leathery and bear spines, respiratory features or locomotory paddles. In other groups, described as "coarctate", the appendages are not visible. In these, the outer surface is a puparium , formed from the last larval skin, and the actual pupa is concealed within. When the adult insect is ready to emerge from this tough, desiccation-resistant capsule, it inflates a balloon-like structure on its head, and forces its way out. The adult stage is usually short, its function is only to mate and lay eggs. The genitalia of male flies are rotated to a varying degree from the position found in other insects. In some flies, this is a temporary rotation during mating, but in others, it is a permanent torsion of the organs that occurs during the pupal stage. This torsion may lead to the anus being below the genitals, or, in the case of 360° torsion, to the sperm duct being wrapped around the gut and the external organs being in their usual position. When flies mate, the male initially flies on top of the female, facing in the same direction, but then turns around to face in the opposite direction. This forces the male to lie on his back for his genitalia to remain engaged with those of the female, or the torsion of the male genitals allows the male to mate while remaining upright. This leads to flies having more reproduction abilities than most insects, and much quicker. Flies occur in large populations due to their ability to mate effectively and quickly during the mating season. More primitive groups mates in the air during swarming, but most of the more advanced species with a 360° torsion mate on a substrate. As ubiquitous insects, dipterans play an important role at various trophic levels both as consumers and as prey. In some groups the larvae complete their development without feeding, and in others the adults do not feed. The larvae can be herbivores, scavengers, decomposers, predators or parasites, with the consumption of decaying organic matter being one of the most prevalent feeding behaviours. The fruit or detritus is consumed along with the associated micro-organisms, a sieve-like filter in the pharynx being used to concentrate the particles, while flesh-eating larvae have mouth-hooks to help shred their food. The larvae of some groups feed on or in the living tissues of plants and fungi, and some of these are serious pests of agricultural crops. Some aquatic larvae consume the films of algae that form underwater on rocks and plants. Many of the parasitoid larvae grow inside and eventually kill other arthropods, while parasitic larvae may attack vertebrate hosts. Whereas many dipteran larvae are aquatic or live in enclosed terrestrial locations, the majority of adults live above ground and are capable of flight. Predominantly they feed on nectar or plant or animal exudates, such as honeydew, for which their lapping mouthparts are adapted. Some flies have functional mandibles that may be used for biting. The flies that feed on vertebrate blood have sharp stylets that pierce the skin, with some species having anticoagulant saliva that is regurgitated before absorbing the blood that flows; in this process, certain diseases can be transmitted. The bot flies (Oestridae) have evolved to parasitize mammals. Many species complete their life cycle inside the bodies of their hosts. The larvae of a few fly groups (Agromyzidae, Anthomyiidae, Cecidomyiidae) are capable of inducing plant galls. Some dipteran larvae are leaf-miners. The larvae of many brachyceran families are predaceous. In many dipteran groups, swarming is a feature of adult life, with clouds of insects gathering in certain locations; these insects are mostly males, and the swarm may serve the purpose of making their location more visible to females. Most adult diptera have their mouthparts modified to sponge up fluid. The adults of many species of flies (e.g. Anthomyia sp., Steganopsis melanogaster ) that feed on liquid food will regurgitate fluid in a behaviour termed as "bubbling" which has been thought to help the insects evaporate water and concentrate food or possibly to cool by evaporation. Some adult diptera are known for kleptoparasitism such as members of the Sarcophagidae. The miltogramminae are known as "satellite flies" for their habit of following wasps and stealing their stung prey or laying their eggs into them. Phorids, milichids and the genus Bengalia are known to steal food carried by ants. Adults of Ephydra hians forage underwater, and have special hydrophobic hairs that trap a bubble of air that lets them breathe underwater. Flies are eaten by other animals at all stages of their development. The eggs and larvae are parasitised by other insects and are eaten by many creatures, some of which specialise in feeding on flies but most of which consume them as part of a mixed diet. Birds, bats, frogs, lizards, dragonflies and spiders are among the predators of flies. Many flies have evolved mimetic resemblances that aid their protection. Batesian mimicry is widespread with many hoverflies resembling bees and wasps, ants and some species of tephritid fruit fly resembling spiders. Some species of hoverfly are myrmecophilous —their young live and grow within the nests of ants. They are protected from the ants by imitating chemical odours given by ant colony members. Bombyliid bee flies such as Bombylius major are short-bodied, round, furry, and distinctly bee-like as they visit flowers for nectar, and are likely also Batesian mimics of bees. In contrast, Drosophila subobscura , a species of fly in the genus Drosophila , lacks a category of hemocytes that are present in other studied species of Drosophila , leading to an inability to defend against parasitic attacks, a form of innate immunodeficiency. Flies are eaten by other animals at all stages of their development. The eggs and larvae are parasitised by other insects and are eaten by many creatures, some of which specialise in feeding on flies but most of which consume them as part of a mixed diet. Birds, bats, frogs, lizards, dragonflies and spiders are among the predators of flies. Many flies have evolved mimetic resemblances that aid their protection. Batesian mimicry is widespread with many hoverflies resembling bees and wasps, ants and some species of tephritid fruit fly resembling spiders. Some species of hoverfly are myrmecophilous —their young live and grow within the nests of ants. They are protected from the ants by imitating chemical odours given by ant colony members. Bombyliid bee flies such as Bombylius major are short-bodied, round, furry, and distinctly bee-like as they visit flowers for nectar, and are likely also Batesian mimics of bees. In contrast, Drosophila subobscura , a species of fly in the genus Drosophila , lacks a category of hemocytes that are present in other studied species of Drosophila , leading to an inability to defend against parasitic attacks, a form of innate immunodeficiency. Flies play a variety of symbolic roles in different cultures. These include both positive and negative roles in religion. In the traditional Navajo religion, Big Fly is an important spirit being. In Christian demonology , Beelzebub is a demonic fly, the "Lord of the Flies", and a god of the Philistines . Flies have appeared in literature since ancient Sumer . In a Sumerian poem, a fly helps the goddess Inanna when her husband Dumuzid is being chased by galla demons. In the Mesopotamian versions of the flood myth , the dead corpses floating on the waters are compared to flies. Later, the gods are said to swarm "like flies" around the hero Utnapishtim 's offering. Flies appear on Old Babylonian seals as symbols of Nergal , the god of death. Fly-shaped lapis lazuli beads were often worn in ancient Mesopotamia, along with other kinds of fly-jewellery. In a little-known Greek myth , a very chatty and talkative maiden named Myia (meaning "fly") enraged the moon-goddess Selene by attempting to seduce her lover, the sleeping Endymion , and was thus turned by the angry goddess into a fly, who now always deprives people of their sleep in memory of her past life. In Prometheus Bound , which is attributed to the Athenian tragic playwright Aeschylus , a gadfly sent by Zeus 's wife Hera pursues and torments his mistress Io , who has been transformed into a cow and is watched constantly by the hundred eyes of the herdsman Argus : "Io: Ah! Hah! Again the prick, the stab of gadfly-sting! O earth, earth, hide, the hollow shape—Argus—that evil thing—the hundred-eyed." William Shakespeare , inspired by Aeschylus, has Tom o'Bedlam in King Lear , "Whom the foul fiend hath led through fire and through flame, through ford and whirlpool, o'er bog and quagmire", driven mad by the constant pursuit. In Antony and Cleopatra , Shakespeare similarly likens Cleopatra's hasty departure from the Actium battlefield to that of a cow chased by a gadfly. More recently, in 1962 the biologist Vincent Dethier wrote To Know a Fly , introducing the general reader to the behaviour and physiology of the fly. Musca depicta ("painted fly" in Latin) is a depiction of a fly as an inconspicuous element of various paintings. This feature was widespread in 15th and 16th centuries paintings and its presence may be explained by various reasons. Flies appear in popular culture in concepts such as fly-on-the-wall documentary -making in film and television production . The metaphoric name suggests that events are seen candidly , as a fly might see them. Flies have inspired the design of miniature flying robots. Steven Spielberg 's 1993 film Jurassic Park relied on the idea that DNA could be preserved in the stomach contents of a blood-sucking fly fossilised in amber , though the mechanism has been discounted by scientists. Dipterans are an important group of insects and have a considerable impact on the environment. Some leaf-miner flies (Agromyzidae), fruit flies (Tephritidae and Drosophilidae) and gall midges (Cecidomyiidae) are pests of agricultural crops; others such as tsetse flies , screwworm and botflies (Oestridae) attack livestock, causing wounds, spreading disease, and creating significant economic harm. See article: Parasitic flies of domestic animals . A few can even cause myiasis in humans. Still others such as mosquitoes (Culicidae), blackflies (Simuliidae) and drain flies (Psychodidae) impact human health, acting as vectors of major tropical diseases. Among these, Anopheles mosquitoes transmit malaria , filariasis , and arboviruses ; Aedes aegypti mosquitoes carry dengue fever and the Zika virus ; blackflies carry river blindness ; sand flies carry leishmaniasis . Other dipterans are a nuisance to humans, especially when present in large numbers; these include houseflies, which contaminate food and spread food-borne illnesses; the biting midges and sandflies (Ceratopogonidae) and the houseflies and stable flies (Muscidae). In tropical regions, eye flies ( Chloropidae ) which visit the eye in search of fluids can be a nuisance in some seasons. Many dipterans serve roles that are useful to humans. Houseflies, blowflies and fungus gnats (Mycetophilidae) are scavengers and aid in decomposition. Robber flies (Asilidae), tachinids (Tachinidae) and dagger flies and balloon flies (Empididae) are predators and parasitoids of other insects, helping to control a variety of pests. Many dipterans such as bee flies (Bombyliidae) and hoverflies (Syrphidae) are pollinators of crop plants. Drosophila melanogaster , a fruit fly, has long been used as a model organism in research because of the ease with which it can be bred and reared in the laboratory, its small genome , and the fact that many of its genes have counterparts in higher eukaryotes . A large number of genetic studies have been undertaken based on this species; these have had a profound impact on the study of gene expression , gene regulatory mechanisms and mutation . Other studies have investigated physiology , microbial pathogenesis and development among other research topics. The studies on dipteran relationships by Willi Hennig helped in the development of cladistics , techniques that he applied to morphological characters but now adapted for use with molecular sequences in phylogenetics. Maggots found on corpses are useful to forensic entomologists . Maggot species can be identified by their anatomical features and by matching their DNA . Maggots of different species of flies visit corpses and carcases at fairly well-defined times after the death of the victim, and so do their predators, such as beetles in the family Histeridae . Thus, the presence or absence of particular species provides evidence for the time since death, and sometimes other details such as the place of death, when species are confined to particular habitats such as woodland . Some species of maggots such as blowfly larvae (gentles) and bluebottle larvae ( casters ) are bred commercially; they are sold as bait in angling , and as food for carnivorous animals (kept as pets, in zoos, or for research) such as some mammals , fishes , reptiles , and birds . It has been suggested that fly larvae could be used at a large scale as food for farmed chickens, pigs, and fish. However, consumers are opposed to the inclusion of insects in their food, and the use of insects in animal feed remains illegal in areas such as the European Union . Fly larvae can be used as a biomedical tool for wound care and treatment. Maggot debridement therapy (MDT) is the use of blow fly larvae to remove the dead tissue from wounds, most commonly being amputations. Historically, this has been used for centuries, both intentional and unintentional, on battlefields and in early hospital settings. Removing the dead tissue promotes cell growth and healthy wound healing. The larvae also have biochemical properties such as antibacterial activity found in their secretions as they feed. These medicinal maggots are a safe and effective treatment for chronic wounds. The Sardinian cheese casu marzu is exposed to flies known as cheese skippers such as Piophila casei , members of the family Piophilidae . The digestive activities of the fly larvae soften the cheese and modify the aroma as part of the process of maturation. At one time European Union authorities banned sale of the cheese and it was becoming hard to find, but the ban has been lifted on the grounds that the cheese is a traditional local product made by traditional methods. Flies play a variety of symbolic roles in different cultures. These include both positive and negative roles in religion. In the traditional Navajo religion, Big Fly is an important spirit being. In Christian demonology , Beelzebub is a demonic fly, the "Lord of the Flies", and a god of the Philistines . Flies have appeared in literature since ancient Sumer . In a Sumerian poem, a fly helps the goddess Inanna when her husband Dumuzid is being chased by galla demons. In the Mesopotamian versions of the flood myth , the dead corpses floating on the waters are compared to flies. Later, the gods are said to swarm "like flies" around the hero Utnapishtim 's offering. Flies appear on Old Babylonian seals as symbols of Nergal , the god of death. Fly-shaped lapis lazuli beads were often worn in ancient Mesopotamia, along with other kinds of fly-jewellery. In a little-known Greek myth , a very chatty and talkative maiden named Myia (meaning "fly") enraged the moon-goddess Selene by attempting to seduce her lover, the sleeping Endymion , and was thus turned by the angry goddess into a fly, who now always deprives people of their sleep in memory of her past life. In Prometheus Bound , which is attributed to the Athenian tragic playwright Aeschylus , a gadfly sent by Zeus 's wife Hera pursues and torments his mistress Io , who has been transformed into a cow and is watched constantly by the hundred eyes of the herdsman Argus : "Io: Ah! Hah! Again the prick, the stab of gadfly-sting! O earth, earth, hide, the hollow shape—Argus—that evil thing—the hundred-eyed." William Shakespeare , inspired by Aeschylus, has Tom o'Bedlam in King Lear , "Whom the foul fiend hath led through fire and through flame, through ford and whirlpool, o'er bog and quagmire", driven mad by the constant pursuit. In Antony and Cleopatra , Shakespeare similarly likens Cleopatra's hasty departure from the Actium battlefield to that of a cow chased by a gadfly. More recently, in 1962 the biologist Vincent Dethier wrote To Know a Fly , introducing the general reader to the behaviour and physiology of the fly. Musca depicta ("painted fly" in Latin) is a depiction of a fly as an inconspicuous element of various paintings. This feature was widespread in 15th and 16th centuries paintings and its presence may be explained by various reasons. Flies appear in popular culture in concepts such as fly-on-the-wall documentary -making in film and television production . The metaphoric name suggests that events are seen candidly , as a fly might see them. Flies have inspired the design of miniature flying robots. Steven Spielberg 's 1993 film Jurassic Park relied on the idea that DNA could be preserved in the stomach contents of a blood-sucking fly fossilised in amber , though the mechanism has been discounted by scientists. Dipterans are an important group of insects and have a considerable impact on the environment. Some leaf-miner flies (Agromyzidae), fruit flies (Tephritidae and Drosophilidae) and gall midges (Cecidomyiidae) are pests of agricultural crops; others such as tsetse flies , screwworm and botflies (Oestridae) attack livestock, causing wounds, spreading disease, and creating significant economic harm. See article: Parasitic flies of domestic animals . A few can even cause myiasis in humans. Still others such as mosquitoes (Culicidae), blackflies (Simuliidae) and drain flies (Psychodidae) impact human health, acting as vectors of major tropical diseases. Among these, Anopheles mosquitoes transmit malaria , filariasis , and arboviruses ; Aedes aegypti mosquitoes carry dengue fever and the Zika virus ; blackflies carry river blindness ; sand flies carry leishmaniasis . Other dipterans are a nuisance to humans, especially when present in large numbers; these include houseflies, which contaminate food and spread food-borne illnesses; the biting midges and sandflies (Ceratopogonidae) and the houseflies and stable flies (Muscidae). In tropical regions, eye flies ( Chloropidae ) which visit the eye in search of fluids can be a nuisance in some seasons. Many dipterans serve roles that are useful to humans. Houseflies, blowflies and fungus gnats (Mycetophilidae) are scavengers and aid in decomposition. Robber flies (Asilidae), tachinids (Tachinidae) and dagger flies and balloon flies (Empididae) are predators and parasitoids of other insects, helping to control a variety of pests. Many dipterans such as bee flies (Bombyliidae) and hoverflies (Syrphidae) are pollinators of crop plants. Drosophila melanogaster , a fruit fly, has long been used as a model organism in research because of the ease with which it can be bred and reared in the laboratory, its small genome , and the fact that many of its genes have counterparts in higher eukaryotes . A large number of genetic studies have been undertaken based on this species; these have had a profound impact on the study of gene expression , gene regulatory mechanisms and mutation . Other studies have investigated physiology , microbial pathogenesis and development among other research topics. The studies on dipteran relationships by Willi Hennig helped in the development of cladistics , techniques that he applied to morphological characters but now adapted for use with molecular sequences in phylogenetics. Maggots found on corpses are useful to forensic entomologists . Maggot species can be identified by their anatomical features and by matching their DNA . Maggots of different species of flies visit corpses and carcases at fairly well-defined times after the death of the victim, and so do their predators, such as beetles in the family Histeridae . Thus, the presence or absence of particular species provides evidence for the time since death, and sometimes other details such as the place of death, when species are confined to particular habitats such as woodland . Some species of maggots such as blowfly larvae (gentles) and bluebottle larvae ( casters ) are bred commercially; they are sold as bait in angling , and as food for carnivorous animals (kept as pets, in zoos, or for research) such as some mammals , fishes , reptiles , and birds . It has been suggested that fly larvae could be used at a large scale as food for farmed chickens, pigs, and fish. However, consumers are opposed to the inclusion of insects in their food, and the use of insects in animal feed remains illegal in areas such as the European Union . Fly larvae can be used as a biomedical tool for wound care and treatment. Maggot debridement therapy (MDT) is the use of blow fly larvae to remove the dead tissue from wounds, most commonly being amputations. Historically, this has been used for centuries, both intentional and unintentional, on battlefields and in early hospital settings. Removing the dead tissue promotes cell growth and healthy wound healing. The larvae also have biochemical properties such as antibacterial activity found in their secretions as they feed. These medicinal maggots are a safe and effective treatment for chronic wounds. The Sardinian cheese casu marzu is exposed to flies known as cheese skippers such as Piophila casei , members of the family Piophilidae . The digestive activities of the fly larvae soften the cheese and modify the aroma as part of the process of maturation. At one time European Union authorities banned sale of the cheese and it was becoming hard to find, but the ban has been lifted on the grounds that the cheese is a traditional local product made by traditional methods. Flies are a health hazard and are attracted to toilets because of their smell. The New Scientist magazine suggested a trap for these flies. A pipe acting as a chimney was fitted to the toilet which let in some light to attract these flies up to the end of this pipe where a gauze covering prevented escape to the air outside so that they were trapped and died. Toilets are generally dark inside particularly if the door is closed.

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West Nile

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Juma Oris

Juma Abdalla Oris [lower-alpha 1] (died in March 2001) was a Ugandan military officer and government minister under the dictatorship of Idi Amin . After fleeing his country during the Uganda–Tanzania War , he became leader of the West Nile Bank Front (WNBF), a rebel group active in the West Nile region of Uganda during the 1990s.Juma Abdalla Oris was born in northern Uganda, or Nimule in southern Sudan. He was an ethnic Madi and/or Nubian , as well as a Muslim. Oris received only minimal education, and eventually joined the Uganda Army , becoming a high-ranking colonel by the early 1970s. Following the 1971 Ugandan coup d'état , he rose to one of the leading figures in Idi Amin 's government. He first became acting Minister of Foreign Affairs , and was appointed full foreign minister on 25 May 1975. He stayed in this position until 1978, while also serving as Minister of Information and Broadcasting . Following his takeover of the Information Ministry, a series of new directives and restrictions were handed down to the Ugandan news industry. All newspapers had to print Amin's statements in full, and Radio Uganda and Uganda Television had to transmit them in full. In addition to this, the latter two had to open and close every broadcast with a daily national prayer. Oris also sharply criticised Uganda's two private newspapers, Munno and Taifa , for supposedly conveying false information about Amin because they were not printing the same stories as the government daily, the Voice of Uganda . He was regarded as follower of Vice President Mustafa Adrisi . Oris was dismissed from his position as foreign minister as well as all of his ministerial portfolios by Amin in 1978, probably as part of a political purge following Adrisi's removal from power. Officially, Amin claimed that Oris had been fired because Uganda's image abroad had been mismanaged and Ugandan diplomats had not been paid regularly under his tenure. Shortly thereafter in late 1978, Ugandan troops invaded neighboring Tanzania under unclear circumstances, causing the Uganda–Tanzania War . Tanzania responded with a counter-invasion, and Amin's government began to collapse. Oris was one of the few Ugandan officers who remained loyal throughout most of the conflict. By 1979, he had been appointed Minister for Animal Resources and Minister of Lands. On 4 April 1979, Amin organized a four‐member war planning committee which consisted of his most trusted followers, including Oris. By this point, the Uganda Army had mostly disintegrated. After the Fall of Kampala , Oris fled with 3,000 cattle into exile to Sudan. He had good connections to the Sudanese security services by this point, and even joined the Sudanese Armed Forces as a mercenary at one point. He recruited West Nile people for a Sudanese contingent that fought in the Iran–Iraq War on behalf of Iraq. Using these connections, Oris helped to organize a coalition of ex-Uganda Army groups in the refugee camps of Sudan. These rebels launched an insurgency in 1980, starting the Ugandan Bush War . Oris became a member of the Former Uganda National Army (FUNA) as well as the Uganda National Rescue Front (UNRF), both of which fought in the Bush War. In the late 1980s and early 1990s Joseph Kony , the leader of the rebel group known as the Lord's Resistance Army claimed to be possessed by the spirit of Juma Oris. It appears he was unaware that Oris was at the time still alive—something which he discovered when the two men eventually met in person. Oris founded his own rebel army, called the " West Nile Bank Front " (WNBF), in 1994. Though founded in Zaire with the blessing of Mobutu Sese Seko , the group was mostly supported by the government of Sudan , as Mobutu's regime was already in terminal decline by this point. The WNBF fought for the secession of the West Nile sub-region or the restoration of Idi Amin as President of Uganda . Oris managed to gain support in northern Uganda by exploiting ethnic tensions and the lack of development opportunities in the area, offering potential recruits money in exchange for joining the WNBF. While waging an insurgency against the Ugandan government, Oris allegedly committed human rights violations by planting landmines in ambush attempts. He also fought with his followers in the Second Sudanese Civil War on the side of the Sudanese government. In March 1997, the WNBF and its allies suffered a heavy defeat when South Sudanese rebels of the SPLA overran their bases in Zaire and Sudan, and then ambushed their retreating forces near Yei during Operation Thunderbolt . Oris was badly wounded during this battle, and the WNBF almost completely destroyed. Most WNBF fighters, including deputy commander Abdulatif Tiyua , were killed or captured. Oris and the remnants of his militia subsequently fled to Juba . From then on, the WNBF was "essentially spent" as fighting force. Having suffered a stroke in late 1999, Oris was bedridden from then on. His condition worsened in early 2001, and he died at his home in Juba or Khartoum in March 2001. This disproved earlier reports according to which he had been killed in battle with the Uganda Peoples' Defence Forces. Oris was buried in Sudan.

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West Nile

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Northern cardinal

19 subspecies, see text Loxia cardinalis Linnaeus, 1758 The northern cardinal ( Cardinalis cardinalis ), known colloquially as the redbird , common cardinal , red cardinal , or just cardinal , is a bird in the genus Cardinalis . It can be found in southeastern Canada, through the eastern United States from Maine to Minnesota to Texas , New Mexico , southern Arizona , southern California, and south through Mexico, Belize , and Guatemala . It is also an introduced species in a few locations such as Bermuda and Hawaii. Its habitat includes woodlands, gardens, shrublands, and wetlands. It is the state bird of Illinois , Indiana , Kentucky , North Carolina , Ohio , Virginia , and West Virginia . The northern cardinal is a mid-sized perching songbird with a body length of 21–23 cm (8.3–9.1 in) and a crest on the top of the head. The species expresses sexual dimorphism : Females are a reddish olive color, and have a gray mask around the beak, while males are a vibrant red color, and have a black mask on the face, as well as a larger crest. Juvenile cardinals do not have the distinctive red-orange beak seen in adult birds until they are almost fully mature. On hatching, their beaks are grayish-black and they do not become the trademark orange-red color until they acquire their final adult plumage in the fall. The northern cardinal is mainly granivorous , but also feeds on insects and fruit. The male behaves territorially , marking out his territory with song. During courtship, the male feeds seed to the female beak-to-beak. The northern cardinal's clutch typically contains three to four eggs, with two to four clutches produced each year. It was once prized as a pet, but its sale was banned in the United States by the Migratory Bird Treaty Act of 1918 .The northern cardinal was described by Carl Linnaeus in the 1758 10th edition of Systema Naturae . It was originally categorized as Loxia cardinalis , a genus which now contains only crossbills. In 1838, it was recategorized as Cardinalis virginianus . In 1918, the scientific name was sometimes replaced with Richmondena cardinalis . In 1983, the scientific name was changed again to Cardinalis cardinalis and the common name was changed to "northern cardinal", to avoid confusion with the several other species also termed cardinals. The cardinal is named after cardinals of the Roman Catholic Church , who wear distinctive red robes and caps. The term "northern" in the common name refers to its range, as it is the northernmost cardinal species known. Northern cardinals are numerous across the eastern United States from the southern half of Maine to Minnesota to the Texas -Mexico border and in Canada in the southern portions of Ontario , Quebec, New Brunswick and Nova Scotia , all the way east to Cape Breton Island. Its range also extends south through Mexico to the Isthmus of Tehuantepec , northern Guatemala , and northern Belize . An allopatric population is found on the Pacific slope of Mexico from Jalisco to Oaxaca (this population is not shown on the range map) . The species was introduced to Bermuda in 1700. It has also been introduced in Hawaii, southern California, and southern Arizona . Its natural habitat is in woodlands, gardens, shrublands, and wetlands. In 1929, Forbush described the species as rare, and by 1955 Griscom reported the bird to be "pushing northward" when recorded annually at feeding stations. Audubon data shows that the population has grown rapidly in Massachusetts since 1960. In Massachusetts, the species is most abundant in the east, especially in areas where dense cover is interspersed with open areas, such as woodland edges, brushy fields, wooded wetlands, parks, and suburban areas. They tend to avoid extensive woodlands. The northern cardinal is a mid-sized songbird with a body length of 21–23.5 cm (8.3–9.3 in) and a wingspan of 25–31 cm (9.8–12.2 in) . The adult weighs from 33.6–65 g (1.19–2.29 oz) , with an average 44.8 g (1.58 oz) . The male averages slightly larger than the female. The adult male is a brilliant crimson red color with a black face mask over the eyes, extending to the upper chest. The color becomes duller and darker on the back and wings. The female is fawn-colored, with mostly grayish-brown tones and a slight reddish tint on the wings, crest, and tail feathers. The face mask of the female is gray to black and is less defined than that of the male. Both sexes possess prominent raised crests and bright coral-colored beaks. The beak is cone-shaped and strong. Young birds, both male and female, show coloring similar to the adult female until the fall, when they molt and grow adult feathers. They are brown above and red-brown below, with brick-colored crest, forehead, wings, and tail. The legs and feet are a dark pink-brown. The iris of the eye is brown. The plumage color of the males is produced from carotenoid pigments in the diet. Coloration is produced from both red pigments and yellow carotenoid pigments. Northern cardinal males metabolize carotenoid pigments to create plumage pigmentation of a color different from the ingested pigment. When fed only yellow pigments, males become a pale red color. A few rare " yellow morph " cardinals lack the enzyme to convert carotenoids into red pigments, and have a yellow beak and feathers (except for black face mask). During winter, cardinals will fluff up their down feathers in order to retain warm air next to their body. The down feathers are small and hairlike at the base of each flight feather . The legs and feet of are thin and lack feathers, and are vulnerable to rapid heat loss. In cold temperatures, cardinals will shiver and tense their muscles, especially breast muscles, to generate heat. Cardinals have the ability to drop their body temperature 3 to 6° if needed in order to survive cold temperatures. [ citation needed ] Both sexes sing clear, whistled song patterns, which are repeated several times, then varied. Some common phrases are described as "cheeeer-a-dote, cheeer-a-dote-dote-dote", "purdy, purdy, purdy...whoit, whoit, whoit, whoit", "what-cheer, what-cheer... wheet, wheet, wheet, wheet" and "cheer, cheer, cheer, what, what, what, what". The northern cardinal has a distinctive alarm call, a short metallic chip sound. This call often is given when predators approach the nest, in order to give warning to the female and nestlings. The songs of the two sexes of the northern cardinal, although not distinguishable by the human ear, are sexually dimorphic. It is suggested that this is because of the differences in levels of hormones of the two sexes. The diet of the adult northern cardinal consists mainly (up to 90%) of weed seeds, grains, and fruits. It is a ground feeder and finds food while hopping on the ground through trees or shrubbery. It will also consume snails and insects, including beetles, cicadas , and grasshoppers , and the young are fed almost entirely on insects. Other common items include corn , oats , sunflower seeds , the blossoms and bark of elm trees , and drinks of maple sap from holes made by sapsuckers . The northern cardinal is a territorial song bird. The male sings in a loud, clear whistle from the top of a tree or another high location to defend his territory. He will chase off other males entering his territory. He may mistake his image on various reflective surfaces as an invading male and will fight his reflection relentlessly. The northern cardinal learns its songs, and as a result the songs vary regionally. Mated pairs often travel together. The songs of a northern cardinal will usually overlap more in syllables when compared to other northern cardinals near it than those far away from it. Pairs may mate for successive years, but some also "divorce" between seasons or choose a new mate when one dies. Pairs generally stay together year-round but are not necessarily monogamous. DNA studies of two populations of cardinals found that 9–35% of nestlings were not fathered by the female's mate. Mated pairs sometimes sing together before nesting. During courtship they may also participate in a bonding behavior where the male collects food and brings it to the female, feeding her beak-to-beak. The cardinals' nest is made of thin twigs, bark strips, and grasses, lined with grasses or other plant fibers. Males sometimes bring nest material to the female, who does most of the building. She crushes twigs with her beak until they are pliable, then turns in the nest to bend the twigs around her body and push them into a cup shape with her feet. The cup has four layers: coarse twigs (and sometimes bits of trash) covered in a leafy mat, then lined with grapevine bark (when available) and finally grasses, stems, rootlets, and pine needles (where available). The nest typically takes three to nine days to build; the finished product is 5.1–7.6 cm (2.0–3.0 in) tall, 10.1 cm (4.0 in) across, with an inner diameter of about 7.6 cm (3.0 in) . Cardinals do not usually use their nests more than once. The female builds a cup nest in a well-concealed spot in dense shrub or a low tree 1–3 m (3.3–9.8 ft) off the ground. The oldest wild cardinal banded by researchers lived at least 15 years and 9 months, although 28.5 years was achieved by a captive bird. Annual survival rates for adult northern cardinals have been estimated at 60–65%. The adult male is a brilliant crimson red color with a black face mask over the eyes, extending to the upper chest. The color becomes duller and darker on the back and wings. The female is fawn-colored, with mostly grayish-brown tones and a slight reddish tint on the wings, crest, and tail feathers. The face mask of the female is gray to black and is less defined than that of the male. Both sexes possess prominent raised crests and bright coral-colored beaks. The beak is cone-shaped and strong. Young birds, both male and female, show coloring similar to the adult female until the fall, when they molt and grow adult feathers. They are brown above and red-brown below, with brick-colored crest, forehead, wings, and tail. The legs and feet are a dark pink-brown. The iris of the eye is brown. The plumage color of the males is produced from carotenoid pigments in the diet. Coloration is produced from both red pigments and yellow carotenoid pigments. Northern cardinal males metabolize carotenoid pigments to create plumage pigmentation of a color different from the ingested pigment. When fed only yellow pigments, males become a pale red color. A few rare " yellow morph " cardinals lack the enzyme to convert carotenoids into red pigments, and have a yellow beak and feathers (except for black face mask). During winter, cardinals will fluff up their down feathers in order to retain warm air next to their body. The down feathers are small and hairlike at the base of each flight feather . The legs and feet of are thin and lack feathers, and are vulnerable to rapid heat loss. In cold temperatures, cardinals will shiver and tense their muscles, especially breast muscles, to generate heat. Cardinals have the ability to drop their body temperature 3 to 6° if needed in order to survive cold temperatures. [ citation needed ]Both sexes sing clear, whistled song patterns, which are repeated several times, then varied. Some common phrases are described as "cheeeer-a-dote, cheeer-a-dote-dote-dote", "purdy, purdy, purdy...whoit, whoit, whoit, whoit", "what-cheer, what-cheer... wheet, wheet, wheet, wheet" and "cheer, cheer, cheer, what, what, what, what". The northern cardinal has a distinctive alarm call, a short metallic chip sound. This call often is given when predators approach the nest, in order to give warning to the female and nestlings. The songs of the two sexes of the northern cardinal, although not distinguishable by the human ear, are sexually dimorphic. It is suggested that this is because of the differences in levels of hormones of the two sexes. The diet of the adult northern cardinal consists mainly (up to 90%) of weed seeds, grains, and fruits. It is a ground feeder and finds food while hopping on the ground through trees or shrubbery. It will also consume snails and insects, including beetles, cicadas , and grasshoppers , and the young are fed almost entirely on insects. Other common items include corn , oats , sunflower seeds , the blossoms and bark of elm trees , and drinks of maple sap from holes made by sapsuckers . The northern cardinal is a territorial song bird. The male sings in a loud, clear whistle from the top of a tree or another high location to defend his territory. He will chase off other males entering his territory. He may mistake his image on various reflective surfaces as an invading male and will fight his reflection relentlessly. The northern cardinal learns its songs, and as a result the songs vary regionally. Mated pairs often travel together. The songs of a northern cardinal will usually overlap more in syllables when compared to other northern cardinals near it than those far away from it. Pairs may mate for successive years, but some also "divorce" between seasons or choose a new mate when one dies. Pairs generally stay together year-round but are not necessarily monogamous. DNA studies of two populations of cardinals found that 9–35% of nestlings were not fathered by the female's mate. Mated pairs sometimes sing together before nesting. During courtship they may also participate in a bonding behavior where the male collects food and brings it to the female, feeding her beak-to-beak. The cardinals' nest is made of thin twigs, bark strips, and grasses, lined with grasses or other plant fibers. Males sometimes bring nest material to the female, who does most of the building. She crushes twigs with her beak until they are pliable, then turns in the nest to bend the twigs around her body and push them into a cup shape with her feet. The cup has four layers: coarse twigs (and sometimes bits of trash) covered in a leafy mat, then lined with grapevine bark (when available) and finally grasses, stems, rootlets, and pine needles (where available). The nest typically takes three to nine days to build; the finished product is 5.1–7.6 cm (2.0–3.0 in) tall, 10.1 cm (4.0 in) across, with an inner diameter of about 7.6 cm (3.0 in) . Cardinals do not usually use their nests more than once. The female builds a cup nest in a well-concealed spot in dense shrub or a low tree 1–3 m (3.3–9.8 ft) off the ground. The oldest wild cardinal banded by researchers lived at least 15 years and 9 months, although 28.5 years was achieved by a captive bird. Annual survival rates for adult northern cardinals have been estimated at 60–65%. There are usually three or four eggs per nest, though there are sometimes as few as one or as many as five. The eggs are white, with a tint of green, blue, or brown, and are marked with lavender, gray, or brown blotches which are thicker around the larger end. The shell is smooth and slightly glossy. Eggs measure approximately 26 mm × 19 mm (1.02 in × 0.75 in) in size. Eggs are laid one to six days following the completion of the nest. Three or four eggs are laid in each clutch . The female generally incubates the eggs. The male may incubate for brief periods of time, though this is rare. Incubation takes 12 or 13 days. Young fledge 10 or 11 days after hatching. Two or three, and even four, broods are raised each year. The male cares for and feeds each brood as the female incubates the next clutch of eggs. Cardinals in Massachusetts have been observed to nest in thick and dense shrubs, trees, and vine tangles, making nests out of twigs, grass, and plant fibers. The eggs are usually incubated by female cardinals, who have brood patches , while the male cardinal forages for food. Newly hatched cardinals weigh an average of 3–3.5 grams, are naked, blind, and immobile, and do not have feathers until they are 4–5 days old. Unlike adults, their diet is mainly composed of insects, which adults crush with their beaks and feed to them. They gain weight at a rate of about 2–3 grams per day, but grow a bit slower until day 2, faster from day 2 to day 7 or 8, and then slower for the day or two before fledging. Nestlings vocalize to attract parents for feeding. Very young nestlings will beg if the nest is moved, but as they grow older, they start to only respond to their parents' presence or their songs. Nestlings defecate in the form of a fecal sac, where the fecal matter is enclosed by a tough mucus membrane. They are produced every 3 or 4 feedings, and female cardinals sometimes stimulate defecation by poking the nestling near the cloaca. Fecal sacs from the first 4- or 5 days of nesting are eaten by the parents, and later sacs are carried away from the nest and dropped. There are usually three or four eggs per nest, though there are sometimes as few as one or as many as five. The eggs are white, with a tint of green, blue, or brown, and are marked with lavender, gray, or brown blotches which are thicker around the larger end. The shell is smooth and slightly glossy. Eggs measure approximately 26 mm × 19 mm (1.02 in × 0.75 in) in size. Eggs are laid one to six days following the completion of the nest. Three or four eggs are laid in each clutch . The female generally incubates the eggs. The male may incubate for brief periods of time, though this is rare. Incubation takes 12 or 13 days. Young fledge 10 or 11 days after hatching. Two or three, and even four, broods are raised each year. The male cares for and feeds each brood as the female incubates the next clutch of eggs. Cardinals in Massachusetts have been observed to nest in thick and dense shrubs, trees, and vine tangles, making nests out of twigs, grass, and plant fibers. The eggs are usually incubated by female cardinals, who have brood patches , while the male cardinal forages for food. Newly hatched cardinals weigh an average of 3–3.5 grams, are naked, blind, and immobile, and do not have feathers until they are 4–5 days old. Unlike adults, their diet is mainly composed of insects, which adults crush with their beaks and feed to them. They gain weight at a rate of about 2–3 grams per day, but grow a bit slower until day 2, faster from day 2 to day 7 or 8, and then slower for the day or two before fledging. Nestlings vocalize to attract parents for feeding. Very young nestlings will beg if the nest is moved, but as they grow older, they start to only respond to their parents' presence or their songs. Nestlings defecate in the form of a fecal sac, where the fecal matter is enclosed by a tough mucus membrane. They are produced every 3 or 4 feedings, and female cardinals sometimes stimulate defecation by poking the nestling near the cloaca. Fecal sacs from the first 4- or 5 days of nesting are eaten by the parents, and later sacs are carried away from the nest and dropped. Northern cardinals are preyed upon by a wide variety of predators native to North America, including falcons , all Accipiter hawks, shrikes , bald eagles , golden eagles and several owls, including long-eared owls , and eastern screech owls . Predators of chicks and eggs include milk snakes , coluber constrictors , blue jays , crows , eastern gray squirrels , fox squirrels , eastern chipmunks , and domestic cats . Cowbirds have been observed to parasitize their nests. Northern cardinals are preyed upon by a wide variety of predators native to North America, including falcons , all Accipiter hawks, shrikes , bald eagles , golden eagles and several owls, including long-eared owls , and eastern screech owls . Predators of chicks and eggs include milk snakes , coluber constrictors , blue jays , crows , eastern gray squirrels , fox squirrels , eastern chipmunks , and domestic cats . Cowbirds have been observed to parasitize their nests. The northern cardinal is found in residential areas throughout its range. Bird feeders attract it by using feeders containing seeds, particularly sunflower seeds and safflower seeds. An increase in backyard feeding by humans has increased the range of this species, with an estimated global range of 5,800,000 km 2 (2,200,000 sq mi) and a global population of some 100 million. Populations appear to remain stable or increasing. Cardinals were once prized as pets due to their bright color and distinctive song. In the United States, this species is protected under the Migratory Bird Treaty Act of 1918, which also banned their sale as cage birds. It is illegal to take, kill, or possess northern cardinals, and violation of the law is punishable by a fine of up to US$15,000 and imprisonment of up to six months. It is also protected by the Convention for the Protection of Migratory Birds in Canada. A study conducted in 2016 in Atlanta, Georgia, on West Nile virus transmission in the United States found that unlike other species, northern cardinals biologically suppress the disease upon infection. In the United States, the northern cardinal (referred to as just "cardinal") is the mascot of numerous athletic teams; however, most teams portray the bird with a yellow beak and legs. In professional sports, it is the mascot of the St. Louis Cardinals of Major League Baseball 's National League and the Arizona Cardinals of the National Football League , which for many years were also based in St. Louis. In college athletics, it is the mascot of many schools, including Ball State University , The Catholic University of America , Illinois State University , the University of the Incarnate Word , Lamar University , the University of Louisville , the Massachusetts College of Pharmacy and Health Sciences , North Central College , North Idaho College , Otterbein University , Saint John Fisher College , the State University of New York at Plattsburgh , Wesleyan University , Wheeling University , and William Jewell College . The northern cardinal is the state bird of seven U.S. states, more than any other species: Illinois , Indiana , Kentucky , North Carolina , Ohio , Virginia , and West Virginia ; although in each case the particular state just refers to the bird as "cardinal". It was also a candidate to become the state bird of Delaware but lost to the Delaware Blue Hen . In the United States, the northern cardinal (referred to as just "cardinal") is the mascot of numerous athletic teams; however, most teams portray the bird with a yellow beak and legs. In professional sports, it is the mascot of the St. Louis Cardinals of Major League Baseball 's National League and the Arizona Cardinals of the National Football League , which for many years were also based in St. Louis. In college athletics, it is the mascot of many schools, including Ball State University , The Catholic University of America , Illinois State University , the University of the Incarnate Word , Lamar University , the University of Louisville , the Massachusetts College of Pharmacy and Health Sciences , North Central College , North Idaho College , Otterbein University , Saint John Fisher College , the State University of New York at Plattsburgh , Wesleyan University , Wheeling University , and William Jewell College . The northern cardinal is the state bird of seven U.S. states, more than any other species: Illinois , Indiana , Kentucky , North Carolina , Ohio , Virginia , and West Virginia ; although in each case the particular state just refers to the bird as "cardinal". It was also a candidate to become the state bird of Delaware but lost to the Delaware Blue Hen . There are 19 subspecies: C. c. cardinalis (Linnaeus, 1758) C. c. affinis Nelson, 1899 C. c. canicaudus Chapman, 1891 C. c. carneus (Lesson, 1842) C. c. clintoni (Banks, 1963) C. c. coccineus Ridgway, 1873 C. c. flammiger J.L. Peters, 1913 C. c. floridanus Ridgway, 1896 C. c. igneus S.F. Baird, 1860 C. c. littoralis Nelson, 1897 C. c. magnirostris Bangs, 1903 C. c. mariae Nelson, 1898 C. c. phillipsi Parkes, 1997 C. c. saturatus Ridgway, 1885 C. c. seftoni (Huey, 1940) C. c. sinaloensis Nelson, 1899 C. c. superbus Ridgway, 1885 C. c. townsendi (van Rossem, 1932) C. c. yucatanicus Ridgway, 1887

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West Nile

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Uganda Army (1971–1980)

The Uganda Army (abbreviated UA ), also known as Uganda Armed Forces , served as the national armed forces of Uganda during the dictatorship of Idi Amin (1971–1979). It mostly collapsed during the Uganda–Tanzania War , but remnants continued to operate in exile from 1979. These pro-Amin rebel forces continued to be called the "Uganda Army" and maintained a semblance of cohesion until 1980, when they fully fractured into rival factions. Following Uganda's independence in 1962, colonial units were transformed into the country's first national military which became known as the " Uganda Army ". The military suffered from increasing ethnic and political tensions until UA commander Idi Amin overthrew President Milton Obote in 1971. The military was subsequently purged of perceived pro-Obote elements, resulting in a transformation of its setup and organization. Under Amin's rule, the UA became dominated by people of northwestern Ugandan, Sudanese, and Zairean origin, resulting in it being increasingly perceived as foreign mercenary force by most Ugandans. It was massively expanded and modernized, mostly with weaponry of Eastern Bloc origin, though Uganda's difficult international relations resulted in shortcomings in the supply of spare parts. To maintain power, Amin used a complex patronage system through which he rewarded the Uganda Army's troops and maintained the soldiers' loyalty. As time went on, this system resulted in extreme corruption, growing indiscipline, and internal rivalries. Despite its numerical growth and good equipment, the fighting capabilities of the Uganda Army consequently deteriorated. Regardless, it remained a powerful force, and defeated several uprisings, coup attempts, and rebel invasions. In late 1978, parts of the Uganda Army invaded the neighboring Tanzania under unclear circumstances, resulting in the Uganda–Tanzania War. The military proved to be ineffective and badly motivated during this conflict, and most soldiers defected, deserted or mutinied after March 1979. Loyalist elements of the Uganda Army managed to retreat into Sudan and Zaire, however, from where they prepared to retake Uganda. The Uganda Army's remnants launched two successful invasions in 1980, capturing most of the West Nile region. Thereafter conflicts between its commanders and different factions resulted in a complete fragmentation of the remaining Uganda Army troops. One of these successor groups, the so-called Former Uganda National Army , maintained to be the continuation of the Uganda Army.After Uganda gained independence from the United Kingdom in 1962, 4th Battalion, King's African Rifles , at Jinja , was transformed into the country's first military force, the Uganda Rifles. The Uganda Rifles later became the Uganda Army. In the following years, the military was gradually expanded from 700 personnel in 1962 to 4,500 in 1965. Parliament passed the Armed Forces Act in 1964 to organise and regulate the army in place of older British ordinances. The measure provided for additional military expansion, including the establishment of the Uganda Army Air Force. Besides defending the country from external foes such as during the Congo Crisis and battling regional insurgencies like the Rwenzururu movement , the Uganda Army was politicized. It became dominated by people from northern Uganda such as the Acholi , Langi , and West Nile tribal people. Over the course of the Mengo Crisis of 1966, Prime Minister Milton Obote and his protégé , Uganda Army commander Idi Amin , used the military to oust the country's president, Mutesa II of Buganda , and establish a de facto dictatorship. This event marked the full entry of the military into the political arena, and the start of ethnic purges in the Uganda Army, as many Bantu and Teso troops were ousted from the ranks. Obote subsequently assumed the presidency and Amin was appointed head of the Uganda Army, but rifts soon emerged between the two allies. Obote feared that the Uganda Army had become too dominated by West Nile tribesmen who were regarded as partisans of Idi Amin, and reacted by ordering the recruitment of more Langi and Acholi. By 1968, the Uganda Army had been expanded to about 9,800 personnel. By 1971 it was rumoured that Obote would have Amin arrested. The rivalry culminated in Amin's successful coup d'état of 25 January 1971, when Obote was on a trip abroad. The takeover was achieved with the support of a small coterie of low ranking army officers—most of whom were of Nubian or West Nile origin—who felt their positions would have been threatened by Amin's arrest. Idi Amin's seizure of power meant that the Uganda Army had assumed full state power, ending the previous era during which civilian elites ruled in cooperation with military figures. The new administration and its more down-to-earth ruling style was initially welcomed by much of the population. Amin declared the " Second Republic of Uganda " to showcase his commitment to republicanism. He also released a manifesto justifying the coup; among other points it attacked Obote's "lack of support for the Army" and favoritism of other state security institutions. The week following the coup, Amin issued a decree declaring the creation of a Defence Council "consisting of the Commander-in-Chief, who shall be the chairman, the Army Chief of Staff, the Chief of the Air Staff, and such persons as the Commander-in-Chief may, by writing under his hand, appoint". The Defence Council was supposed to assist Amin and civilian officials in instituting a democratic transition, but this never occurred and soon the council came to supplant the cabinet as the key decision-making institution in the country. The new regime immediately embarked on a programme of military expansion. An Israeli firm was contracted to build two new army bases and several airfields. New mechanised battalions were established, as well as a paratrooper unit. Portions of the Uganda Army Air Force were redeployed from its main installation in Entebbe to the new airfields. [lower-alpha 1] Foreign equipment was ordered and procured with the assistance of France, Egypt and various Arab states, though the acquisitions depleted Uganda's foreign exchange reserves. The coup created unrest in the Uganda Army, as tensions rose between the pre-existing Acholi and Langi-dominated hierarchy and the new command structure consisting of the junior officers who had supported Amin's takeover. Amin actually promised reforms in the army to make it more ethnically representative and improve its discipline. Despite this, hundreds of soldiers were massacred in the coup's immediate aftermath—including chief of staff Suleiman Hussein . The early killings—as well as arrests—were largely selective and meant to remove potential dissidents. Nevertheless, the repression disproportionately affected Acholi and Langi officers and thus provoked the flight of hundreds of Acholi and Langi soldiers from the country, who went into exile to link up with Obote. In April 1971 the full extent of the exodus was revealed when Sudanese authorities interned hundreds of army deserters and returned them to Uganda, where they were then massacred. Realizing that it could not effectively prevent the flight of army personnel from the country and fearing that more Acholi and Langi would join with Obote, Amin's regime resorted to indiscriminate violence and moved to systematically purge the Uganda Army of Acholi, Langi, and Teso soldiers. Teso soldiers were targeted by Amin's supporters despite the fact that many of them did not resist the coup. Researcher Thomas Lowman interviewed several Ugandans who had witnessed the killings of Teso personnel, and all of them said the massacres of these soldiers were a result of "confusion rather than strategy". Lowman concluded that the Teso soldiers were "erroneously targeted". About 5,000 Acholi and Langi soldiers were killed or forcibly disappeared in the next months. Journalist Patrick Keatley estimated that as much as two thirds of the original military personnel were killed within a year. The most severe purges took place in July 1971, when fighting broke out at the military barracks of Mbarara , Jinja and Moroto . The Ugandan government maintained that pro-Obote guerrillas had attacked the barracks, whereas a pro-opposition source stated that the fighting had erupted due to tribal rivalries and 900 Acholi as well as Lango troops being massacred by Amin's supporters. A large number of the Acholi and Langi exiles joined Obote's "People Army" and " Kikosi Maalum " force which aimed at overthrowing Amin. These insurgents found a haven in Tanzania which opposed Amin's seizure of power, causing tensions that resulted in border clashes in August 1971. In August 1971, FRONASA rebels attempted to set up a guerrilla base on Mount Elgon , but they were quickly discovered and mostly arrested by Ugandan security forces. In order to replace the purged troops and consolidate his power, Amin enlisted tribesmen belonging to ethnic groups that lived in the West Nile District, Sudan, Zaire, Kenya, and Rwanda. These tribes such as the Kakwa , Nubians , Madi , Lugbara , and Alur were believed to be more loyal to Amin, and their fortunes were tied to the survival of his regime. In addition, ex- Simba and ex- Anyanya rebels became an important force among the restructured Uganda Army. Most promotions were granted to Muslim soldiers. In the course of 1971, Amin recruited 19,742 new soldiers, nominally increasing the Uganda Army to 27,000. This massive intake of untrained troops, along with the political purges and the expanded patronage system caused widespread indiscipline. By the end of the year, just 11,409 soldiers were actually accounted for. Tom Cooper and Adrien Fontanellaz described the military as being in a state of "near-anarchy" from this point onwards. The government could not financially sustain this expansion, and subsequently reduced the number of personnel. In early 1972, Amin ordered another purge of Uganda Army troops that were suspected of being disloyal, killing "thousands" of Luo soldiers. About 600 soldiers who had been imprisoned since the coup were also executed. At the same time, Amin strengthened the military's rule by stationing troops in every village of the country, ostensibly to aid rural development. In fact, it mostly helped to keep the population under control. He also expelled Uganda's Asian minority in early August 1972, and redistributed their wealth to his supporters, including the military. Amin also wielded the army as the country's main arm of law enforcement, which facilitated soldiers' abuse of power over civilians and subverted the authority of the police and non-military institutions. Given wide latitude to act, soldiers could shoot civilians with the justification that they were "resisting investigation". They also began conducting public executions. When Obote's loyalists launched invasions in 1972 from Tanzania and southern Sudan, they were completely defeated by Amin's troops and allied Libyan soldiers. This failed invasion marked the beginning of "a new and unprecedently violent phase" of Amin's reign. His regime greatly empowered and further expanded the military, allowed soldiers to act with impunity, and ultimately caused a "destructive spiral of violence" that destabilized the country. As result of the increasing brutality and the growing number of troops of West Nile origin whose primary language was Swahili , Ugandan civilians increasingly began to perceive the military as a "foreign" force. At the same time, Amin's following gradually became narrower as he grew paranoid and his resources to buy the troops' loyalty shrank amid Uganda's economic decline. The Alur were the first West Nile group that fell from power. As they were quite numerous and related to the Acholi and Langi, Amin's regime began to regard them as a security risk and purged them. The highest-ranking Alur officer, Lieutenant Colonel Valentine Ochima, was removed from the Defence Council and imprisoned in July 1971. Following Obote's invasion, Ochima was shot and all other Alur officers removed from important posts. Next, the Madi were disempowered mostly because they opposed the growing influence of Muslims in the regime. Madi soldiers were also accused of being undisciplined and aiding anti-Amin insurgents. The Lugbara also fell under suspicion as they were the largest West Nile tribe. To replace the purged troops, Amin began to enlist a growing number of Sudanese. The First Sudanese Civil War had ended in March 1972, and many Anyanya rebels opted to cross the border and enlist in the Uganda Army instead of remaining in their home country. [lower-alpha 2] Some Lugbara, Madi, and Alur officers wanted to stop the growing chaos in Uganda by overthrowing Amin, but their conspiracy was crushed in July 1973. The year also witnessed another purge of the military. By the end of 1973, the Alur, Lugbara, and Madi were marginalized, and several high-ranking commanders belonging to these tribes had been ousted from the Uganda Army or killed. The army also proved incapable of containing incursions from Turkana cattle raiders from Kenya, though on several occasions they crossed the border in pursuit and carried out reprisals on Kenyans both there and in Uganda. In addition, Ugandan soldiers who had been sent for a training mission to Libya were ordered by Libyan leader Muammar Gaddafi to assist in the Libyan occupation of the Aouzou Strip in Chad in 1973. [...] when some army officers are promoted they run for big cars and stop buying suits. Some of them are dressed like cowboys in bell-bottom trousers. —President Idi Amin, 1974, about the indiscipline in the Uganda Army At the same time, many native Ugandan officers felt marginalized by the growing number of foreigners in the military. Led by Brigadier Charles Arube (a Kakwa) and Lieutenant Colonel Elly Aseni, some of these officers plotted to overthrow Amin. In response to the murder of a Lugbara foreign minister, the remaining Lugbara in the army joined this plot. The coup attempt, later known as " Arube uprising ", was launched in March 1974, as the Lugbara troops initiated an uprising at the Malire Barracks in Kampala and Arube led a strike force to arrest or kill Amin. The plot failed when the President shot Arube dead, throwing the coup plotters into chaos. The revolt was subsequently put down with force, and over 100 soldiers were killed. After the purge of the Lugbara commander of the Suicide Battalion, another uprising broke out, in November 1974. Lugbara troops mutinied at the Mbuya barracks, and revolting Suicide Battalion troops had to be defeated at Mbarara. At least 15 soldiers were killed, and several others deserted. Thereafter, the Lugbara were no longer powerful enough to act as "counterweight to the Amin regime". From 1975, the "Kakwa-Nubi-Anyanya core" was dominant in the military. Despite their loss of power, most Madi, Lugbara, and Alur remained at least nominally loyal, as they still benefited from Amin's regime. "Substantial" numbers of Madi, Lugbara, and Alur were also kept in the military. In June 1976, Amin allowed pro-Palestinian militants to land a hijacked Airbus A300 jet airliner at Entebbe. Israel launched a counter-terrorist hostage-rescue mission, known as " Operation Entebbe " in the following month, freeing most of the airliner's passengers after killing dozens of Ugandan soldiers and all of the hijackers. The Israeli forces consequently destroyed most of the Ugandan aircraft present at Entebbe airport to prevent the Ugandans from pursuing them. The raid greatly damaged the Uganda Army, and though it was able to mostly replace the lost war materiel, internal rifts continued to worsen. Around August 1976, the Uganda Army experienced another purge, while rogue troops went on an ethnically charged rampage in Jinja and Makerere , killing or expelling all Kenyans they could find. Around this time, the Uganda Army also launched operations against armed smugglers operating on Lake Victoria . Researcher Aiden Southall argued that these operations were so intense that they amounted to "warfare". In the end, the military was unable to suppress the smuggling. In January 1977 President Amin removed General Mustafa Adrisi from his post as army chief of staff and appointed him Vice President of Uganda. Amin had ruled Uganda without a vice president for six years, and his decision to give Adrisi the job probably stemmed from his wish to appease soldiers who wanted the dismissal of Brigadier Hussein Marella , an ally of Amin who had killed a prominent Lugbara officer. In 1977, the Uganda Army was subjected to more ethnic purges. These were often met with resistance, and flagrant armed insubordination in the army increased. In one case, soldiers were hired by a businessman to rescue his brother, resulting in a successful attack on the prison at Iganga and the freeing of 600 prisoners. While one lieutenant colonel in the Bondo garrison personally oversaw the instructed execution of his Acholi officers, another opted to send his Acholi and Langi subordinates on leave so that they could flee. The largely Acholi and Langi Chui Battalion began denying access of their barracks to agents of the State Research Bureau , Amin's state security organisation, which was usually tasked with enforcing purges. Over time they began shooting at the agents when they entered their environs. The purges also sparked additional desertions, as more Acholi and Langi personnel fled the country to join Obote's rebel group. Members of the Malire Battalion and air force attempted to kill Amin during Operation Mafuta Mingi in June. In late 1977, a rebel group known as "Uganda Liberation Movement" attempted to invade from Kenya , but the insurgents were easily defeated by the Uganda Army. Following the bloodshed of 1977, Amin declared that 1978 would be a "year of peace". Nevertheless, infighting and factionalism in the army increased. Beginning in 1977, the Uganda Army had been affected by growing tensions between supporters of Amin and soldiers loyal to Vice President Adrisi. Adrisi intended to purge foreigners in the military, particularly Sudanese, as he felt that foreigners were not dependent enough on the regime to support it, and would at their convenience flee back to their lands of origin. He thought that it would be best if the Uganda Army was made up of northern Ugandans who had a larger stake in fighting for it. By this point, Uganda was already in a state of acute crisis, as its economy and infrastructure collapsed, and the different factions in the Uganda Army increasingly competed for the remaining resources. Adrisi was outmaneuvered by his political opponents, and relieved of his ministerial portfolios after being injured in a car accident in early 1978. Amin consequently purged Adrisi's loyalists from the military, including chief of staff Isaac Lumago and other ranking officers such as Moses Ali , Juma Oris , and Nasur Ezega. Ultimately, almost 3,000 troops were removed by Amin. These purges reinforced suspicions that Adrisi's "car accident" had been an assassination attempt. The Lugbara troops were especially upset about Adrisi's fall from power. Several "disturbances" took place at various army barracks in the next months, as soldiers mutinied or were purged. One major revolt took place in August, as a clique of officers attempted to forcibly restore a civilian government. In September 1978, Amin announced that he had recruited an additional 10,000 foreigners for the military, causing further discontent among the other troops of the Uganda Army. According to a Ugandan soldier interviewed by the Drum magazine, a significant number of these new recruits were actually Ugandans, many of them children, who had been forcibly conscripted. Researcher Aiden Southall argued that by this point Ugandan soldiers had been increasingly substituted by "Sudanese and Zairois guerrillas and mercenaries", while Paul Nugent said that this development "amounted to the disappearance of a national army in the conventional sense of the term." On 27 October, members of the military's southern and western commands allegedly met at Kabamba and drafted a 12‐point petition to Amin, demanding the end of corruption, factionalism, and favoritism of Nubian troops; the curtailing of the State Research Bureau's powers; the reinstatement of Adrisi and Lumago; the enforcement of religious tolerance; and an end of the alliance with various Arab powers . In late October 1978, the Uganda Army crossed the border to Tanzania and invaded the Kagera salient . The circumstances of this invasion remains unclear. Several experts and politicians have argued that Amin directly ordered the invasion to distract the Ugandan military and public from the crisis at home. Researcher Amii Omara-Otunnu stated that "the technological superiority of his armaments had blinded [Amin] from seeing the ineptitude and indiscipline of his troops." On the other side, diplomats such as Paul Etiang and other purported eyewitnesses claimed that troops loyal to Adrisi had allegedly mutinied and almost killed Amin, but were eventually defeated by loyalist troops. The Uganda Army then chased after the mutineers who crossed the border to Tanzania, resulting in the invasion. The New York Times reporter John Darnton pieced together several accounts by refugees, and argued that the invasion was possibly part of an elaborate plan by Amin. The President had sent soldiers loyal to Adrisi to the border, and then ordered them to invade Tanzania. This was supposed to be a suicide mission, and the weakened survivors would be purged by other units upon returning to Uganda. When one officer learned of this plan, he and his men revolted. However, Darnton also cautioned that the refugees were not necessarily reliable sources of information. Researchers Andrew Mambo and Julian Schofield discounted the theory about the mutinies as unlikely, noting that the battalions that were said to have mutinied remained relatively loyal to Amin's cause throughout the war with Tanzania. Mambo, Schofield, and some Ugandan commanders instead argued that the invasion was the result of violent incidents along the border which had spiralled out of control or been exploited by glory-seeking soldiers. Accordingly, the invading Ugandan troops acted on their own causing Amin to sanction the invasion post facto to save face. In any case, the invasion resulted in open war with Tanzania. Even though the Uganda Army overwhelmed the weak border defenses and successfully occupied Kagera, the invasion already exposed its catastrophic weaknesses. The Ugandan troops and their officers focused on looting the occupied territory instead of continuing their advance or preparing any defenses. They also raped local women and shot and killed about 1,500 civilians. According to a Ugandan soldier interviewed by the Drum magazine, thousands of Uganda Army soldiers took their loot and then deserted. When it became clear that the Tanzanians were preparing a counter-offensive, the Ugandan forces began to withdraw from Kagera. The Tanzania People's Defence Force (TPDF) counter-attacked in November 1978, encountering almost no resistance and retaking all lost territory. Amin's problem isn't lack of hardware. His problem is that his army is no damn good. —An unnamed Western diplomat on the Uganda Army's poor performance during the Uganda–Tanzania War In January 1979, the Tanzanians and allied Ugandan rebels crossed the border, and defeated the Uganda Army in the Battle of Mutukula . The Tanzanians used BM-21 Grad rocket launchers along the border with particular effectiveness. The Ugandans lacked weaponry which was able to counter the Tanzanian artillery, and were terrified by the destructive capabilities of the BM-21 Grads. Amin dispatched a team of officers to Spain to investigate the purchase of aircraft and napalm bombs to counter the rockets, but ultimately no munitions were acquired. The Uganda military suffered further reversals during the next month: Its southern defenses were overrun during the Battles of Simba Hills and Gayaza Hills , though at the latter it executed a successful ambush on a Tanzanian battalion. These failures were followed by another defeat in the Battle of Masaka and the loss of Mbarara . By late February, southern Uganda was occupied by Tanzanian-led forces. In addition, the Uganda Army Air Force had suffered such heavy losses during these operations that it was effectively eliminated as a fighting force. The ability of the Uganda Army's ground forces to resist the TPDF was hampered by organizational chaos, indiscipline, and the widespread lack of combat experience among its troops. Well equipped with armoured personnel carriers , the Ugandan soldiers usually chose to fight along the country's roads, but deployed their vehicles ineffectively against well-armed Tanzanian troops, resulting in many losses. Though the Uganda Army employed at least 20,000 personnel by 1978/79, only 3,000 Ugandan soldiers at most were deployed at the front lines at any given time. The 10,000 new recruits had little training, and were used to man roadblocks instead of serving at the front lines. Despite being regarded as Amin's "elite" troops, the foreign soldiers of the Uganda Army proved unreliable and often put up little resistance. One former Uganda Army officer later attributed his military's inability to organize a proper resistance to the soldiers being more interested in protecting their wealth and families rather than fight; the troops were not properly trained and many had become more akin to wealthy civilians than actual soldiers. Despite support by the Palestine Liberation Organisation and Libya, the Uganda Army was defeated in the war's decisive Battle of Lukaya on 10–11 March 1979. Thereafter, the Ugandan military completely disintegrated. In late March 1979, Darnton estimated that Amin could only rely on about 2,500 Nubians in the Uganda Army; "the loyalty or at least will to fight" of the other troops was "questionable". In April 1979, the TPDF and its allies captured Kampala ; Amin fled into exile. Some Uganda Army troops continued their resistance, but were defeated during Tanzanian mopping-up operations from April to June 1979. About 3,000 Uganda Army personnel were taken prisoner during the war. Most fleeing soldiers focused on plundering shops and banks as well as on stealing cars in hopes of escaping with as much loot as possible. The Uganda Army was replaced as Uganda's national armed forces by the Uganda National Liberation Army (UNLA), a former pro-Tanzanian alliance of rebel militias. The air force was left completely destroyed by the war, as was the army's lake patrol force. Meanwhile, Obote returned to power and became president following the disputed general election of 1980. Thousands or even tens of thousands of Uganda Army troops managed to flee across the borders to Zaire and Sudan, however, where they reorganized as insurgents and rallied under the leadership of officers such as Emilio Mondo , Isaac Lumago, Isaac Maliyamungu , Elly Hassan , Christopher Mawadri , and Moses Ali. Most of the Anyanya veterans successfully escaped to Juba . Other veterans remained in Uganda, and the new Tanzanian-backed government soon announced that they should assemble in Kampala. Many went, expecting to be enlisted in the UNLA, but they were instead imprisoned without trial. The new government viewed them as criminals due to their association with Amin's regime. They remained incarcerated for years, though most were gradually pardoned by the successive Ugandan governments. The reasoning of the pardons often remained unclear, though authorities often requested testimonies by the soldiers' communities to determine "whether they would be a danger to the public when released." In other cases, the veterans were acquitted after their families or local leaders asked for their release. In autumn 1980, about 7,100 Uganda Army troops successfully invaded northwestern Uganda , starting the Ugandan Bush War . Despite capturing most of the West Nile region from the UNLA, the Uganda Army remained highly factious. Its remaining forces were not truly unified but split into several bands with differing agendas. Some Uganda Army groups wanted to restore Amin to presidency, whereas others wanted to distance themselves from him. [lower-alpha 3] Some troops without larger political goals simply did not wish to give up their arms return to civilian livelihoods. This rift culminated in open war between two rival factions which became known as the " Uganda National Rescue Front " (UNRF) under Moses Ali, and the "Former Uganda National Army" (FUNA), led by Elly Hassan. UNRF mostly defeated FUNA in July 1981, but both factions continued to be active in the West Nile region. FUNA maintained its claim to be the continuation of the Uganda Army during this time. In August 1985, FUNA leader Isaac Lumago even claimed that the "structure of the army that went into exile after Amin's overthrow remains intact in southern Sudan and eastern Zaire". In 1985, President Obote was overthrown by a clique of UNLA officers led by Tito Okello . Okello's regime consequently convinced several ex-Uganda Army rebel groups to join his forces. The UNLA was defeated by National Resistance Army (NRA) rebels in 1986. As result, the National Resistance Movement (NRM) assumed power, Yoweri Museveni was installed as president, and the NRA became Uganda's new national military. When the NRA advanced into the West Nile region, the local elders convinced most ex-Uganda Army soldiers to peacefully surrender and reconcile with Museveni's government. Some ex-Uganda Army forces even managed to make favorable deals with the NRM. Moses Ali integrated his private army into the National Resistance Army and subsequently became a high-ranking military officer and official in Museveni's government. Some elements of FUNA and UNRF refused to lay down their weapons, but were consequently forced to retreat back into Zaire and Sudan. Though FUNA and UNRF dissolved afterwards, ex-Uganda Army soldiers formed the West Nile Bank Front and UNRF (II) which battled Museveni's government in the 1980s and 1990s. Some militant Amin loyalists and Uganda Army veterans such as Dusman Sabuni eventually joined the Allied Democratic Forces that continue to wage an insurgency up until the present day. I am called Amin's man but I did not join in Amin's time. We are called Amin's men but we did not join to help Amin. Now we are in peace, the poorest of soldiers. And where is Amin? — Yusuf Gowon , former Uganda Army chief of staff, 2017 The Uganda Army became closely associated with Idi Amin among Uganda's population, and its veterans remain popularly known as "Amin's soldiers" ( Kiswahili : Omusilikale wa Amin ) or "Amin's men". In the decades since Amin's downfall, the term maintained a negative connotation in much of Uganda due to the Uganda Army's indiscipline, brutal conduct, and corruption. "Amin's soldiers" were stereotypically believed to be uneducated northerners who had only joined the military to maintain Amin's power, despite the existence of many veterans who did not correspond to this image. This negative perception affected their attempted reintegration into civilian communities; their military service was seen as a "shame", they were monitored by authorities, and many were not granted their full pensions. There were also differences between the veterans, as some of those who had peacefully surrendered after the Uganda–Tanzania War became outcasts, whereas those who had joined rebel groups were later "welcomed back to Uganda". Some veterans came to resent Amin, especially as he had continued to live in luxury in exile, leaving them to their fate. Many issues also remained unresolved in regard to questions of guilt. Victims of Amin's regime believe that many soldiers who had committed human rights violations essentially walked free. This problem is exacerbated by the reconciliation policies of the NRM government that governs Uganda since 1986. Since the 1990s, many Uganda Army veterans have also begun to lobby for their cause, and publicly criticised their stereotypical perception as perpetrators, arguing that they should not be generally blamed for Amin's crimes. In the early 2000s veterans of the army from the 1960s and 1970s formed the Uganda Army Service Men Development Association and sued the government, demanding to be properly compensated for their service. In 2007 the Ugandan Court of Appeal ruled that since the Armed Forces of Act of 1964 had not been officially superseded by other legislation until 1992, "the Uganda Army technically remained the national army side by side with the NRA" up to that point and thus its 45,000 members required compensation for those years of duty. The government appealed the case to the Supreme Court , which nullified the award. Despite this, President Museveni declared that his government would reimburse the veterans alongside other former members of Ugandan armies to signify his government's appreciation for their national service. Over the subsequent years the government began making payouts at a gradual pace. After Uganda gained independence from the United Kingdom in 1962, 4th Battalion, King's African Rifles , at Jinja , was transformed into the country's first military force, the Uganda Rifles. The Uganda Rifles later became the Uganda Army. In the following years, the military was gradually expanded from 700 personnel in 1962 to 4,500 in 1965. Parliament passed the Armed Forces Act in 1964 to organise and regulate the army in place of older British ordinances. The measure provided for additional military expansion, including the establishment of the Uganda Army Air Force. Besides defending the country from external foes such as during the Congo Crisis and battling regional insurgencies like the Rwenzururu movement , the Uganda Army was politicized. It became dominated by people from northern Uganda such as the Acholi , Langi , and West Nile tribal people. Over the course of the Mengo Crisis of 1966, Prime Minister Milton Obote and his protégé , Uganda Army commander Idi Amin , used the military to oust the country's president, Mutesa II of Buganda , and establish a de facto dictatorship. This event marked the full entry of the military into the political arena, and the start of ethnic purges in the Uganda Army, as many Bantu and Teso troops were ousted from the ranks. Obote subsequently assumed the presidency and Amin was appointed head of the Uganda Army, but rifts soon emerged between the two allies. Obote feared that the Uganda Army had become too dominated by West Nile tribesmen who were regarded as partisans of Idi Amin, and reacted by ordering the recruitment of more Langi and Acholi. By 1968, the Uganda Army had been expanded to about 9,800 personnel. By 1971 it was rumoured that Obote would have Amin arrested. The rivalry culminated in Amin's successful coup d'état of 25 January 1971, when Obote was on a trip abroad. The takeover was achieved with the support of a small coterie of low ranking army officers—most of whom were of Nubian or West Nile origin—who felt their positions would have been threatened by Amin's arrest. Idi Amin's seizure of power meant that the Uganda Army had assumed full state power, ending the previous era during which civilian elites ruled in cooperation with military figures. The new administration and its more down-to-earth ruling style was initially welcomed by much of the population. Amin declared the " Second Republic of Uganda " to showcase his commitment to republicanism. He also released a manifesto justifying the coup; among other points it attacked Obote's "lack of support for the Army" and favoritism of other state security institutions. The week following the coup, Amin issued a decree declaring the creation of a Defence Council "consisting of the Commander-in-Chief, who shall be the chairman, the Army Chief of Staff, the Chief of the Air Staff, and such persons as the Commander-in-Chief may, by writing under his hand, appoint". The Defence Council was supposed to assist Amin and civilian officials in instituting a democratic transition, but this never occurred and soon the council came to supplant the cabinet as the key decision-making institution in the country. The new regime immediately embarked on a programme of military expansion. An Israeli firm was contracted to build two new army bases and several airfields. New mechanised battalions were established, as well as a paratrooper unit. Portions of the Uganda Army Air Force were redeployed from its main installation in Entebbe to the new airfields. [lower-alpha 1] Foreign equipment was ordered and procured with the assistance of France, Egypt and various Arab states, though the acquisitions depleted Uganda's foreign exchange reserves. The coup created unrest in the Uganda Army, as tensions rose between the pre-existing Acholi and Langi-dominated hierarchy and the new command structure consisting of the junior officers who had supported Amin's takeover. Amin actually promised reforms in the army to make it more ethnically representative and improve its discipline. Despite this, hundreds of soldiers were massacred in the coup's immediate aftermath—including chief of staff Suleiman Hussein . The early killings—as well as arrests—were largely selective and meant to remove potential dissidents. Nevertheless, the repression disproportionately affected Acholi and Langi officers and thus provoked the flight of hundreds of Acholi and Langi soldiers from the country, who went into exile to link up with Obote. In April 1971 the full extent of the exodus was revealed when Sudanese authorities interned hundreds of army deserters and returned them to Uganda, where they were then massacred. Realizing that it could not effectively prevent the flight of army personnel from the country and fearing that more Acholi and Langi would join with Obote, Amin's regime resorted to indiscriminate violence and moved to systematically purge the Uganda Army of Acholi, Langi, and Teso soldiers. Teso soldiers were targeted by Amin's supporters despite the fact that many of them did not resist the coup. Researcher Thomas Lowman interviewed several Ugandans who had witnessed the killings of Teso personnel, and all of them said the massacres of these soldiers were a result of "confusion rather than strategy". Lowman concluded that the Teso soldiers were "erroneously targeted". About 5,000 Acholi and Langi soldiers were killed or forcibly disappeared in the next months. Journalist Patrick Keatley estimated that as much as two thirds of the original military personnel were killed within a year. The most severe purges took place in July 1971, when fighting broke out at the military barracks of Mbarara , Jinja and Moroto . The Ugandan government maintained that pro-Obote guerrillas had attacked the barracks, whereas a pro-opposition source stated that the fighting had erupted due to tribal rivalries and 900 Acholi as well as Lango troops being massacred by Amin's supporters. A large number of the Acholi and Langi exiles joined Obote's "People Army" and " Kikosi Maalum " force which aimed at overthrowing Amin. These insurgents found a haven in Tanzania which opposed Amin's seizure of power, causing tensions that resulted in border clashes in August 1971. In August 1971, FRONASA rebels attempted to set up a guerrilla base on Mount Elgon , but they were quickly discovered and mostly arrested by Ugandan security forces. In order to replace the purged troops and consolidate his power, Amin enlisted tribesmen belonging to ethnic groups that lived in the West Nile District, Sudan, Zaire, Kenya, and Rwanda. These tribes such as the Kakwa , Nubians , Madi , Lugbara , and Alur were believed to be more loyal to Amin, and their fortunes were tied to the survival of his regime. In addition, ex- Simba and ex- Anyanya rebels became an important force among the restructured Uganda Army. Most promotions were granted to Muslim soldiers. In the course of 1971, Amin recruited 19,742 new soldiers, nominally increasing the Uganda Army to 27,000. This massive intake of untrained troops, along with the political purges and the expanded patronage system caused widespread indiscipline. By the end of the year, just 11,409 soldiers were actually accounted for. Tom Cooper and Adrien Fontanellaz described the military as being in a state of "near-anarchy" from this point onwards. The government could not financially sustain this expansion, and subsequently reduced the number of personnel. In early 1972, Amin ordered another purge of Uganda Army troops that were suspected of being disloyal, killing "thousands" of Luo soldiers. About 600 soldiers who had been imprisoned since the coup were also executed. At the same time, Amin strengthened the military's rule by stationing troops in every village of the country, ostensibly to aid rural development. In fact, it mostly helped to keep the population under control. He also expelled Uganda's Asian minority in early August 1972, and redistributed their wealth to his supporters, including the military. Amin also wielded the army as the country's main arm of law enforcement, which facilitated soldiers' abuse of power over civilians and subverted the authority of the police and non-military institutions. Given wide latitude to act, soldiers could shoot civilians with the justification that they were "resisting investigation". They also began conducting public executions. When Obote's loyalists launched invasions in 1972 from Tanzania and southern Sudan, they were completely defeated by Amin's troops and allied Libyan soldiers. This failed invasion marked the beginning of "a new and unprecedently violent phase" of Amin's reign. His regime greatly empowered and further expanded the military, allowed soldiers to act with impunity, and ultimately caused a "destructive spiral of violence" that destabilized the country. As result of the increasing brutality and the growing number of troops of West Nile origin whose primary language was Swahili , Ugandan civilians increasingly began to perceive the military as a "foreign" force. At the same time, Amin's following gradually became narrower as he grew paranoid and his resources to buy the troops' loyalty shrank amid Uganda's economic decline. The Alur were the first West Nile group that fell from power. As they were quite numerous and related to the Acholi and Langi, Amin's regime began to regard them as a security risk and purged them. The highest-ranking Alur officer, Lieutenant Colonel Valentine Ochima, was removed from the Defence Council and imprisoned in July 1971. Following Obote's invasion, Ochima was shot and all other Alur officers removed from important posts. Next, the Madi were disempowered mostly because they opposed the growing influence of Muslims in the regime. Madi soldiers were also accused of being undisciplined and aiding anti-Amin insurgents. The Lugbara also fell under suspicion as they were the largest West Nile tribe. To replace the purged troops, Amin began to enlist a growing number of Sudanese. The First Sudanese Civil War had ended in March 1972, and many Anyanya rebels opted to cross the border and enlist in the Uganda Army instead of remaining in their home country. [lower-alpha 2] Some Lugbara, Madi, and Alur officers wanted to stop the growing chaos in Uganda by overthrowing Amin, but their conspiracy was crushed in July 1973. The year also witnessed another purge of the military. By the end of 1973, the Alur, Lugbara, and Madi were marginalized, and several high-ranking commanders belonging to these tribes had been ousted from the Uganda Army or killed. The army also proved incapable of containing incursions from Turkana cattle raiders from Kenya, though on several occasions they crossed the border in pursuit and carried out reprisals on Kenyans both there and in Uganda. In addition, Ugandan soldiers who had been sent for a training mission to Libya were ordered by Libyan leader Muammar Gaddafi to assist in the Libyan occupation of the Aouzou Strip in Chad in 1973. [...] when some army officers are promoted they run for big cars and stop buying suits. Some of them are dressed like cowboys in bell-bottom trousers. —President Idi Amin, 1974, about the indiscipline in the Uganda Army At the same time, many native Ugandan officers felt marginalized by the growing number of foreigners in the military. Led by Brigadier Charles Arube (a Kakwa) and Lieutenant Colonel Elly Aseni, some of these officers plotted to overthrow Amin. In response to the murder of a Lugbara foreign minister, the remaining Lugbara in the army joined this plot. The coup attempt, later known as " Arube uprising ", was launched in March 1974, as the Lugbara troops initiated an uprising at the Malire Barracks in Kampala and Arube led a strike force to arrest or kill Amin. The plot failed when the President shot Arube dead, throwing the coup plotters into chaos. The revolt was subsequently put down with force, and over 100 soldiers were killed. After the purge of the Lugbara commander of the Suicide Battalion, another uprising broke out, in November 1974. Lugbara troops mutinied at the Mbuya barracks, and revolting Suicide Battalion troops had to be defeated at Mbarara. At least 15 soldiers were killed, and several others deserted. Thereafter, the Lugbara were no longer powerful enough to act as "counterweight to the Amin regime". From 1975, the "Kakwa-Nubi-Anyanya core" was dominant in the military. Despite their loss of power, most Madi, Lugbara, and Alur remained at least nominally loyal, as they still benefited from Amin's regime. "Substantial" numbers of Madi, Lugbara, and Alur were also kept in the military. In June 1976, Amin allowed pro-Palestinian militants to land a hijacked Airbus A300 jet airliner at Entebbe. Israel launched a counter-terrorist hostage-rescue mission, known as " Operation Entebbe " in the following month, freeing most of the airliner's passengers after killing dozens of Ugandan soldiers and all of the hijackers. The Israeli forces consequently destroyed most of the Ugandan aircraft present at Entebbe airport to prevent the Ugandans from pursuing them. The raid greatly damaged the Uganda Army, and though it was able to mostly replace the lost war materiel, internal rifts continued to worsen. Around August 1976, the Uganda Army experienced another purge, while rogue troops went on an ethnically charged rampage in Jinja and Makerere , killing or expelling all Kenyans they could find. Around this time, the Uganda Army also launched operations against armed smugglers operating on Lake Victoria . Researcher Aiden Southall argued that these operations were so intense that they amounted to "warfare". In the end, the military was unable to suppress the smuggling. In January 1977 President Amin removed General Mustafa Adrisi from his post as army chief of staff and appointed him Vice President of Uganda. Amin had ruled Uganda without a vice president for six years, and his decision to give Adrisi the job probably stemmed from his wish to appease soldiers who wanted the dismissal of Brigadier Hussein Marella , an ally of Amin who had killed a prominent Lugbara officer. In 1977, the Uganda Army was subjected to more ethnic purges. These were often met with resistance, and flagrant armed insubordination in the army increased. In one case, soldiers were hired by a businessman to rescue his brother, resulting in a successful attack on the prison at Iganga and the freeing of 600 prisoners. While one lieutenant colonel in the Bondo garrison personally oversaw the instructed execution of his Acholi officers, another opted to send his Acholi and Langi subordinates on leave so that they could flee. The largely Acholi and Langi Chui Battalion began denying access of their barracks to agents of the State Research Bureau , Amin's state security organisation, which was usually tasked with enforcing purges. Over time they began shooting at the agents when they entered their environs. The purges also sparked additional desertions, as more Acholi and Langi personnel fled the country to join Obote's rebel group. Members of the Malire Battalion and air force attempted to kill Amin during Operation Mafuta Mingi in June. In late 1977, a rebel group known as "Uganda Liberation Movement" attempted to invade from Kenya , but the insurgents were easily defeated by the Uganda Army. Following the bloodshed of 1977, Amin declared that 1978 would be a "year of peace". Nevertheless, infighting and factionalism in the army increased. Beginning in 1977, the Uganda Army had been affected by growing tensions between supporters of Amin and soldiers loyal to Vice President Adrisi. Adrisi intended to purge foreigners in the military, particularly Sudanese, as he felt that foreigners were not dependent enough on the regime to support it, and would at their convenience flee back to their lands of origin. He thought that it would be best if the Uganda Army was made up of northern Ugandans who had a larger stake in fighting for it. By this point, Uganda was already in a state of acute crisis, as its economy and infrastructure collapsed, and the different factions in the Uganda Army increasingly competed for the remaining resources. Adrisi was outmaneuvered by his political opponents, and relieved of his ministerial portfolios after being injured in a car accident in early 1978. Amin consequently purged Adrisi's loyalists from the military, including chief of staff Isaac Lumago and other ranking officers such as Moses Ali , Juma Oris , and Nasur Ezega. Ultimately, almost 3,000 troops were removed by Amin. These purges reinforced suspicions that Adrisi's "car accident" had been an assassination attempt. The Lugbara troops were especially upset about Adrisi's fall from power. Several "disturbances" took place at various army barracks in the next months, as soldiers mutinied or were purged. One major revolt took place in August, as a clique of officers attempted to forcibly restore a civilian government. In September 1978, Amin announced that he had recruited an additional 10,000 foreigners for the military, causing further discontent among the other troops of the Uganda Army. According to a Ugandan soldier interviewed by the Drum magazine, a significant number of these new recruits were actually Ugandans, many of them children, who had been forcibly conscripted. Researcher Aiden Southall argued that by this point Ugandan soldiers had been increasingly substituted by "Sudanese and Zairois guerrillas and mercenaries", while Paul Nugent said that this development "amounted to the disappearance of a national army in the conventional sense of the term." On 27 October, members of the military's southern and western commands allegedly met at Kabamba and drafted a 12‐point petition to Amin, demanding the end of corruption, factionalism, and favoritism of Nubian troops; the curtailing of the State Research Bureau's powers; the reinstatement of Adrisi and Lumago; the enforcement of religious tolerance; and an end of the alliance with various Arab powers . In late October 1978, the Uganda Army crossed the border to Tanzania and invaded the Kagera salient . The circumstances of this invasion remains unclear. Several experts and politicians have argued that Amin directly ordered the invasion to distract the Ugandan military and public from the crisis at home. Researcher Amii Omara-Otunnu stated that "the technological superiority of his armaments had blinded [Amin] from seeing the ineptitude and indiscipline of his troops." On the other side, diplomats such as Paul Etiang and other purported eyewitnesses claimed that troops loyal to Adrisi had allegedly mutinied and almost killed Amin, but were eventually defeated by loyalist troops. The Uganda Army then chased after the mutineers who crossed the border to Tanzania, resulting in the invasion. The New York Times reporter John Darnton pieced together several accounts by refugees, and argued that the invasion was possibly part of an elaborate plan by Amin. The President had sent soldiers loyal to Adrisi to the border, and then ordered them to invade Tanzania. This was supposed to be a suicide mission, and the weakened survivors would be purged by other units upon returning to Uganda. When one officer learned of this plan, he and his men revolted. However, Darnton also cautioned that the refugees were not necessarily reliable sources of information. Researchers Andrew Mambo and Julian Schofield discounted the theory about the mutinies as unlikely, noting that the battalions that were said to have mutinied remained relatively loyal to Amin's cause throughout the war with Tanzania. Mambo, Schofield, and some Ugandan commanders instead argued that the invasion was the result of violent incidents along the border which had spiralled out of control or been exploited by glory-seeking soldiers. Accordingly, the invading Ugandan troops acted on their own causing Amin to sanction the invasion post facto to save face. In any case, the invasion resulted in open war with Tanzania. Even though the Uganda Army overwhelmed the weak border defenses and successfully occupied Kagera, the invasion already exposed its catastrophic weaknesses. The Ugandan troops and their officers focused on looting the occupied territory instead of continuing their advance or preparing any defenses. They also raped local women and shot and killed about 1,500 civilians. According to a Ugandan soldier interviewed by the Drum magazine, thousands of Uganda Army soldiers took their loot and then deserted. When it became clear that the Tanzanians were preparing a counter-offensive, the Ugandan forces began to withdraw from Kagera. The Tanzania People's Defence Force (TPDF) counter-attacked in November 1978, encountering almost no resistance and retaking all lost territory. Amin's problem isn't lack of hardware. His problem is that his army is no damn good. —An unnamed Western diplomat on the Uganda Army's poor performance during the Uganda–Tanzania War In January 1979, the Tanzanians and allied Ugandan rebels crossed the border, and defeated the Uganda Army in the Battle of Mutukula . The Tanzanians used BM-21 Grad rocket launchers along the border with particular effectiveness. The Ugandans lacked weaponry which was able to counter the Tanzanian artillery, and were terrified by the destructive capabilities of the BM-21 Grads. Amin dispatched a team of officers to Spain to investigate the purchase of aircraft and napalm bombs to counter the rockets, but ultimately no munitions were acquired. The Uganda military suffered further reversals during the next month: Its southern defenses were overrun during the Battles of Simba Hills and Gayaza Hills , though at the latter it executed a successful ambush on a Tanzanian battalion. These failures were followed by another defeat in the Battle of Masaka and the loss of Mbarara . By late February, southern Uganda was occupied by Tanzanian-led forces. In addition, the Uganda Army Air Force had suffered such heavy losses during these operations that it was effectively eliminated as a fighting force. The ability of the Uganda Army's ground forces to resist the TPDF was hampered by organizational chaos, indiscipline, and the widespread lack of combat experience among its troops. Well equipped with armoured personnel carriers , the Ugandan soldiers usually chose to fight along the country's roads, but deployed their vehicles ineffectively against well-armed Tanzanian troops, resulting in many losses. Though the Uganda Army employed at least 20,000 personnel by 1978/79, only 3,000 Ugandan soldiers at most were deployed at the front lines at any given time. The 10,000 new recruits had little training, and were used to man roadblocks instead of serving at the front lines. Despite being regarded as Amin's "elite" troops, the foreign soldiers of the Uganda Army proved unreliable and often put up little resistance. One former Uganda Army officer later attributed his military's inability to organize a proper resistance to the soldiers being more interested in protecting their wealth and families rather than fight; the troops were not properly trained and many had become more akin to wealthy civilians than actual soldiers. Despite support by the Palestine Liberation Organisation and Libya, the Uganda Army was defeated in the war's decisive Battle of Lukaya on 10–11 March 1979. Thereafter, the Ugandan military completely disintegrated. In late March 1979, Darnton estimated that Amin could only rely on about 2,500 Nubians in the Uganda Army; "the loyalty or at least will to fight" of the other troops was "questionable". In April 1979, the TPDF and its allies captured Kampala ; Amin fled into exile. Some Uganda Army troops continued their resistance, but were defeated during Tanzanian mopping-up operations from April to June 1979. About 3,000 Uganda Army personnel were taken prisoner during the war. Most fleeing soldiers focused on plundering shops and banks as well as on stealing cars in hopes of escaping with as much loot as possible. The Uganda Army was replaced as Uganda's national armed forces by the Uganda National Liberation Army (UNLA), a former pro-Tanzanian alliance of rebel militias. The air force was left completely destroyed by the war, as was the army's lake patrol force. Meanwhile, Obote returned to power and became president following the disputed general election of 1980. Idi Amin's seizure of power meant that the Uganda Army had assumed full state power, ending the previous era during which civilian elites ruled in cooperation with military figures. The new administration and its more down-to-earth ruling style was initially welcomed by much of the population. Amin declared the " Second Republic of Uganda " to showcase his commitment to republicanism. He also released a manifesto justifying the coup; among other points it attacked Obote's "lack of support for the Army" and favoritism of other state security institutions. The week following the coup, Amin issued a decree declaring the creation of a Defence Council "consisting of the Commander-in-Chief, who shall be the chairman, the Army Chief of Staff, the Chief of the Air Staff, and such persons as the Commander-in-Chief may, by writing under his hand, appoint". The Defence Council was supposed to assist Amin and civilian officials in instituting a democratic transition, but this never occurred and soon the council came to supplant the cabinet as the key decision-making institution in the country. The new regime immediately embarked on a programme of military expansion. An Israeli firm was contracted to build two new army bases and several airfields. New mechanised battalions were established, as well as a paratrooper unit. Portions of the Uganda Army Air Force were redeployed from its main installation in Entebbe to the new airfields. [lower-alpha 1] Foreign equipment was ordered and procured with the assistance of France, Egypt and various Arab states, though the acquisitions depleted Uganda's foreign exchange reserves. The coup created unrest in the Uganda Army, as tensions rose between the pre-existing Acholi and Langi-dominated hierarchy and the new command structure consisting of the junior officers who had supported Amin's takeover. Amin actually promised reforms in the army to make it more ethnically representative and improve its discipline. Despite this, hundreds of soldiers were massacred in the coup's immediate aftermath—including chief of staff Suleiman Hussein . The early killings—as well as arrests—were largely selective and meant to remove potential dissidents. Nevertheless, the repression disproportionately affected Acholi and Langi officers and thus provoked the flight of hundreds of Acholi and Langi soldiers from the country, who went into exile to link up with Obote. In April 1971 the full extent of the exodus was revealed when Sudanese authorities interned hundreds of army deserters and returned them to Uganda, where they were then massacred. Realizing that it could not effectively prevent the flight of army personnel from the country and fearing that more Acholi and Langi would join with Obote, Amin's regime resorted to indiscriminate violence and moved to systematically purge the Uganda Army of Acholi, Langi, and Teso soldiers. Teso soldiers were targeted by Amin's supporters despite the fact that many of them did not resist the coup. Researcher Thomas Lowman interviewed several Ugandans who had witnessed the killings of Teso personnel, and all of them said the massacres of these soldiers were a result of "confusion rather than strategy". Lowman concluded that the Teso soldiers were "erroneously targeted". About 5,000 Acholi and Langi soldiers were killed or forcibly disappeared in the next months. Journalist Patrick Keatley estimated that as much as two thirds of the original military personnel were killed within a year. The most severe purges took place in July 1971, when fighting broke out at the military barracks of Mbarara , Jinja and Moroto . The Ugandan government maintained that pro-Obote guerrillas had attacked the barracks, whereas a pro-opposition source stated that the fighting had erupted due to tribal rivalries and 900 Acholi as well as Lango troops being massacred by Amin's supporters. A large number of the Acholi and Langi exiles joined Obote's "People Army" and " Kikosi Maalum " force which aimed at overthrowing Amin. These insurgents found a haven in Tanzania which opposed Amin's seizure of power, causing tensions that resulted in border clashes in August 1971. In August 1971, FRONASA rebels attempted to set up a guerrilla base on Mount Elgon , but they were quickly discovered and mostly arrested by Ugandan security forces. In order to replace the purged troops and consolidate his power, Amin enlisted tribesmen belonging to ethnic groups that lived in the West Nile District, Sudan, Zaire, Kenya, and Rwanda. These tribes such as the Kakwa , Nubians , Madi , Lugbara , and Alur were believed to be more loyal to Amin, and their fortunes were tied to the survival of his regime. In addition, ex- Simba and ex- Anyanya rebels became an important force among the restructured Uganda Army. Most promotions were granted to Muslim soldiers. In the course of 1971, Amin recruited 19,742 new soldiers, nominally increasing the Uganda Army to 27,000. This massive intake of untrained troops, along with the political purges and the expanded patronage system caused widespread indiscipline. By the end of the year, just 11,409 soldiers were actually accounted for. Tom Cooper and Adrien Fontanellaz described the military as being in a state of "near-anarchy" from this point onwards. The government could not financially sustain this expansion, and subsequently reduced the number of personnel. In early 1972, Amin ordered another purge of Uganda Army troops that were suspected of being disloyal, killing "thousands" of Luo soldiers. About 600 soldiers who had been imprisoned since the coup were also executed. At the same time, Amin strengthened the military's rule by stationing troops in every village of the country, ostensibly to aid rural development. In fact, it mostly helped to keep the population under control. He also expelled Uganda's Asian minority in early August 1972, and redistributed their wealth to his supporters, including the military. Amin also wielded the army as the country's main arm of law enforcement, which facilitated soldiers' abuse of power over civilians and subverted the authority of the police and non-military institutions. Given wide latitude to act, soldiers could shoot civilians with the justification that they were "resisting investigation". They also began conducting public executions. When Obote's loyalists launched invasions in 1972 from Tanzania and southern Sudan, they were completely defeated by Amin's troops and allied Libyan soldiers. This failed invasion marked the beginning of "a new and unprecedently violent phase" of Amin's reign. His regime greatly empowered and further expanded the military, allowed soldiers to act with impunity, and ultimately caused a "destructive spiral of violence" that destabilized the country. As result of the increasing brutality and the growing number of troops of West Nile origin whose primary language was Swahili , Ugandan civilians increasingly began to perceive the military as a "foreign" force. At the same time, Amin's following gradually became narrower as he grew paranoid and his resources to buy the troops' loyalty shrank amid Uganda's economic decline. The Alur were the first West Nile group that fell from power. As they were quite numerous and related to the Acholi and Langi, Amin's regime began to regard them as a security risk and purged them. The highest-ranking Alur officer, Lieutenant Colonel Valentine Ochima, was removed from the Defence Council and imprisoned in July 1971. Following Obote's invasion, Ochima was shot and all other Alur officers removed from important posts. Next, the Madi were disempowered mostly because they opposed the growing influence of Muslims in the regime. Madi soldiers were also accused of being undisciplined and aiding anti-Amin insurgents. The Lugbara also fell under suspicion as they were the largest West Nile tribe. To replace the purged troops, Amin began to enlist a growing number of Sudanese. The First Sudanese Civil War had ended in March 1972, and many Anyanya rebels opted to cross the border and enlist in the Uganda Army instead of remaining in their home country. [lower-alpha 2] Some Lugbara, Madi, and Alur officers wanted to stop the growing chaos in Uganda by overthrowing Amin, but their conspiracy was crushed in July 1973. The year also witnessed another purge of the military. By the end of 1973, the Alur, Lugbara, and Madi were marginalized, and several high-ranking commanders belonging to these tribes had been ousted from the Uganda Army or killed. The army also proved incapable of containing incursions from Turkana cattle raiders from Kenya, though on several occasions they crossed the border in pursuit and carried out reprisals on Kenyans both there and in Uganda. In addition, Ugandan soldiers who had been sent for a training mission to Libya were ordered by Libyan leader Muammar Gaddafi to assist in the Libyan occupation of the Aouzou Strip in Chad in 1973. [...] when some army officers are promoted they run for big cars and stop buying suits. Some of them are dressed like cowboys in bell-bottom trousers. —President Idi Amin, 1974, about the indiscipline in the Uganda Army At the same time, many native Ugandan officers felt marginalized by the growing number of foreigners in the military. Led by Brigadier Charles Arube (a Kakwa) and Lieutenant Colonel Elly Aseni, some of these officers plotted to overthrow Amin. In response to the murder of a Lugbara foreign minister, the remaining Lugbara in the army joined this plot. The coup attempt, later known as " Arube uprising ", was launched in March 1974, as the Lugbara troops initiated an uprising at the Malire Barracks in Kampala and Arube led a strike force to arrest or kill Amin. The plot failed when the President shot Arube dead, throwing the coup plotters into chaos. The revolt was subsequently put down with force, and over 100 soldiers were killed. After the purge of the Lugbara commander of the Suicide Battalion, another uprising broke out, in November 1974. Lugbara troops mutinied at the Mbuya barracks, and revolting Suicide Battalion troops had to be defeated at Mbarara. At least 15 soldiers were killed, and several others deserted. Thereafter, the Lugbara were no longer powerful enough to act as "counterweight to the Amin regime". From 1975, the "Kakwa-Nubi-Anyanya core" was dominant in the military. Despite their loss of power, most Madi, Lugbara, and Alur remained at least nominally loyal, as they still benefited from Amin's regime. "Substantial" numbers of Madi, Lugbara, and Alur were also kept in the military. In June 1976, Amin allowed pro-Palestinian militants to land a hijacked Airbus A300 jet airliner at Entebbe. Israel launched a counter-terrorist hostage-rescue mission, known as " Operation Entebbe " in the following month, freeing most of the airliner's passengers after killing dozens of Ugandan soldiers and all of the hijackers. The Israeli forces consequently destroyed most of the Ugandan aircraft present at Entebbe airport to prevent the Ugandans from pursuing them. The raid greatly damaged the Uganda Army, and though it was able to mostly replace the lost war materiel, internal rifts continued to worsen. Around August 1976, the Uganda Army experienced another purge, while rogue troops went on an ethnically charged rampage in Jinja and Makerere , killing or expelling all Kenyans they could find. Around this time, the Uganda Army also launched operations against armed smugglers operating on Lake Victoria . Researcher Aiden Southall argued that these operations were so intense that they amounted to "warfare". In the end, the military was unable to suppress the smuggling. In January 1977 President Amin removed General Mustafa Adrisi from his post as army chief of staff and appointed him Vice President of Uganda. Amin had ruled Uganda without a vice president for six years, and his decision to give Adrisi the job probably stemmed from his wish to appease soldiers who wanted the dismissal of Brigadier Hussein Marella , an ally of Amin who had killed a prominent Lugbara officer. In 1977, the Uganda Army was subjected to more ethnic purges. These were often met with resistance, and flagrant armed insubordination in the army increased. In one case, soldiers were hired by a businessman to rescue his brother, resulting in a successful attack on the prison at Iganga and the freeing of 600 prisoners. While one lieutenant colonel in the Bondo garrison personally oversaw the instructed execution of his Acholi officers, another opted to send his Acholi and Langi subordinates on leave so that they could flee. The largely Acholi and Langi Chui Battalion began denying access of their barracks to agents of the State Research Bureau , Amin's state security organisation, which was usually tasked with enforcing purges. Over time they began shooting at the agents when they entered their environs. The purges also sparked additional desertions, as more Acholi and Langi personnel fled the country to join Obote's rebel group. Members of the Malire Battalion and air force attempted to kill Amin during Operation Mafuta Mingi in June. In late 1977, a rebel group known as "Uganda Liberation Movement" attempted to invade from Kenya , but the insurgents were easily defeated by the Uganda Army. Following the bloodshed of 1977, Amin declared that 1978 would be a "year of peace". Nevertheless, infighting and factionalism in the army increased. Beginning in 1977, the Uganda Army had been affected by growing tensions between supporters of Amin and soldiers loyal to Vice President Adrisi. Adrisi intended to purge foreigners in the military, particularly Sudanese, as he felt that foreigners were not dependent enough on the regime to support it, and would at their convenience flee back to their lands of origin. He thought that it would be best if the Uganda Army was made up of northern Ugandans who had a larger stake in fighting for it. By this point, Uganda was already in a state of acute crisis, as its economy and infrastructure collapsed, and the different factions in the Uganda Army increasingly competed for the remaining resources. Adrisi was outmaneuvered by his political opponents, and relieved of his ministerial portfolios after being injured in a car accident in early 1978. Amin consequently purged Adrisi's loyalists from the military, including chief of staff Isaac Lumago and other ranking officers such as Moses Ali , Juma Oris , and Nasur Ezega. Ultimately, almost 3,000 troops were removed by Amin. These purges reinforced suspicions that Adrisi's "car accident" had been an assassination attempt. The Lugbara troops were especially upset about Adrisi's fall from power. Several "disturbances" took place at various army barracks in the next months, as soldiers mutinied or were purged. One major revolt took place in August, as a clique of officers attempted to forcibly restore a civilian government. In September 1978, Amin announced that he had recruited an additional 10,000 foreigners for the military, causing further discontent among the other troops of the Uganda Army. According to a Ugandan soldier interviewed by the Drum magazine, a significant number of these new recruits were actually Ugandans, many of them children, who had been forcibly conscripted. Researcher Aiden Southall argued that by this point Ugandan soldiers had been increasingly substituted by "Sudanese and Zairois guerrillas and mercenaries", while Paul Nugent said that this development "amounted to the disappearance of a national army in the conventional sense of the term." On 27 October, members of the military's southern and western commands allegedly met at Kabamba and drafted a 12‐point petition to Amin, demanding the end of corruption, factionalism, and favoritism of Nubian troops; the curtailing of the State Research Bureau's powers; the reinstatement of Adrisi and Lumago; the enforcement of religious tolerance; and an end of the alliance with various Arab powers . In late October 1978, the Uganda Army crossed the border to Tanzania and invaded the Kagera salient . The circumstances of this invasion remains unclear. Several experts and politicians have argued that Amin directly ordered the invasion to distract the Ugandan military and public from the crisis at home. Researcher Amii Omara-Otunnu stated that "the technological superiority of his armaments had blinded [Amin] from seeing the ineptitude and indiscipline of his troops." On the other side, diplomats such as Paul Etiang and other purported eyewitnesses claimed that troops loyal to Adrisi had allegedly mutinied and almost killed Amin, but were eventually defeated by loyalist troops. The Uganda Army then chased after the mutineers who crossed the border to Tanzania, resulting in the invasion. The New York Times reporter John Darnton pieced together several accounts by refugees, and argued that the invasion was possibly part of an elaborate plan by Amin. The President had sent soldiers loyal to Adrisi to the border, and then ordered them to invade Tanzania. This was supposed to be a suicide mission, and the weakened survivors would be purged by other units upon returning to Uganda. When one officer learned of this plan, he and his men revolted. However, Darnton also cautioned that the refugees were not necessarily reliable sources of information. Researchers Andrew Mambo and Julian Schofield discounted the theory about the mutinies as unlikely, noting that the battalions that were said to have mutinied remained relatively loyal to Amin's cause throughout the war with Tanzania. Mambo, Schofield, and some Ugandan commanders instead argued that the invasion was the result of violent incidents along the border which had spiralled out of control or been exploited by glory-seeking soldiers. Accordingly, the invading Ugandan troops acted on their own causing Amin to sanction the invasion post facto to save face. In any case, the invasion resulted in open war with Tanzania. Even though the Uganda Army overwhelmed the weak border defenses and successfully occupied Kagera, the invasion already exposed its catastrophic weaknesses. The Ugandan troops and their officers focused on looting the occupied territory instead of continuing their advance or preparing any defenses. They also raped local women and shot and killed about 1,500 civilians. According to a Ugandan soldier interviewed by the Drum magazine, thousands of Uganda Army soldiers took their loot and then deserted. When it became clear that the Tanzanians were preparing a counter-offensive, the Ugandan forces began to withdraw from Kagera. The Tanzania People's Defence Force (TPDF) counter-attacked in November 1978, encountering almost no resistance and retaking all lost territory. Amin's problem isn't lack of hardware. His problem is that his army is no damn good. —An unnamed Western diplomat on the Uganda Army's poor performance during the Uganda–Tanzania War In January 1979, the Tanzanians and allied Ugandan rebels crossed the border, and defeated the Uganda Army in the Battle of Mutukula . The Tanzanians used BM-21 Grad rocket launchers along the border with particular effectiveness. The Ugandans lacked weaponry which was able to counter the Tanzanian artillery, and were terrified by the destructive capabilities of the BM-21 Grads. Amin dispatched a team of officers to Spain to investigate the purchase of aircraft and napalm bombs to counter the rockets, but ultimately no munitions were acquired. The Uganda military suffered further reversals during the next month: Its southern defenses were overrun during the Battles of Simba Hills and Gayaza Hills , though at the latter it executed a successful ambush on a Tanzanian battalion. These failures were followed by another defeat in the Battle of Masaka and the loss of Mbarara . By late February, southern Uganda was occupied by Tanzanian-led forces. In addition, the Uganda Army Air Force had suffered such heavy losses during these operations that it was effectively eliminated as a fighting force. The ability of the Uganda Army's ground forces to resist the TPDF was hampered by organizational chaos, indiscipline, and the widespread lack of combat experience among its troops. Well equipped with armoured personnel carriers , the Ugandan soldiers usually chose to fight along the country's roads, but deployed their vehicles ineffectively against well-armed Tanzanian troops, resulting in many losses. Though the Uganda Army employed at least 20,000 personnel by 1978/79, only 3,000 Ugandan soldiers at most were deployed at the front lines at any given time. The 10,000 new recruits had little training, and were used to man roadblocks instead of serving at the front lines. Despite being regarded as Amin's "elite" troops, the foreign soldiers of the Uganda Army proved unreliable and often put up little resistance. One former Uganda Army officer later attributed his military's inability to organize a proper resistance to the soldiers being more interested in protecting their wealth and families rather than fight; the troops were not properly trained and many had become more akin to wealthy civilians than actual soldiers. Despite support by the Palestine Liberation Organisation and Libya, the Uganda Army was defeated in the war's decisive Battle of Lukaya on 10–11 March 1979. Thereafter, the Ugandan military completely disintegrated. In late March 1979, Darnton estimated that Amin could only rely on about 2,500 Nubians in the Uganda Army; "the loyalty or at least will to fight" of the other troops was "questionable". In April 1979, the TPDF and its allies captured Kampala ; Amin fled into exile. Some Uganda Army troops continued their resistance, but were defeated during Tanzanian mopping-up operations from April to June 1979. About 3,000 Uganda Army personnel were taken prisoner during the war. Most fleeing soldiers focused on plundering shops and banks as well as on stealing cars in hopes of escaping with as much loot as possible. The Uganda Army was replaced as Uganda's national armed forces by the Uganda National Liberation Army (UNLA), a former pro-Tanzanian alliance of rebel militias. The air force was left completely destroyed by the war, as was the army's lake patrol force. Meanwhile, Obote returned to power and became president following the disputed general election of 1980. Thousands or even tens of thousands of Uganda Army troops managed to flee across the borders to Zaire and Sudan, however, where they reorganized as insurgents and rallied under the leadership of officers such as Emilio Mondo , Isaac Lumago, Isaac Maliyamungu , Elly Hassan , Christopher Mawadri , and Moses Ali. Most of the Anyanya veterans successfully escaped to Juba . Other veterans remained in Uganda, and the new Tanzanian-backed government soon announced that they should assemble in Kampala. Many went, expecting to be enlisted in the UNLA, but they were instead imprisoned without trial. The new government viewed them as criminals due to their association with Amin's regime. They remained incarcerated for years, though most were gradually pardoned by the successive Ugandan governments. The reasoning of the pardons often remained unclear, though authorities often requested testimonies by the soldiers' communities to determine "whether they would be a danger to the public when released." In other cases, the veterans were acquitted after their families or local leaders asked for their release. In autumn 1980, about 7,100 Uganda Army troops successfully invaded northwestern Uganda , starting the Ugandan Bush War . Despite capturing most of the West Nile region from the UNLA, the Uganda Army remained highly factious. Its remaining forces were not truly unified but split into several bands with differing agendas. Some Uganda Army groups wanted to restore Amin to presidency, whereas others wanted to distance themselves from him. [lower-alpha 3] Some troops without larger political goals simply did not wish to give up their arms return to civilian livelihoods. This rift culminated in open war between two rival factions which became known as the " Uganda National Rescue Front " (UNRF) under Moses Ali, and the "Former Uganda National Army" (FUNA), led by Elly Hassan. UNRF mostly defeated FUNA in July 1981, but both factions continued to be active in the West Nile region. FUNA maintained its claim to be the continuation of the Uganda Army during this time. In August 1985, FUNA leader Isaac Lumago even claimed that the "structure of the army that went into exile after Amin's overthrow remains intact in southern Sudan and eastern Zaire". In 1985, President Obote was overthrown by a clique of UNLA officers led by Tito Okello . Okello's regime consequently convinced several ex-Uganda Army rebel groups to join his forces. The UNLA was defeated by National Resistance Army (NRA) rebels in 1986. As result, the National Resistance Movement (NRM) assumed power, Yoweri Museveni was installed as president, and the NRA became Uganda's new national military. When the NRA advanced into the West Nile region, the local elders convinced most ex-Uganda Army soldiers to peacefully surrender and reconcile with Museveni's government. Some ex-Uganda Army forces even managed to make favorable deals with the NRM. Moses Ali integrated his private army into the National Resistance Army and subsequently became a high-ranking military officer and official in Museveni's government. Some elements of FUNA and UNRF refused to lay down their weapons, but were consequently forced to retreat back into Zaire and Sudan. Though FUNA and UNRF dissolved afterwards, ex-Uganda Army soldiers formed the West Nile Bank Front and UNRF (II) which battled Museveni's government in the 1980s and 1990s. Some militant Amin loyalists and Uganda Army veterans such as Dusman Sabuni eventually joined the Allied Democratic Forces that continue to wage an insurgency up until the present day. I am called Amin's man but I did not join in Amin's time. We are called Amin's men but we did not join to help Amin. Now we are in peace, the poorest of soldiers. And where is Amin? — Yusuf Gowon , former Uganda Army chief of staff, 2017 The Uganda Army became closely associated with Idi Amin among Uganda's population, and its veterans remain popularly known as "Amin's soldiers" ( Kiswahili : Omusilikale wa Amin ) or "Amin's men". In the decades since Amin's downfall, the term maintained a negative connotation in much of Uganda due to the Uganda Army's indiscipline, brutal conduct, and corruption. "Amin's soldiers" were stereotypically believed to be uneducated northerners who had only joined the military to maintain Amin's power, despite the existence of many veterans who did not correspond to this image. This negative perception affected their attempted reintegration into civilian communities; their military service was seen as a "shame", they were monitored by authorities, and many were not granted their full pensions. There were also differences between the veterans, as some of those who had peacefully surrendered after the Uganda–Tanzania War became outcasts, whereas those who had joined rebel groups were later "welcomed back to Uganda". Some veterans came to resent Amin, especially as he had continued to live in luxury in exile, leaving them to their fate. Many issues also remained unresolved in regard to questions of guilt. Victims of Amin's regime believe that many soldiers who had committed human rights violations essentially walked free. This problem is exacerbated by the reconciliation policies of the NRM government that governs Uganda since 1986. Since the 1990s, many Uganda Army veterans have also begun to lobby for their cause, and publicly criticised their stereotypical perception as perpetrators, arguing that they should not be generally blamed for Amin's crimes. In the early 2000s veterans of the army from the 1960s and 1970s formed the Uganda Army Service Men Development Association and sued the government, demanding to be properly compensated for their service. In 2007 the Ugandan Court of Appeal ruled that since the Armed Forces of Act of 1964 had not been officially superseded by other legislation until 1992, "the Uganda Army technically remained the national army side by side with the NRA" up to that point and thus its 45,000 members required compensation for those years of duty. The government appealed the case to the Supreme Court , which nullified the award. Despite this, President Museveni declared that his government would reimburse the veterans alongside other former members of Ugandan armies to signify his government's appreciation for their national service. Over the subsequent years the government began making payouts at a gradual pace. The Uganda Army was Idi Amin's primary base of power. He consequently granted the soldiers rewards to keep them loyal and developed an "advanced clientage and patronage system". As part of this system, the Uganda Army was both the main channel in Uganda through which rewards were distributed, as well as the primary recipient. In general, soldiers were granted great leeway in their relations with civilians, and allowed to demand service from many businesses without payment. This was not unprecedented, as the Ugandan troops had already been allowed to act in this way during the previous Obote administration. Nevertheless, the extent of the military's misbehavior greatly increased under Amin. The soldiers were also given access to luxury hotels, and provided with money, alcohol, cigars, petrol, and cars. In this regard, the so-called "whisky run", "Whisky-Airline", or "Ugandan Connection" was of great importance. This was an almost nightly air transport service by cargo planes that traveled from Entebbe Airport to London Stansted Airport and back. Guarded by State Research Bureau agents, the planes brought coffee for sale to England, and returned to Uganda with alcohol, cigars, cars, various luxury items, and supplies for the military and police. Other goods included linen and electronics, which were stored in the State House in Entebbe for safekeeping. Soldiers would either buy these goods for their own use or sell them on the black market for a profit. Along with similar air services to the United States, the "whisky run" acted as "Amin's lifeline" and won him a "shaky loyalty" among the military, and especially among the officers who received most of the rewards. The expulsion of Asians was also motivated by Amin's desire to redistribute their wealth and thereby ensure the Uganda Army's support. Soldiers were given the majority of the property expropriated from the expelled Asian community. During Amin's time here was nothing. Because when he came here, what he did based here was recuit all the youth [...]. OK, from the army they got ranks and so on. That is what they benefited from. But there was no tangible development here, not here, but people were enjoying themselves all over, all over the big shops in the city, everywhere and so on. —An unnamed elder from the West Nile region Loyal soldiers were also promoted in such great numbers that it created chaos in the chain of command. As result of the great power wielded by soldiers, businesses were forced into clientage relationships with officers to avoid being constantly harassed or stolen from. Taken together with the President's own system of favors, the military developed a patronage system in which high-ranking military men combined "military, political, administrative, commercial, and agricultural operations into composite fiefs", becoming autonomous warlords. To keep these officers from becoming too powerful, Amin allowed and even encouraged lower-ranks to ignore their commanders' orders and take orders directly from himself. Troops were also allowed to bend rules and disregard many laws. As result, many soldiers also acted as bandits, were willing to loan or sell their weapons to civilians, and operated as guns for hire. Soldiers also frequently engaged in poaching in national parks and game reserves, dramatically decreasing wildlife populations in the country. As they were generally more wealthy and had better access to various goods, clinics, and schools, soldiers were among the most eligible men in the country for marriage. Many Uganda Army troops used their weapons and status to rape women without suffering consequences. In general, service in the Uganda Army provided great economic and social incentives, providing military men with wealth and power in an increasingly dysfunctional country. Military service was especially attractive to West Nile people due to their home area's poverty. Amin did little to actually help West Nile's development during his rule, and the Uganda Army remained one of the few actual employment opportunities for locals. Researcher Mark Leopold consequently described the West Nile soldiers during Amin's rule as " lumpen militariat ", a term originally developed by Ali Mazrui based on the Marxist concept of Lumpenproletariat . In addition, the Ugandan urban poor and people from rural low-income families in Zaire as well as Sudan were targeted by recruiters with promises of patronage, power, and adventure. By 1977, the higher-ranking officers were effectively the country's economic elite, possessing cars, villas, clubs, and their own duty-free shop in Kampala, while the country's economy had fallen into chaos. Even though this patronage system succeeded to keep much of the military somewhat loyal, it negatively affected the Uganda Army's ability to function. Corruption and indiscipline were widespread, and the soldiers were often unpredictable, especially when they were drunk. In addition, the morale of the troops was bound to Amin's ability to keep their needs satisfied. This was especially the case for the military's foreign troops who were operating as mercenaries and thus only loyal as long as they received their remuneration on time. Idi Amin's rule thus remained precarious and he faced repeated coup attempts by dissatisfied elements in the Uganda Army. With the Ugandan economy shrinking, Amin was also unable to provide all troops with ample rewards. He responded by reducing his following, promoting factionalism in the military and repeatedly purging senior ranks, thereby making concentrated actions against his regime unlikely. The factionalism in the military further reduced the Uganda Army's cohesion, and caused violent infighting. By 1978, many troops were discontent due to the lack of proper uniforms and delays in pay which resulted in soldiers regularly robbing shopkeepers during "foraging expeditions". When the Uganda–Tanzania War erupted the British authorities also stopped the "whisky run". According to German news magazine Der Spiegel , this demoralised the cut-off Ugandan troops and negatively affected their willingness to keep fighting. Had ours been a civilized army, [the brigadier] would have simply ordered the colonel to drop the idea and that would have been that. However, ours was a different army. A brigadier was too powerless to check a colonel's powers. —Ugandan soldier Bernard Rwehururu on the haphazard command structure of the army The Uganda Army suffered from organizational chaos during Idi Amin's rule. Many soldiers did not stay at their respective unit's barracks, and senior officers were regularly moved from one position to another to prevent them from gaining firm influence over the troops. In addition, the military was affected by factional infighting and regular purges, and many officers whom Amin promoted were completely unqualified and corrupt. Their rise in the ranks was attributed to their loyalty to the President and their ethnicity. Amin initially had the support of a handful of educated, high-ranking officers in the army, while several more did not oppose him and were accepting of him as President. Over time this group came into repeated conflict with the group of less-educated soldiers whom Amin promoted. The formal chain of command ceased to function and the ranks of officers gradually became meaningless. People wielded influence in accordance to their connection to Amin, and a junior officer who was liked by the President could easily circumvent or even command a senior officer who was less well connected. The power of individuals was also tied to the ability to provide economic resources to supporters. In order to keep the officers in line, Amin would often call high-ranking commanders in the middle of the night and accuse them of treason "just to shake them up a bit". The army's headquarters was located in Republic House in Kampala. The military was factually controlled by the Defence Council which mostly consisted of Amin's inner circle. As the President was illiterate, he issued orders to officers personally or via telephone. The Uganda Army was highly factionalised under Idi Amin's rule, with different groups and people rising and then falling from power. In general, tribal identities were of great importance to determine a soldier's standing, though this was a complex issue. Amin's regime actually wanted to reduce the ethnic and religious lines of division in the country which would have helped to keep its rule stable. The President himself was known for his repeated criticism of tribalism, and pledged to combat it. A few of his appointments of officers did reflect this intention to defuse ethnic tensions. At the same time, Amin's government mostly "acted within ethnic categories" and ultimately fueled ethnic favoritism. Indian diplomat Madanjeet Singh wrote that Amin "had a cunning grasp of the tribal mentality, and shrewdly played upon intertribal and interreligious rivalries, quarrels and envy to control the army". This paradox resulted from the regime's most important concern, namely to ensure its survival. Certain ethnic groups were judged to be simply more loyal than others due to familial and economic circumstances. As result, they were empowered, but this increased factionalism and in turn led to more strife, necessitating even more reliance on trusted elements. Amin's government was never able to solve this problem, and many of its initiatives were driven by the anxiety of losing control. In addition, ethnic affiliation and tribalism were problematic issues in Uganda. This was due to Ugandan "tribes" being often ill-defined and changeable, as no firm tribal structures existed among many West Nile peoples, while intermarriage also occurred. Amin himself was of mixed ethnic origin. [lower-alpha 4] In fact, the much-favored Nubians were "an extremely fluid category" and Amin himself stated that members of different tribes could become Nubians. [lower-alpha 5] According to Henry Kyemba , the Sudanese Anyanya fighters who joined Amin's forces preferred to identify themselves as Nubians. The monetary and status enhancement accompanying military service was especially attractive to Ugandan Nubians as they mostly belonged to poor urban families and were traditionally subjected to discrimination by other Ugandans. Tribalism is the biggest enemy in Africa today. Many people confuse the word tribalism with tribe. When we say we do not want tribalism, we do not mean there should be no tribe. Tribes are here to stay. —President Idi Amin Besides ethnicity and security concerns, favoritism in the military was also determined by the political relations of the Ugandan government. When Amin began to forge strong links with various Muslim Arab powers, religion grew in importance and Muslims became more favored in the Uganda Army. As result, members of traditionally favored tribes who identified as Christians became marginalized, resulting in strife. In the end, Amin could not even rely on members of his own tribe, the Kakwa, to always stay loyal. Most prominently, Charles Arube was a Kakwa yet attempted a coup when he was marginalized by another officer, Hussein Malera. Overall, ethnicity was less important than personal connections in Amin's military. For example, one of the President's most important security agencies was led by a Lango by 1976. Several high-ranking officers who were Christian or did not belong to the favored tribes also remained in the Uganda Army up until Amin's regime collapsed, with Ali Fadhul and Isaac Maliyamungu being notable examples. Overall, the military remained a diverse force whose troops had a wide variety of backgrounds and accordingly different views on the character of their service. A large number continued to regard themselves as "career military professionals". As result of all these factors, the factions in the military and its ethnic makeup changed significantly in course of Amin's presidency. According to researcher Andrew Rice, there were "cliques upon cliques" in the military which Amin empowered or disempowered as he saw fit. After the 1971 coup, Amin initially preferred to recruit and promote Kakwa, Nubians, Madi, Lugbara, and Alur, while members of other ethnic groups were gradually removed from the Uganda Army, as they were suspected of being disloyal. By 1973, about 35–50% of the military was made up of West Nile tribesmen; almost half of these were Lugbara. As result of repeated coup attempts and other factors, the Lugbara, Madi, and Alur also came under suspicion and were partially purged by 1973, leaving just the Kakwa and Nubians as core faction of the Uganda Army. At the same time, the growing number of Nubian soldiers also resulted from the blurring lines of tribal identities in the West Nile. Muslim and Kakwa troops were increasingly regarded as Nubians regardless of ethnic origin. By 1973, the Nubians constituted about 25–30% of the army. Despite the repeated purges, however, many Madi, Lugbara, and Alur soldiers remained in the army, though their influence was greatly reduced. Even the Nubians and Kakwa remained a potential threat, so that Amin increasingly opted to rely on foreigners to keep the military loyal to his regime. The Uganda Army's foreign members were recruited from various neighboring countries, most importantly Sudan and Zaire. They were "lifted above both the ethnic pattern and religious affiliation". These troops were often ex-members of rebel groups with whom Amin had forged good relations such as the Anyanya from southern Sudan. They acted as de facto mercenaries. According to researcher Holger Bernt Hansen, the mercenary role of the Sudanese recruits was especially evident as the Anyanya rebels had fought against Islamization in their home areas, yet supported Amin's regime that favored Muslims. Amin believed the foreigners to be more dependent and therefore more loyal than most native Ugandans. By 1973, about 20–25% of the Uganda Army were foreigners, most being ex-Anyanya. Researchers Paul Nugent and Samuel Decalo estimated that as much as three-quarters of the military eventually consisted of foreigners. A anonymous UA major concurred, estimating that half of the military were Sudanese and Nubians, a quarter of Zairean origin, and another quarter of Ugandan natives by the 1978–79 war. Even though the foreigners often claimed membership in the same tribes to which the native Ugandan troops belonged, the latter saw them as outsiders and often held them in low regard. For example, Ugandan Nubians in Bombo , Kitgum , and Gulu resented the foreign Nubians as ruthless mercenaries. Accordingly, the foreigners were "seen as an instrument to neutralize the predominance of the ethnic factor" by Amin, though ultimately they did not ease ethnic tensions. Instead, rivalries developed between the foreign and native troops of the Uganda Army. A system of courts and military justice was established by the Armed Forces Act of 1964. Further broad guarantees of the right to a fair trial were assured by Uganda's succession of constitutions in the 1960s. Military tribunals convened by Amin during his rule frequently ignored constitutional and legal prescriptions. Most men called to serve on the panels were selected on the basis of their loyalty to the President and their willingness to convict political opponents of the regime; many were illiterate and had no understanding of Ugandan law. Defendants were often presumed to be guilty at the start of proceedings and were usually denied legal counsel. Most persons found guilty of an offence by a military tribunal were executed via firing squad. Many cases were prosecuted in secret and in some instances without the knowledge of the accused party. Though upon taking power Amin declared that he would subject soldiers accused of offences to tribunals, in practice many were killed without any legal process. In 1973 Amin issued a decree expanding the reach of military tribunals to include the trial of civilians accused of committing capital offences. He also empowered himself to convene such tribunals for civilians believed to have been acting in a fashion to bring the government or army into disrepute. The President further expanded their jurisdiction into non-military matters with another decree in 1975. The strength of the Uganda Army is not known for certain during the 1971–1979 period. As result of massive recruitment drives, coupled with regular purges, the number of military personnel fluctuated greatly. Accordingly, there exist estimates ranging from about 10,000 to more than 40,000 troops. The Associated Press stated in 1974 that the army was around 15,000 strong. According to Cooper and Fontanellaz, the Uganda Army was at least nominally 19,000 soldiers strong by January 1976, of whom 658 were officers, while the German newspaper Der Spiegel put its strength at 21,000 in 1977. A Ugandan major captured by the TPDF stated that the Uganda Army numbered 25,000 by 1978/79. One Ugandan officer claimed that the TPDF outnumbered the Uganda Army "by 3-1 ratio" during the conflict. It is often estimated that about 20,000 troops served in the Uganda Army on average during Amin's rule. It was one of the largest militaries in Africa at the time. The Uganda Army consisted of its ground forces and the Uganda Army Air Force. It had no official navy. President Amin created a "small lake patrol" in 1977, though it was still in development at the time of his overthrow. Uganda had already acquired patrol boats and amphibious vehicles which marines operated on Lake Victoria by this time. UAAF Ugandan Air ForceHad ours been a civilized army, [the brigadier] would have simply ordered the colonel to drop the idea and that would have been that. However, ours was a different army. A brigadier was too powerless to check a colonel's powers. —Ugandan soldier Bernard Rwehururu on the haphazard command structure of the army The Uganda Army suffered from organizational chaos during Idi Amin's rule. Many soldiers did not stay at their respective unit's barracks, and senior officers were regularly moved from one position to another to prevent them from gaining firm influence over the troops. In addition, the military was affected by factional infighting and regular purges, and many officers whom Amin promoted were completely unqualified and corrupt. Their rise in the ranks was attributed to their loyalty to the President and their ethnicity. Amin initially had the support of a handful of educated, high-ranking officers in the army, while several more did not oppose him and were accepting of him as President. Over time this group came into repeated conflict with the group of less-educated soldiers whom Amin promoted. The formal chain of command ceased to function and the ranks of officers gradually became meaningless. People wielded influence in accordance to their connection to Amin, and a junior officer who was liked by the President could easily circumvent or even command a senior officer who was less well connected. The power of individuals was also tied to the ability to provide economic resources to supporters. In order to keep the officers in line, Amin would often call high-ranking commanders in the middle of the night and accuse them of treason "just to shake them up a bit". The army's headquarters was located in Republic House in Kampala. The military was factually controlled by the Defence Council which mostly consisted of Amin's inner circle. As the President was illiterate, he issued orders to officers personally or via telephone. The Uganda Army was highly factionalised under Idi Amin's rule, with different groups and people rising and then falling from power. In general, tribal identities were of great importance to determine a soldier's standing, though this was a complex issue. Amin's regime actually wanted to reduce the ethnic and religious lines of division in the country which would have helped to keep its rule stable. The President himself was known for his repeated criticism of tribalism, and pledged to combat it. A few of his appointments of officers did reflect this intention to defuse ethnic tensions. At the same time, Amin's government mostly "acted within ethnic categories" and ultimately fueled ethnic favoritism. Indian diplomat Madanjeet Singh wrote that Amin "had a cunning grasp of the tribal mentality, and shrewdly played upon intertribal and interreligious rivalries, quarrels and envy to control the army". This paradox resulted from the regime's most important concern, namely to ensure its survival. Certain ethnic groups were judged to be simply more loyal than others due to familial and economic circumstances. As result, they were empowered, but this increased factionalism and in turn led to more strife, necessitating even more reliance on trusted elements. Amin's government was never able to solve this problem, and many of its initiatives were driven by the anxiety of losing control. In addition, ethnic affiliation and tribalism were problematic issues in Uganda. This was due to Ugandan "tribes" being often ill-defined and changeable, as no firm tribal structures existed among many West Nile peoples, while intermarriage also occurred. Amin himself was of mixed ethnic origin. [lower-alpha 4] In fact, the much-favored Nubians were "an extremely fluid category" and Amin himself stated that members of different tribes could become Nubians. [lower-alpha 5] According to Henry Kyemba , the Sudanese Anyanya fighters who joined Amin's forces preferred to identify themselves as Nubians. The monetary and status enhancement accompanying military service was especially attractive to Ugandan Nubians as they mostly belonged to poor urban families and were traditionally subjected to discrimination by other Ugandans. Tribalism is the biggest enemy in Africa today. Many people confuse the word tribalism with tribe. When we say we do not want tribalism, we do not mean there should be no tribe. Tribes are here to stay. —President Idi Amin Besides ethnicity and security concerns, favoritism in the military was also determined by the political relations of the Ugandan government. When Amin began to forge strong links with various Muslim Arab powers, religion grew in importance and Muslims became more favored in the Uganda Army. As result, members of traditionally favored tribes who identified as Christians became marginalized, resulting in strife. In the end, Amin could not even rely on members of his own tribe, the Kakwa, to always stay loyal. Most prominently, Charles Arube was a Kakwa yet attempted a coup when he was marginalized by another officer, Hussein Malera. Overall, ethnicity was less important than personal connections in Amin's military. For example, one of the President's most important security agencies was led by a Lango by 1976. Several high-ranking officers who were Christian or did not belong to the favored tribes also remained in the Uganda Army up until Amin's regime collapsed, with Ali Fadhul and Isaac Maliyamungu being notable examples. Overall, the military remained a diverse force whose troops had a wide variety of backgrounds and accordingly different views on the character of their service. A large number continued to regard themselves as "career military professionals". As result of all these factors, the factions in the military and its ethnic makeup changed significantly in course of Amin's presidency. According to researcher Andrew Rice, there were "cliques upon cliques" in the military which Amin empowered or disempowered as he saw fit. After the 1971 coup, Amin initially preferred to recruit and promote Kakwa, Nubians, Madi, Lugbara, and Alur, while members of other ethnic groups were gradually removed from the Uganda Army, as they were suspected of being disloyal. By 1973, about 35–50% of the military was made up of West Nile tribesmen; almost half of these were Lugbara. As result of repeated coup attempts and other factors, the Lugbara, Madi, and Alur also came under suspicion and were partially purged by 1973, leaving just the Kakwa and Nubians as core faction of the Uganda Army. At the same time, the growing number of Nubian soldiers also resulted from the blurring lines of tribal identities in the West Nile. Muslim and Kakwa troops were increasingly regarded as Nubians regardless of ethnic origin. By 1973, the Nubians constituted about 25–30% of the army. Despite the repeated purges, however, many Madi, Lugbara, and Alur soldiers remained in the army, though their influence was greatly reduced. Even the Nubians and Kakwa remained a potential threat, so that Amin increasingly opted to rely on foreigners to keep the military loyal to his regime. The Uganda Army's foreign members were recruited from various neighboring countries, most importantly Sudan and Zaire. They were "lifted above both the ethnic pattern and religious affiliation". These troops were often ex-members of rebel groups with whom Amin had forged good relations such as the Anyanya from southern Sudan. They acted as de facto mercenaries. According to researcher Holger Bernt Hansen, the mercenary role of the Sudanese recruits was especially evident as the Anyanya rebels had fought against Islamization in their home areas, yet supported Amin's regime that favored Muslims. Amin believed the foreigners to be more dependent and therefore more loyal than most native Ugandans. By 1973, about 20–25% of the Uganda Army were foreigners, most being ex-Anyanya. Researchers Paul Nugent and Samuel Decalo estimated that as much as three-quarters of the military eventually consisted of foreigners. A anonymous UA major concurred, estimating that half of the military were Sudanese and Nubians, a quarter of Zairean origin, and another quarter of Ugandan natives by the 1978–79 war. Even though the foreigners often claimed membership in the same tribes to which the native Ugandan troops belonged, the latter saw them as outsiders and often held them in low regard. For example, Ugandan Nubians in Bombo , Kitgum , and Gulu resented the foreign Nubians as ruthless mercenaries. Accordingly, the foreigners were "seen as an instrument to neutralize the predominance of the ethnic factor" by Amin, though ultimately they did not ease ethnic tensions. Instead, rivalries developed between the foreign and native troops of the Uganda Army. A system of courts and military justice was established by the Armed Forces Act of 1964. Further broad guarantees of the right to a fair trial were assured by Uganda's succession of constitutions in the 1960s. Military tribunals convened by Amin during his rule frequently ignored constitutional and legal prescriptions. Most men called to serve on the panels were selected on the basis of their loyalty to the President and their willingness to convict political opponents of the regime; many were illiterate and had no understanding of Ugandan law. Defendants were often presumed to be guilty at the start of proceedings and were usually denied legal counsel. Most persons found guilty of an offence by a military tribunal were executed via firing squad. Many cases were prosecuted in secret and in some instances without the knowledge of the accused party. Though upon taking power Amin declared that he would subject soldiers accused of offences to tribunals, in practice many were killed without any legal process. In 1973 Amin issued a decree expanding the reach of military tribunals to include the trial of civilians accused of committing capital offences. He also empowered himself to convene such tribunals for civilians believed to have been acting in a fashion to bring the government or army into disrepute. The President further expanded their jurisdiction into non-military matters with another decree in 1975. The strength of the Uganda Army is not known for certain during the 1971–1979 period. As result of massive recruitment drives, coupled with regular purges, the number of military personnel fluctuated greatly. Accordingly, there exist estimates ranging from about 10,000 to more than 40,000 troops. The Associated Press stated in 1974 that the army was around 15,000 strong. According to Cooper and Fontanellaz, the Uganda Army was at least nominally 19,000 soldiers strong by January 1976, of whom 658 were officers, while the German newspaper Der Spiegel put its strength at 21,000 in 1977. A Ugandan major captured by the TPDF stated that the Uganda Army numbered 25,000 by 1978/79. One Ugandan officer claimed that the TPDF outnumbered the Uganda Army "by 3-1 ratio" during the conflict. It is often estimated that about 20,000 troops served in the Uganda Army on average during Amin's rule. It was one of the largest militaries in Africa at the time. The Uganda Army consisted of its ground forces and the Uganda Army Air Force. It had no official navy. President Amin created a "small lake patrol" in 1977, though it was still in development at the time of his overthrow. Uganda had already acquired patrol boats and amphibious vehicles which marines operated on Lake Victoria by this time. UAAF Ugandan Air ForceUAAF Ugandan Air ForceThe Uganda Army was well-equipped with weaponry during the rule of Idi Amin. Beginning in 1973, he imported large quantities of arms from the Soviet Union and Libya, ranging from tanks to aircraft to missiles. Amin reportedly "loved military pageantry and weaponry", investing much energying in equipping the Uganda Army with military hardware. The standard infantry rifle was the Heckler & Koch G3 . The Uganda Army's armoured fighting vehicle force was regarded as one of the strongest of the region. The country had already possessed 12 M4A1(76) Sherman tanks , around 20 Ferret armoured cars , and 12 OT-64B armoured personnel carriers (APCs) before the 1971 coup. Amin consequently imported large quantities of armoured fighting vehicles from the Soviet Union and Libya. Uganda received 16 T-55A tanks and 62 APCS from the Soviets, as well as 16 Alvis Saracen armoured cars from Libya in 1973 and 1974. In 1975, the Soviet Union provided Uganda with military suppiles worth $48 million, compared with just $12 million in economic aid. From this time onward, however, relations with the Soviet Union worsened, resulting in the reduction of military aid and supplies. Libya also gifted Uganda ten T-34/85 tanks in 1976. From 1977 onward the army made fewer foreign acquisitions. By 1978, the Uganda Army's ground forces possessed 10 T-34, 15 T-54/T-55 , and 10 M-4 tanks, 250 Alvis Saracen armoured cars, and an unspecified number of BRDM amphibious vehicles, OT-64 APCs, as well as Ferret, BTR-40 , and BTR-152 armoured cars. At the time of the outbreak of the war with Tanzania, the Uganda Army was one of the most mechanised forces in Africa. The Uganda Army's artillery included 76 mm and 122 mm cannons, 82 mm and 120 mmm mortars, Sagger anti-tank missiles , and fifty 40 mm anti-aircraft guns by 1978. The Uganda Army Air Force (UAAF) was also expanded during Amin's presidency. Before Operation Entebbe, about 65 aircraft and helicopters were in use. In 1976 a helicopter and some small transport aircraft were purchased from the United States. By 1979, the UAAF still had access to several dozen fighter and trainer aircraft, though the exact number remains unclear. It possessed MiG-21MFs , MiG-21UMs , MiG-17s , MiG-15UTIs , and L-29s . Furthermore, several transport aircraft were in service, including a Lockheed C-130 Hercules cargo transport. Under Idi Amin's rule, several foreign countries supported the Uganda Army by sending advisers. The first military mission from the Soviet Union was sent to Uganda in 1973. By Amin's late reign, the Soviet experts were headed by Colonel Datsenko until January 1979 when he was replaced by Colonel Protassenia. In addition, Ugandan soldiers were trained and aided by Palestine Liberation Organisation militants, Pakistani experts, and Iraqi advisors. Military attachés were also attached to several embassies in Kampala and occasionally called on for help by Ugandan authorities. Thousands of Ugandan troops were sent for training into the Soviet Union, Second Czechoslovak Republic , Libya, and North Korea .

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Ruffed grouse

Tetrao umbellus Linnaeus, 1766 The ruffed grouse ( Bonasa umbellus ) is a medium-sized grouse occurring in forests from the Appalachian Mountains across Canada to Alaska . It is the most widely distributed game bird in North America. It is non-migratory . It is the only species in the genus Bonasa . The ruffed grouse is sometimes incorrectly referred to as a " partridge ", an unrelated phasianid , and occasionally confused with the grey partridge , a bird of open areas rather than woodlands. The ruffed grouse is the state game bird of Pennsylvania , United States. Bonasa umbellus was first described by Carl Linnaeus in his 1766 12th edition of Systema Naturae . He classified it as Tetrao umbellus , placing it in a subfamily with Eurasian grouse. The genus Bonasa was applied by British naturalist John Francis Stephens in 1819. Ruffed grouse is the preferred common name because it applies only to this species. Misleading vernacular names abound, however, and it is often called partridge (sometimes rendered pa'tridge, or shortened to pat), pheasant, or prairie chicken, all of which are properly applied to other birds. Other nicknames for ruffed grouse include drummer or thunder-chicken. The ruffed grouse has 13 recognized subspecies: Ruffed grouse are chunky, medium-sized birds that weigh from 450–750 g (0.99–1.65 lb) , measure from 40 to 50 cm (16 to 20 in) in length and span 50–64 cm (20–25 in) across their short, strong wings. They have two distinct morphs : grey and brown. In the grey morph, the head, neck, and back are grey-brown; the breast is light with barring. There is much white on the underside and flanks. Overall, the birds have a variegated appearance; the throat is often distinctly lighter. The tail is essentially the same brownish grey, with regular barring and a broad black band near the end ("subterminal"). Brown-morph birds have tails of the same color and pattern. However, the rest of the plumage is much more brown, giving the appearance of a more uniform bird with less light plumage below and a conspicuously grey tail. There are all sorts of intergrades between the most typical morphs; warmer and more humid conditions favor browner birds in general. [ citation needed ] The ruffs are on the sides of the neck in both sexes. They also have a crest on top of their head, which sometimes lies flat. Both sexes are similarly marked and sized, making them difficult to tell apart, even in hand. The female often has a broken subterminal tail band. At the same time, males tend to have unbroken tail bands, though the opposite of either can occur. Females may also do a display similar to the male. Another fairly accurate sign is that rump feathers with a single white dot indicate a female; rump feathers with more than one white dot indicate a male. [ citation needed ] The average life span of a ruffed grouse is one year, although some birds are thought to live for as long as eleven years. Ruffed grouse are polygynous , and males may mate with several females during the breeding season. [ citation needed ]Like most grouse, they spend most of their time on the ground; mixed woodland rich in aspen seems to be particularly well-liked. These birds forage on the ground or in trees. They are omnivores , eating buds, leaves, berries , seeds , and insects. According to nature writer Don L. Johnson : More than any other characteristic, it is the ruffed grouse's ability to thrive on a wide range of foods that has allowed it to adapt to such a wide and varied range of habitat on this continent. A complete menu of grouse fare might itself fill a book. One grouse crop yielded a live salamander in a salad of watercress . Another contained a small snake. Hunting of the ruffed grouse is common in the northern and far western United States as well as Canada, often with shotguns. Dogs may also be used. Hunting of the ruffed grouse can be challenging. This is because the grouse spends most of its time in thick brush, aspen stands, and second growth pines. It is also very hard to detect a foraging grouse bobbing about in the thicket due to their camouflage. With adequate snow cover, they will burrow under the snow. The ruffed grouse will maintain trails through the underbrush and pines like other forest creatures. These can often be found by looking for the bird's feathers on the ground and twigs at the edges of its trail. Hunting of the ruffed grouse requires a good ear and lots of stamina as one will be constantly walking and listening for them in the leaves. Ruffed grouse frequently seek gravel and clover along road beds during early morning and late afternoon. These are good areas to walk during this time to flush birds. Also, grouse use sandy roadbeds to dust their feathers to rid themselves of skin pests. Dusting sites are visible as areas of disturbed soils with some signs of feathers. Birds will return to these spots during the late afternoon to bathe in dust and socialize and mate. [ citation needed ]The ruffed grouse differs from other grouse species in its courtship display . The ruffed grouse relies entirely on a non-vocal acoustic display, known as drumming, unlike other grouse species. The drumming itself is a rapid, wing-beating display that creates a low-frequency sound, starting slow and speeding up (thump ... thump ... thump..thump-thump-thump-thump). Even in thick woods, this can be heard for .25 miles (0.40 km) or more. The ruffed grouse spends most of its time quietly on the ground, and when surprised, may explode into flight, beating its wings very loudly. They will burrow into the snow for warmth in the winter and may suddenly burst out of the snow when approached too closely. The male grouse proclaims his property by engaging in a "drumming" display. This sound is made by beating his wings against the air to create a vacuum. It usually stands on a log, stone or mound of dirt when drumming. It does not strike the log to make the noise, it only uses the "drumming log" as a sort of stage. The ruffed grouse population has a cycle, and follows the cycle no matter how much or how little hunting there is. The cycle has puzzled scientists for years, and is simply referred to as the "grouse cycle". In spite of this historical cycle, populations have been declining in Pennsylvania and management plans adopted. Habitat loss has been a concern for the species, but the introduction of the West Nile virus has been seen to be further increasing mortality.

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Nile Ranger

Nile Ranger (born 11 April 1991) is an English professional footballer who plays as a striker . He is currently a free agent . Previously with Crystal Palace and Southampton , Ranger finished his youth career at Newcastle United , where he made his professional debut and was part of their team which won the Football League Championship in 2009–10 . Later on in his spell at St James's Park , he was loaned to Barnsley and Sheffield Wednesday . He played international football for England U19 . After leaving Newcastle by mutual consent in 2013, he went on to play for Swindon Town , Blackpool and Southend United in the English Football League , with his spells at all three clubs being hindered by disciplinary issues including multiple absences from training. Ranger, who was incarcerated for involvement in armed robbery as a teenager, served a prison sentence for fraud in 2017. Born in Wood Green in North London, Ranger attended Alexandra Park School . He began his football career at Crystal Palace Football Academy and was at their development centre from a young age. He was with the Protec Football Development School for a few weeks before being scouted by Southampton . His career was almost over before it began, as whilst playing for the club he was sentenced to 11 weeks in a Young Offender's Institute for his part in an armed street robbery in Muswell Hill committed before signing for the club. He returned to Southampton after completing his sentence, but was eventually released as a player with a bad reputation. He was offered terms by Swindon Town after a successful trial before Newcastle signed him. [ citation needed ]In July 2008, director of football at Newcastle, Dennis Wise , brought Ranger to Newcastle United. Ranger made his academy debut against Leicester City on 23 August 2008 and made his debut for the reserve team against Sunderland at St James' Park on 1 September 2008. He impressed hugely in these levels, finishing with 15 goals for the Under-18s and seven for the reserves in his first season on Tyneside. That resulted in his winning the "Wor Jackie Milburn Trophy" in 2009. He was subsequently rewarded by then-manager Alan Shearer with a new and improved three-and-a-half-year contract. Ranger's Newcastle debut came as an added-time substitute for Shola Ameobi against West Bromwich Albion in the Championship on 8 August 2009. He made his first senior start against Leicester City on 31 August, where he won the man of the match award; he played just over 84 minutes before being substituted and received a standing ovation from fans. He scored his first senior goal for the club in a 2–0 win over Coventry City on 9 December, after coming on as a substitute for Peter Løvenkrands . Ranger scored the second of his two league goals that season in a 2–0 home win against Crystal Palace on 27 January 2010, as Newcastle ended the season as champions and were promoted to the Premier League . After appearing as an unused substitute in the first two Premier League games for Newcastle, he started in the Football League Cup wins over Accrington Stanley and Chelsea . He scored the first equalising goal in the game at Stamford Bridge on 22 September 2010, appearing in a right-wing berth, as Newcastle went on to triumph 4–3. He made his Premier League debut on 16 October, coming off the bench in the 89th minute in a 2–2 draw against Wigan Athletic . He made a host of substitute appearances for Newcastle after that, notably in the 1–0 away win to Arsenal , when he turned past Arsenal defender Laurent Koscielny and was through on goal before the latter tugged him down and received a red card. Ranger signed a new 5 + 1 ⁄ 2 -year contract on 3 December 2010, keeping him at the club until 2016. He also started several games after, for a while, being the club's only fit striker after the sale of Andy Carroll to Liverpool and injuries to Shola Ameobi and Leon Best . On 21 November 2011, having failed to appear for Newcastle in the season up to that date, Ranger signed on loan for Championship club Barnsley until 14 January 2012. In his fifth game for Barnsley, a 1–0 away defeat to West Ham United on 17 December 2011, Ranger injured his foot. His loan was cut short and he returned to Newcastle. [ citation needed ] On 22 March 2012, he joined Sheffield Wednesday in League One on loan until the end of the 2011–12 season. On 19 January 2013, Ranger criticised the Newcastle fans on Twitter for booing the team off after a 2–1 home loss to fellow strugglers Reading . He left Newcastle by mutual consent on 1 March 2013. Ranger joined Swindon Town of League One on a one-year deal, with the option of a second, on 16 August 2013. He was signed despite his ongoing rape case. Ranger scored his first goal for Swindon on 27 August against Queens Park Rangers in the League Cup and his first league goal in the following game four days later, a 5–0 home win against Crewe Alexandra . He was a regular in the side until early November, scoring four more goals. On 14 November he failed to report to the club for training after being given a period of leave. He played one more game before again failing to turn up at the club. Manager Mark Cooper decided Ranger would not appear until he showed "respect for the team". In December Cooper said he would offload Ranger if he failed to train and because of his disciplinary record. On 3 January 2014, Swindon Town chairman Lee Power confirmed in a press conference that the club would be meeting with Ranger and his management in the following days to confirm his sacking due to his disrespect shown towards the club through constant absence during training. Power said "I'm the chairman of the club and I've got to do what's best for the club. Unfortunately, what's best for the club is having to sit down with Nile and talk about parting ways. While this is ongoing Nile is not training with the squad." He was soon recalled to the squad, scoring in a 2–1 win against Peterborough United on 11 January. He continued to play throughout January and early February, scoring three more goals. On 14 February he suffered a hamstring tear in a game against Colchester United , his last game for Swindon. He had played 28 games in all competitions, scoring ten goals. His time with the club had been beset with disciplinary problems and issues with his private life and on 2 May 2014, Ranger and Swindon Town mutually agreed to terminate his contract with immediate effect. On 16 August 2014 Ranger signed for Blackpool of the Championship on a one-year deal. He scored against Millwall on 30 August and against Leeds United on 8 November, both in defeats. After two more league appearances, he went AWOL after being left out of the squad to face Birmingham City in early December. He claimed he had to return to London for "family issues". In late January 2015, Blackpool began to fine the striker for each day he was absent. In May 2015 Blackpool released 17 players following their relegation. They took up an option to extend Ranger's contract for another year. Despite saying he would return to the club for pre-season training in preparation for the 2015–16 season, he failed to do so until 28 July, by which point Blackpool had played four friendlies. I have seen two of my good friends pass away. Whilst overcoming this it has made me realise life is really short and I have really been taking things for granted. I would like to use this opportunity to thank Southampton, Newcastle, Swindon and Blackpool for giving me the chance to experience the dream of being a professional footballer. To add to this I would like to apologise to everyone at these clubs including management, players, staff and fans. I should have given more and been a better role model. I would also like to add I am sorry to my current team-mates at Blackpool for being missing for a long period of time and not attending pre-season and putting in the hard work during this time. Truth be told I'm just a young boy who has been living the dream and playing a game which I do love and miss deeply, and hope that one day I will be able to get back on a pitch and play because life is really too short. On 2 February 2016, Blackpool announced that Ranger had left the club. On 3 August 2016, Southend United announced that they had signed Ranger on a one-year contract. He made his debut 13 days later in a 3–0 win at Sheffield United , his first professional match since November 2014, but was substituted with an injury halfway through the first half. On 12 November, Ranger scored his first goals for the Shrimpers, one in each half of a 4–1 win over Bury at Gigg Lane . On 1 December Ranger signed a new contract with Southend, committing him to the club until 2020. Ranger began the 2017–18 season having served time in prison for online banking fraud. On his release he was subject to a 7pm curfew meaning he could not play games with an evening kick-off. He was also electronically tagged . On 22 September the tag was removed and Ranger was included in the squad to play an away game at Fleetwood . He scored in a 4–2 win; his controversial goal celebration involving removing his boot and using it to mimic the action of someone using a machine gun . Ranger's contract with the club was terminated on 4 January 2018 because of "recurring disciplinary issues". On 29 October 2020, after a stint at Barnet Sunday League side AC United, Ranger signed for Northern Premier League Division One South East club Spalding United . Two days later, he made his debut against Belper Town , scoring one and assisting another in the process. In February 2021, Ranger returned to Southend United, signing on a month-by-month contract. His debut game on 27 February, during his second spell with Southend, lasted only 11 minutes. Coming on as a second-half substitute against Salford City , Ranger sustained a groin injury and was himself substituted off. His injury was so severe that he was reported as being unlikely to play for the remainder of the season. In May 2021, following Southend's relegation into the National League , manager Phil Brown revealed Southend had "severed all ties" with Ranger after the striker failed to attend physiotherapy sessions. Ranger himself claimed that Southend were not funding his travel to the sessions. In December 2021, Ranger signed for National League club Boreham Wood . His contract length was 'undisclosed'. He made his Boreham Wood debut on 6 December coming on as a late substitute in a 4–0 FA Cup second round win against St Albans City . In July 2008, director of football at Newcastle, Dennis Wise , brought Ranger to Newcastle United. Ranger made his academy debut against Leicester City on 23 August 2008 and made his debut for the reserve team against Sunderland at St James' Park on 1 September 2008. He impressed hugely in these levels, finishing with 15 goals for the Under-18s and seven for the reserves in his first season on Tyneside. That resulted in his winning the "Wor Jackie Milburn Trophy" in 2009. He was subsequently rewarded by then-manager Alan Shearer with a new and improved three-and-a-half-year contract. Ranger's Newcastle debut came as an added-time substitute for Shola Ameobi against West Bromwich Albion in the Championship on 8 August 2009. He made his first senior start against Leicester City on 31 August, where he won the man of the match award; he played just over 84 minutes before being substituted and received a standing ovation from fans. He scored his first senior goal for the club in a 2–0 win over Coventry City on 9 December, after coming on as a substitute for Peter Løvenkrands . Ranger scored the second of his two league goals that season in a 2–0 home win against Crystal Palace on 27 January 2010, as Newcastle ended the season as champions and were promoted to the Premier League . After appearing as an unused substitute in the first two Premier League games for Newcastle, he started in the Football League Cup wins over Accrington Stanley and Chelsea . He scored the first equalising goal in the game at Stamford Bridge on 22 September 2010, appearing in a right-wing berth, as Newcastle went on to triumph 4–3. He made his Premier League debut on 16 October, coming off the bench in the 89th minute in a 2–2 draw against Wigan Athletic . He made a host of substitute appearances for Newcastle after that, notably in the 1–0 away win to Arsenal , when he turned past Arsenal defender Laurent Koscielny and was through on goal before the latter tugged him down and received a red card. Ranger signed a new 5 + 1 ⁄ 2 -year contract on 3 December 2010, keeping him at the club until 2016. He also started several games after, for a while, being the club's only fit striker after the sale of Andy Carroll to Liverpool and injuries to Shola Ameobi and Leon Best . On 21 November 2011, having failed to appear for Newcastle in the season up to that date, Ranger signed on loan for Championship club Barnsley until 14 January 2012. In his fifth game for Barnsley, a 1–0 away defeat to West Ham United on 17 December 2011, Ranger injured his foot. His loan was cut short and he returned to Newcastle. [ citation needed ] On 22 March 2012, he joined Sheffield Wednesday in League One on loan until the end of the 2011–12 season. On 19 January 2013, Ranger criticised the Newcastle fans on Twitter for booing the team off after a 2–1 home loss to fellow strugglers Reading . He left Newcastle by mutual consent on 1 March 2013. Ranger joined Swindon Town of League One on a one-year deal, with the option of a second, on 16 August 2013. He was signed despite his ongoing rape case. Ranger scored his first goal for Swindon on 27 August against Queens Park Rangers in the League Cup and his first league goal in the following game four days later, a 5–0 home win against Crewe Alexandra . He was a regular in the side until early November, scoring four more goals. On 14 November he failed to report to the club for training after being given a period of leave. He played one more game before again failing to turn up at the club. Manager Mark Cooper decided Ranger would not appear until he showed "respect for the team". In December Cooper said he would offload Ranger if he failed to train and because of his disciplinary record. On 3 January 2014, Swindon Town chairman Lee Power confirmed in a press conference that the club would be meeting with Ranger and his management in the following days to confirm his sacking due to his disrespect shown towards the club through constant absence during training. Power said "I'm the chairman of the club and I've got to do what's best for the club. Unfortunately, what's best for the club is having to sit down with Nile and talk about parting ways. While this is ongoing Nile is not training with the squad." He was soon recalled to the squad, scoring in a 2–1 win against Peterborough United on 11 January. He continued to play throughout January and early February, scoring three more goals. On 14 February he suffered a hamstring tear in a game against Colchester United , his last game for Swindon. He had played 28 games in all competitions, scoring ten goals. His time with the club had been beset with disciplinary problems and issues with his private life and on 2 May 2014, Ranger and Swindon Town mutually agreed to terminate his contract with immediate effect. On 16 August 2014 Ranger signed for Blackpool of the Championship on a one-year deal. He scored against Millwall on 30 August and against Leeds United on 8 November, both in defeats. After two more league appearances, he went AWOL after being left out of the squad to face Birmingham City in early December. He claimed he had to return to London for "family issues". In late January 2015, Blackpool began to fine the striker for each day he was absent. In May 2015 Blackpool released 17 players following their relegation. They took up an option to extend Ranger's contract for another year. Despite saying he would return to the club for pre-season training in preparation for the 2015–16 season, he failed to do so until 28 July, by which point Blackpool had played four friendlies. I have seen two of my good friends pass away. Whilst overcoming this it has made me realise life is really short and I have really been taking things for granted. I would like to use this opportunity to thank Southampton, Newcastle, Swindon and Blackpool for giving me the chance to experience the dream of being a professional footballer. To add to this I would like to apologise to everyone at these clubs including management, players, staff and fans. I should have given more and been a better role model. I would also like to add I am sorry to my current team-mates at Blackpool for being missing for a long period of time and not attending pre-season and putting in the hard work during this time. Truth be told I'm just a young boy who has been living the dream and playing a game which I do love and miss deeply, and hope that one day I will be able to get back on a pitch and play because life is really too short. On 2 February 2016, Blackpool announced that Ranger had left the club. On 3 August 2016, Southend United announced that they had signed Ranger on a one-year contract. He made his debut 13 days later in a 3–0 win at Sheffield United , his first professional match since November 2014, but was substituted with an injury halfway through the first half. On 12 November, Ranger scored his first goals for the Shrimpers, one in each half of a 4–1 win over Bury at Gigg Lane . On 1 December Ranger signed a new contract with Southend, committing him to the club until 2020. Ranger began the 2017–18 season having served time in prison for online banking fraud. On his release he was subject to a 7pm curfew meaning he could not play games with an evening kick-off. He was also electronically tagged . On 22 September the tag was removed and Ranger was included in the squad to play an away game at Fleetwood . He scored in a 4–2 win; his controversial goal celebration involving removing his boot and using it to mimic the action of someone using a machine gun . Ranger's contract with the club was terminated on 4 January 2018 because of "recurring disciplinary issues". On 29 October 2020, after a stint at Barnet Sunday League side AC United, Ranger signed for Northern Premier League Division One South East club Spalding United . Two days later, he made his debut against Belper Town , scoring one and assisting another in the process. In February 2021, Ranger returned to Southend United, signing on a month-by-month contract. His debut game on 27 February, during his second spell with Southend, lasted only 11 minutes. Coming on as a second-half substitute against Salford City , Ranger sustained a groin injury and was himself substituted off. His injury was so severe that he was reported as being unlikely to play for the remainder of the season. In May 2021, following Southend's relegation into the National League , manager Phil Brown revealed Southend had "severed all ties" with Ranger after the striker failed to attend physiotherapy sessions. Ranger himself claimed that Southend were not funding his travel to the sessions. In December 2021, Ranger signed for National League club Boreham Wood . His contract length was 'undisclosed'. He made his Boreham Wood debut on 6 December coming on as a late substitute in a 4–0 FA Cup second round win against St Albans City . Ranger made his debut for the England U19 team on 25 March 2009 against the Czech Republic U19s. He got his first goal for the Under-19s in his second match, against Bosnia and Herzegovina , with a headed effort. He helped his team to the final of the UEFA U-19 Championship but his team eventually lost the final to host nation Ukraine 2–0 in Donetsk . In 2007, at the age of 15, Ranger was sentenced to 11 weeks in a Young Offenders Institute after being convicted of participating in street robbery in Muswell Hill , London. In May 2011 Ranger was questioned by Newcastle after posing with a replica gun in a photograph. On 27 August 2011, he was arrested on suspicion of assaulting a man in Newcastle city centre, leaving the victim unconscious in the street. Ranger was subsequently dropped to Newcastle United's reserve team. He was found not guilty of the charge in October 2012. In October 2011 he was charged with being drunk and disorderly in Newcastle's Cathedral Square. The charge came only days after Ranger had been reinstated to Newcastle United's first-team training after a three-month exile in the club's reserves. In March 2012, he was fined by The FA for making homophobic comments on social networking website Twitter . In the early hours of 23 September 2012, police were called to a house in Enfield, north London after reports of a disturbance. The front door of the property was badly damaged and Ranger was arrested at the scene and later charged with criminal damage . The charge against Ranger was dropped that November after the court accepted his explanation that he had damaged the door after fearing his girlfriend was being kidnapped. On 25 January 2013, Ranger was arrested on suspicion of rape in a Newcastle hotel room. In connection with the same alleged offence, Ranger was charged with rape on 8 July 2013. On 4 March 2014, he was cleared of the charge at Newcastle Crown Court . On 14 March 2013, Ranger was charged with common assault after an incident in Newcastle city centre. On 23 March 2014, Ranger was arrested on suspicion of causing criminal damage to a taxi in Liverpool. He later pleaded guilty to criminal damage and was fined £1,000 and was ordered to pay compensation to the taxi driver for breaking a window. Ranger said that he was enraged by being called a rapist by the driver. On 28 April 2014, Ranger was charged with criminal damage after an incident at a block of flats in Swindon on 13 April. He was later fined for damage to the door of his flat in relation to this incident which was captured on CCTV, in an incident where he additionally appeared to strike his female companion three times in the face. In May 2014, Ranger was found not guilty of being drunk in charge of his vehicle, after being found asleep in the driver's seat of his car on the M4 motorway . In December 2016, Ranger was charged with conspiracy to defraud and conspiracy to commit money laundering, in respect of offences alleged to have been committed in February 2015. In January 2017, he pleaded guilty to conspiracy to defraud at Wood Green Crown Court . On 23 May 2017, he was sentenced to eight months in prison. On 11 August 2017, he was released after 10 weeks of his sentence due to "his consistently excellent custodial behaviour", remaining under curfew for the next five weeks. Newcastle United England U19

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West Nile

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Disease

A disease is a particular abnormal condition that adversely affects the structure or function of all or part of an organism and is not immediately due to any external injury . Diseases are often known to be medical conditions that are associated with specific signs and symptoms . A disease may be caused by external factors such as pathogens or by internal dysfunctions. For example, internal dysfunctions of the immune system can produce a variety of different diseases, including various forms of immunodeficiency , hypersensitivity , allergies , and autoimmune disorders . In humans, disease is often used more broadly to refer to any condition that causes pain , dysfunction , distress , social problems , or death to the person affected, or similar problems for those in contact with the person. In this broader sense, it sometimes includes injuries , disabilities , disorders , syndromes , infections , isolated symptoms, deviant behaviors , and atypical variations of structure and function, while in other contexts and for other purposes these may be considered distinguishable categories. Diseases can affect people not only physically but also mentally, as contracting and living with a disease can alter the affected person's perspective on life. Death due to disease is called death by natural causes . There are four main types of disease: infectious diseases, deficiency diseases , hereditary diseases (including both genetic and non-genetic hereditary diseases ), and physiological diseases. Diseases can also be classified in other ways, such as communicable versus non-communicable diseases. The deadliest diseases in humans are coronary artery disease (blood flow obstruction), followed by cerebrovascular disease and lower respiratory infections . In developed countries, the diseases that cause the most sickness overall are neuropsychiatric conditions , such as depression and anxiety . The study of disease is called pathology , which includes the study of etiology , or cause.In many cases, terms such as disease , disorder , morbidity , sickness and illness are used interchangeably; however, there are situations when specific terms are considered preferable. In an infectious disease, the incubation period is the time between infection and the appearance of symptoms. The latency period is the time between infection and the ability of the disease to spread to another person, which may precede, follow, or be simultaneous with the appearance of symptoms. Some viruses also exhibit a dormant phase, called viral latency , in which the virus hides in the body in an inactive state. For example, varicella zoster virus causes chickenpox in the acute phase ; after recovery from chickenpox, the virus may remain dormant in nerve cells for many years, and later cause herpes zoster (shingles).In many cases, terms such as disease , disorder , morbidity , sickness and illness are used interchangeably; however, there are situations when specific terms are considered preferable. In an infectious disease, the incubation period is the time between infection and the appearance of symptoms. The latency period is the time between infection and the ability of the disease to spread to another person, which may precede, follow, or be simultaneous with the appearance of symptoms. Some viruses also exhibit a dormant phase, called viral latency , in which the virus hides in the body in an inactive state. For example, varicella zoster virus causes chickenpox in the acute phase ; after recovery from chickenpox, the virus may remain dormant in nerve cells for many years, and later cause herpes zoster (shingles).Diseases may be classified by cause, pathogenesis ( mechanism by which the disease is caused), or by symptoms . Alternatively, diseases may be classified according to the organ system involved, though this is often complicated since many diseases affect more than one organ. A chief difficulty in nosology is that diseases often cannot be defined and classified clearly, especially when cause or pathogenesis are unknown. Thus diagnostic terms often only reflect a symptom or set of symptoms ( syndrome ). Classical classification of human disease derives from the observational correlation between pathological analysis and clinical syndromes. Today it is preferred to classify them by their cause if it is known. The most known and used classification of diseases is the World Health Organization 's ICD . This is periodically updated. Currently, the last publication is the ICD-11 .Diseases can be caused by any number of factors and may be acquired or congenital . Microorganisms , genetics, the environment or a combination of these can contribute to a diseased state. Only some diseases such as influenza are contagious and commonly believed infectious. The microorganisms that cause these diseases are known as pathogens and include varieties of bacteria, viruses, protozoa, and fungi. Infectious diseases can be transmitted, e.g. by hand-to-mouth contact with infectious material on surfaces, by bites of insects or other carriers of the disease, and from contaminated water or food (often via fecal contamination), etc. Also, there are sexually transmitted diseases . In some cases, microorganisms that are not readily spread from person to person play a role, while other diseases can be prevented or ameliorated with appropriate nutrition or other lifestyle changes. Some diseases, such as most (but not all ) forms of cancer , heart disease , and mental disorders, are non-infectious diseases . Many non-infectious diseases have a partly or completely genetic basis (see genetic disorder ) and may thus be transmitted from one generation to another. Social determinants of health are the social conditions in which people live that determine their health. Illnesses are generally related to social, economic, political, and environmental circumstances . Social determinants of health have been recognized by several health organizations such as the Public Health Agency of Canada and the World Health Organization to greatly influence collective and personal well-being. The World Health Organization's Social Determinants Council also recognizes Social determinants of health in poverty . When the cause of a disease is poorly understood, societies tend to mythologize the disease or use it as a metaphor or symbol of whatever that culture considers evil. For example, until the bacterial cause of tuberculosis was discovered in 1882, experts variously ascribed the disease to heredity , a sedentary lifestyle , depressed mood , and overindulgence in sex, rich food, or alcohol, all of which were social ills at the time. When a disease is caused by a pathogenic organism (e.g., when malaria is caused by Plasmodium ), one should not confuse the pathogen (the cause of the disease) with disease itself. For example, West Nile virus (the pathogen) causes West Nile fever (the disease). The misuse of basic definitions in epidemiology is frequent in scientific publications. Many diseases and disorders can be prevented through a variety of means. These include sanitation , proper nutrition , adequate exercise , vaccinations and other self-care and public health measures, such as obligatory face mask mandates [ citation needed ] .Medical therapies or treatments are efforts to cure or improve a disease or other health problems. In the medical field, therapy is synonymous with the word treatment . Among psychologists, the term may refer specifically to psychotherapy or "talk therapy". Common treatments include medications , surgery , medical devices , and self-care . Treatments may be provided by an organized health care system , or informally, by the patient or family members. Preventive healthcare is a way to avoid an injury, sickness, or disease in the first place. A treatment or cure is applied after a medical problem has already started. A treatment attempts to improve or remove a problem, but treatments may not produce permanent cures, especially in chronic diseases . Cures are a subset of treatments that reverse diseases completely or end medical problems permanently. Many diseases that cannot be completely cured are still treatable. Pain management (also called pain medicine) is that branch of medicine employing an interdisciplinary approach to the relief of pain and improvement in the quality of life of those living with pain. Treatment for medical emergencies must be provided promptly, often through an emergency department or, in less critical situations, through an urgent care facility.Epidemiology is the study of the factors that cause or encourage diseases. Some diseases are more common in certain geographic areas, among people with certain genetic or socioeconomic characteristics, or at different times of the year. Epidemiology is considered a cornerstone methodology of public health research and is highly regarded in evidence-based medicine for identifying risk factors for diseases. In the study of communicable and non-communicable diseases, the work of epidemiologists ranges from outbreak investigation to study design, data collection, and analysis including the development of statistical models to test hypotheses and the documentation of results for submission to peer-reviewed journals. Epidemiologists also study the interaction of diseases in a population, a condition known as a syndemic . Epidemiologists rely on a number of other scientific disciplines such as biology (to better understand disease processes), biostatistics (the current raw information available), Geographic Information Science (to store data and map disease patterns) and social science disciplines (to better understand proximate and distal risk factors). Epidemiology can help identify causes as well as guide prevention efforts. In studying diseases, epidemiology faces the challenge of defining them. Especially for poorly understood diseases, different groups might use significantly different definitions. Without an agreed-on definition, different researchers may report different numbers of cases and characteristics of the disease. Some morbidity databases are compiled with data supplied by states and territories health authorities, at national levels or larger scale (such as European Hospital Morbidity Database (HMDB)) which may contain hospital discharge data by detailed diagnosis, age and sex. The European HMDB data was submitted by European countries to the World Health Organization Regional Office for Europe. Disease burden is the impact of a health problem in an area measured by financial cost, mortality, morbidity, or other indicators. There are several measures used to quantify the burden imposed by diseases on people. The years of potential life lost (YPLL) is a simple estimate of the number of years that a person's life was shortened due to a disease. For example, if a person dies at the age of 65 from a disease, and would probably have lived until age 80 without that disease, then that disease has caused a loss of 15 years of potential life. YPLL measurements do not account for how disabled a person is before dying, so the measurement treats a person who dies suddenly and a person who died at the same age after decades of illness as equivalent. In 2004, the World Health Organization calculated that 932 million years of potential life were lost to premature death. The quality-adjusted life year (QALY) and disability-adjusted life year (DALY) metrics are similar but take into account whether the person was healthy after diagnosis. In addition to the number of years lost due to premature death, these measurements add part of the years lost to being sick. Unlike YPLL, these measurements show the burden imposed on people who are very sick, but who live a normal lifespan. A disease that has high morbidity, but low mortality, has a high DALY and a low YPLL. In 2004, the World Health Organization calculated that 1.5 billion disability-adjusted life years were lost to disease and injury. In the developed world, heart disease and stroke cause the most loss of life, but neuropsychiatric conditions like major depressive disorder cause the most years lost to being sick.Disease burden is the impact of a health problem in an area measured by financial cost, mortality, morbidity, or other indicators. There are several measures used to quantify the burden imposed by diseases on people. The years of potential life lost (YPLL) is a simple estimate of the number of years that a person's life was shortened due to a disease. For example, if a person dies at the age of 65 from a disease, and would probably have lived until age 80 without that disease, then that disease has caused a loss of 15 years of potential life. YPLL measurements do not account for how disabled a person is before dying, so the measurement treats a person who dies suddenly and a person who died at the same age after decades of illness as equivalent. In 2004, the World Health Organization calculated that 932 million years of potential life were lost to premature death. The quality-adjusted life year (QALY) and disability-adjusted life year (DALY) metrics are similar but take into account whether the person was healthy after diagnosis. In addition to the number of years lost due to premature death, these measurements add part of the years lost to being sick. Unlike YPLL, these measurements show the burden imposed on people who are very sick, but who live a normal lifespan. A disease that has high morbidity, but low mortality, has a high DALY and a low YPLL. In 2004, the World Health Organization calculated that 1.5 billion disability-adjusted life years were lost to disease and injury. In the developed world, heart disease and stroke cause the most loss of life, but neuropsychiatric conditions like major depressive disorder cause the most years lost to being sick.How a society responds to diseases is the subject of medical sociology . A condition may be considered a disease in some cultures or eras but not in others. For example, obesity can represent wealth and abundance, and is a status symbol in famine-prone areas and some places hard-hit by HIV/AIDS . Epilepsy is considered a sign of spiritual gifts among the Hmong people . Sickness confers the social legitimization of certain benefits, such as illness benefits, work avoidance, and being looked after by others. The person who is sick takes on a social role called the sick role . A person who responds to a dreaded disease, such as cancer , in a culturally acceptable fashion may be publicly and privately honored with higher social status . In return for these benefits, the sick person is obligated to seek treatment and work to become well once more. As a comparison, consider pregnancy , which is not interpreted as a disease or sickness, even if the mother and baby may both benefit from medical care. Most religions grant exceptions from religious duties to people who are sick. For example, one whose life would be endangered by fasting on Yom Kippur or during Ramadan is exempted from the requirement, or even forbidden from participating. People who are sick are also exempted from social duties. For example, ill health is the only socially acceptable reason for an American to refuse an invitation to the White House . The identification of a condition as a disease, rather than as simply a variation of human structure or function, can have significant social or economic implications. The controversial recognition of diseases such as repetitive stress injury (RSI) and post-traumatic stress disorder (PTSD) has had a number of positive and negative effects on the financial and other responsibilities of governments, corporations, and institutions towards individuals, as well as on the individuals themselves. The social implication of viewing aging as a disease could be profound, though this classification is not yet widespread. Lepers were people who were historically shunned because they had an infectious disease, and the term "leper" still evokes social stigma . Fear of disease can still be a widespread social phenomenon, though not all diseases evoke extreme social stigma. Social standing and economic status affect health. Diseases of poverty are diseases that are associated with poverty and low social status; diseases of affluence are diseases that are associated with high social and economic status. Which diseases are associated with which states vary according to time, place, and technology. Some diseases, such as diabetes mellitus , may be associated with both poverty (poor food choices) and affluence (long lifespans and sedentary lifestyles), through different mechanisms. The term lifestyle diseases describes diseases associated with longevity and that are more common among older people. For example, cancer is far more common in societies in which most members live until they reach the age of 80 than in societies in which most members die before they reach the age of 50. An illness narrative is a way of organizing a medical experience into a coherent story that illustrates the sick individual's personal experience. People use metaphors to make sense of their experiences with disease. The metaphors move disease from an objective thing that exists to an affective experience. The most popular metaphors draw on military concepts: Disease is an enemy that must be feared, fought, battled, and routed. The patient or the healthcare provider is a warrior , rather than a passive victim or bystander. The agents of communicable diseases are invaders ; non-communicable diseases constitute internal insurrection or civil war . Because the threat is urgent, perhaps a matter of life and death, unthinkably radical, even oppressive, measures are society's and the patient's moral duty as they courageously mobilize to struggle against destruction. The War on Cancer is an example of this metaphorical use of language. This language is empowering to some patients, but leaves others feeling like they are failures. Another class of metaphors describes the experience of illness as a journey: The person travels to or from a place of disease, and changes himself, discovers new information, or increases his experience along the way. He may travel "on the road to recovery" or make changes to "get on the right track" or choose "pathways". Some are explicitly immigration-themed: the patient has been exiled from the home territory of health to the land of the ill, changing identity and relationships in the process. This language is more common among British healthcare professionals than the language of physical aggression. Some metaphors are disease-specific. Slavery is a common metaphor for addictions : The alcoholic is enslaved by drink, and the smoker is captive to nicotine. Some cancer patients treat the loss of their hair from chemotherapy as a metonymy or metaphor for all the losses caused by the disease. Some diseases are used as metaphors for social ills: "Cancer" is a common description for anything that is endemic and destructive in society, such as poverty, injustice, or racism. AIDS was seen as a divine judgment for moral decadence, and only by purging itself from the "pollution" of the "invader" could society become healthy again. More recently, when AIDS seemed less threatening, this type of emotive language was applied to avian flu and type 2 diabetes mellitus . Authors in the 19th century commonly used tuberculosis as a symbol and a metaphor for transcendence . People with the disease were portrayed in literature as having risen above daily life to become ephemeral objects of spiritual or artistic achievement. In the 20th century, after its cause was better understood, the same disease became the emblem of poverty, squalor, and other social problems. An illness narrative is a way of organizing a medical experience into a coherent story that illustrates the sick individual's personal experience. People use metaphors to make sense of their experiences with disease. The metaphors move disease from an objective thing that exists to an affective experience. The most popular metaphors draw on military concepts: Disease is an enemy that must be feared, fought, battled, and routed. The patient or the healthcare provider is a warrior , rather than a passive victim or bystander. The agents of communicable diseases are invaders ; non-communicable diseases constitute internal insurrection or civil war . Because the threat is urgent, perhaps a matter of life and death, unthinkably radical, even oppressive, measures are society's and the patient's moral duty as they courageously mobilize to struggle against destruction. The War on Cancer is an example of this metaphorical use of language. This language is empowering to some patients, but leaves others feeling like they are failures. Another class of metaphors describes the experience of illness as a journey: The person travels to or from a place of disease, and changes himself, discovers new information, or increases his experience along the way. He may travel "on the road to recovery" or make changes to "get on the right track" or choose "pathways". Some are explicitly immigration-themed: the patient has been exiled from the home territory of health to the land of the ill, changing identity and relationships in the process. This language is more common among British healthcare professionals than the language of physical aggression. Some metaphors are disease-specific. Slavery is a common metaphor for addictions : The alcoholic is enslaved by drink, and the smoker is captive to nicotine. Some cancer patients treat the loss of their hair from chemotherapy as a metonymy or metaphor for all the losses caused by the disease. Some diseases are used as metaphors for social ills: "Cancer" is a common description for anything that is endemic and destructive in society, such as poverty, injustice, or racism. AIDS was seen as a divine judgment for moral decadence, and only by purging itself from the "pollution" of the "invader" could society become healthy again. More recently, when AIDS seemed less threatening, this type of emotive language was applied to avian flu and type 2 diabetes mellitus . Authors in the 19th century commonly used tuberculosis as a symbol and a metaphor for transcendence . People with the disease were portrayed in literature as having risen above daily life to become ephemeral objects of spiritual or artistic achievement. In the 20th century, after its cause was better understood, the same disease became the emblem of poverty, squalor, and other social problems.

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West Nile

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Religion in Uganda

Religion in Uganda (2014 census) Christianity is the predominant religion in Uganda . According to the 2014 census, over 84 percent of the population was Christian, while about 14 percent of the population adhered to Islam , making it the largest minority religion. Anglicanism and Catholicism are the main Christian denominations in the country. The northern and west Nile regions are dominated by Roman Catholics, and Iganga District in the east of Uganda had the highest percentage of Muslims; Good Friday , Easter Monday , Eid al-Fitr , Eid al-Adha , and Christmas are recognized national holidays. Freedom of religion is guaranteed by the Uganda Constitution, but religions are expected to be registered with the government and then to secure a five-year license; registered groups are exempt from direct taxation. In 2023, the country was scored 3 out of 4 for religious freedom. According to the national census of 2014, Christians of all denominations comprised 85 percent of Uganda's population. The Roman Catholic Church had the largest number of adherents (39.3 percent of the total population). The largest Protestant church was the Anglican Church of Uganda , a part of the worldwide Anglican communion, at 32 percent. The category of Pentecostal/Evangelical/Born Again made up 11.1% of the population, while Seventh-day Adventists made up 1.7%, Baptists 0.3% and Eastern Orthodox 0.1%., although some sources estimate their numbers to more than 3% Jehovah's Witnesses operate in Uganda under the International Bible Students Association name and are working in a total of ten languages, including Swahili and Luganda . Followers of William M. Branham and Branhamism claim numbers in the tens of thousands, thanks in large part to translation and distribution efforts by Voice of God Recordings. The Presbyterian Church in Uganda has 100-200 congregations. The Reformed Presbyterian Church in Uganda was a result in a split in the Presbyterian church. Baptist has its origins in American mission of the Southern Baptist Convention in 1963. The Baptist Union of Uganda was founded in 1974. According to a denomination census released in 2020, it claimed 1,800 churches and 550,000 members. The Church of Jesus Christ of Latter-day Saints claims more than 14,000 members in 27 congregations in Uganda. They also have two family history centers. The Society of Friends has two yearly meetings , Uganda Yearly Meeting, part of Friends United Meeting and Evangelical Friends Church . There were about 3,000 members between the two in 2001. A 2015 study estimated some 35,000 believers in Christ from a Muslim background residing in the country at the time. According to the 2014 National Census, 14 percent of Ugandans adhered to Islam. Most Muslims are Sunni , with a small minority of Shia Muslims. There was a small group of Ahmadis in the country in 2012. There are a small community of Ugandan Jews called the Abayudaya , numbering some 2,000-3,000. The group was formed by Semei Kakungulu in the early 20th century. About 1 percent of Uganda's population follow traditional religions only; however, in 2009, more people practiced traditional religious practices along with other religions such as Christianity or Islam. One survey in 2010 showed that about 27 percent of Ugandans believe that sacrifices to ancestors or spirits can protect them from harm. Uganda has received media attention for interfaith efforts in Mbale . Founded by JJ Keki, the Mirembe Kawomera (Delicious Peace) Fair Trade Coffee Cooperative brings together Muslim, Jewish, and Christian coffee farmers. Members of the cooperative use music to spread their message of peace. The Smithsonian Folkways album "Delicious Peace: Coffee, Music & Interfaith Harmony in Uganda" features songs from members of the cooperative about their interfaith message. The 2014 Census found that there were 13,905 Hindus, making up less than 0.1% of the population. The Bahá'í Faith in Uganda started to grow in 1951 and in four years time there were 500 Bahá'ís in 80 localities, including 13 Bahá'í Local Spiritual Assemblies , representing 30 tribes, and had dispatched 9 Bahá'í pioneers to other African locations. Following the reign of Idi Amin when the Bahá'í Faith was banned and the murder of Bahá'í Hand of the Cause Enoch Olinga and his family, the community continues to grow though estimates of the population range widely from 19,000 to 105,000 and the community's involvements have included diverse efforts to promote the welfare of the Ugandan people. One of only ten Bahá'í Houses of Worship in the world, known as the Mother Temple of Africa, is located on the outskirts of Kampala . The Uganda Buddhist Centre , founded in 2005 by Venerable Buddharakkhita, is an initiative that intends to provide the first stable source of Buddhism in Uganda. Only 0.9 percent of Ugandans claim no religion. The Uganda Humanist Association is a member of the International Humanist and Ethical Union and has been registered since 1996.

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West Nile

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Rock dove

The rock dove , rock pigeon , or common pigeon ( / ˈ p ɪ dʒ . ə n / also / ˈ p ɪ dʒ . ɪ n / ; Columba livia ) is a member of the bird family Columbidae (doves and pigeons). : 624 In common usage, it is often simply referred to as the "pigeon", although this is the wild form of the bird; the pigeons most familiar to people are the domesticated form of the wild rock dove. The domestic pigeon ( Columba livia domestica , which includes about 1,000 different breeds ) descended from this species. Escaped domestic pigeons have increased the populations of feral pigeons around the world. Wild rock doves are pale grey with two black bars on each wing, whereas domestic and feral pigeons vary in the colour and pattern of their plumage . Few differences are seen between males and females; i.e they are not strongly sexually dimorphic . The species is generally monogamous , with two squabs (young) per brood . Both parents care for the young for a time. Habitats include various open and semi-open environments where they are able to forage on the ground. Cliffs and rock ledges are used for roosting and breeding in the wild. Originating in Southern Europe , North Africa , and Western Asia , pigeons have become established in cities around the world. The species is abundant, with an estimated population of 17 to 28 million feral and wild birds in Europe alone and up to 120 million worldwide. The official common name is rock dove , as given by the International Ornithological Congress . The rock dove was formally described in 1789 by the German naturalist Johann Friedrich Gmelin in his revised and expanded edition of Systema Naturae written by Carl Linnaeus . He placed it with all the other doves and pigeons in the genus Columba and coined the binomial name Columba livia . The genus name Columba is the Latin word meaning "pigeon, dove", whose older etymology comes from the Ancient Greek ÎºÏŒÎ»Ï Î¼Î²Î¿Ï‚ ( kolumbos ), "a diver", from ÎºÎ¿Î»Ï Î¼Î²Î¬Ï‰ (kolumbao), "dive, plunge headlong, swim". Aristophanes (Birds, 304) and others use the word ÎºÎ¿Î»Ï Î¼Î²Î¯Ï‚ ( kolumbis ), "diver", for the name of the bird, because of its swimming motion in the air. The specific epithet livia is a medieval Latin variant of livida , "livid, bluish-grey"; this was Theodorus Gaza 's translation of Greek peleia , "dove", itself thought to be derived from pellos , "dark-coloured". : 228 Its closest relative in the genus Columba is the hill pigeon , followed by the other rock pigeons: the snow , speckled , and white-collared pigeons . Pigeon chicks are called "squabs". Note that members of the lesser known pigeon genus Petrophassa and the speckled pigeon ( Columba guinea ), also have the common name " rock pigeon ". The rock dove was first described by German naturalist Johann Gmelin in 1789. The rock dove was central to Charles Darwin 's discovery of evolution , and featured in four of his works from 1859 to 1872. Darwin posited that, despite wide-ranging morphological differences, the many hundreds of breeds of domestic pigeon could all be traced back to the wild rock dove; in essence human selection of pigeon breeds was analogous to natural selection . Nine subspecies are recognised: Nine subspecies are recognised: Centuries of domestication have greatly altered the rock dove. Feral pigeons, which have escaped domestication throughout history, have significant variations in plumage. When not specified, descriptions are for assumed wild type , though the wild type may be on the verge of extinction or already extinct. The adult of the nominate subspecies of the rock dove is 29 to 37 cm (11 to 15 in) long with a 62 to 72 cm (24 to 28 in) wingspan. Weight for wild or feral rock doves ranges from 238–380 g (8.4–13.4 oz) , though overfed domestic and semidomestic individuals can exceed normal weights. It has a dark bluish-grey head, neck, and chest with glossy yellowish, greenish, and reddish-purple iridescence along its neck and wing feathers. The iris is orange, red, or golden with a paler inner ring, and the bare skin round the eye is bluish-grey. The bill is grey-black with a conspicuous off-white cere, and the feet are purplish-red. Among standard measurements, the wing chord is typically around 22.3 cm (8.8 in) , the tail is 9.5 to 11 cm (3.7 to 4.3 in) , the bill is around 1.8 cm (0.71 in) , and the tarsus is 2.6 to 3.5 cm (1.0 to 1.4 in) . The adult female is almost identical in outward appearance to the male, but the iridescence on her neck is less intense and more restricted to the rear and sides, whereas that on the breast is often very obscure. The white lower back of the pure rock dove is its best identification characteristic; the two black bars on its pale grey wings are also distinctive. The tail has a black band on the end, and the outer web of the tail feathers are margined with white. It is strong and quick on the wing, dashing out from sea caves, flying low over the water, its lighter grey rump showing well from above. [ self-published source? ] Young birds show little lustre and are duller. Eye colour of the pigeon is generally orange, but a few pigeons may have white-grey eyes. The eyelids are orange and encapsulated in a grey-white eye ring. The feet are red to pink. The subspecies gymnocycla is smaller and very much darker than the nominate subspecies . It is almost blackish on the head, rump and underparts with a white back and the iridescence of the nape extending onto the head. Subspecies targia is slightly smaller than the nominate, with similar plumage, but the back is concolorous with the mantle instead of white. Subspecies dakhlae is smaller and much paler than the nominate. Subspecies schimperi closely resembles targia , but has a distinctly paler mantle. Subspecies palaestinae is slightly larger than schimperi and has darker plumage. Subspecies gaddi is larger and paler than palaestinae, with which it intergrades in the west. Subspecies neglecta it is similar to the nominate in size but darker, with a stronger and more extensive iridescent sheen on the neck. It intergrades with gaddi in the south. Subspecies intermedia is similar to neglecta but darker, with a less contrasting back. : 176–179 There have been numerous skeletal descriptions of the rock dove and the associated muscles including those of the eye, jaw, neck, and throat. The skull is dominated by the rostrum, eye socket, and braincase. The quadrate bone is relatively small and mobile and connects the rest of the cranium to the lower jaw. The latter has an angled shape in side view because the long-axis of the front half of the lower jaw is at a 30° angle to the back half. Beneath the skull, the hyoid skeleton involves three mid-line structures and a pair of elongate structures that stem from between the junction of the back two structures. The anterior structure (the paraglossum or entoglossum) is unpaired and shaped like an arrowhead. When circling overhead, the white underwing of the bird becomes conspicuous. In its flight, behaviour, and voice, which is more of a dovecot coo than the phrase of the wood pigeon , it is a typical pigeon. Although it is a relatively strong flier, it also glides frequently, holding its wings in a very pronounced V shape as it does. As prey birds, they must keep their vigilance, and when disturbed a pigeon within a flock will take off with a noisy clapping sound that cues for other pigeons to take to flight. The noise of the take-off increases the faster a pigeon beats its wings, thus advertising the magnitude of a perceived threat to its flockmates. Feral pigeons are essentially the same size and shape as the original wild rock dove, but often display far greater variation in colour and pattern compared to their wild ancestors. The blue-barred pattern which the original wild rock dove displays is generally less common in more urban areas. Urban pigeons tend to have darker plumage than those in more rural areas. Pigeons feathers have two types of melanin (pigment) – eumelanin and pheomelanin . A study of melanin in the feathers of both wild rock and domestic pigeons, of different coloration types and known genetic background, measured the concentration, distribution and proportions of eumelanin and pheomelanin and found that gene mutations affecting the distribution, amounts and proportions of pigments accounted for the greater variation of coloration in domesticated birds than in their wild relations. Eumelanin generally causes grey or black coloration, while pheomelanin results in a reddish-brown colour. Other shades of brown may be produced through different combinations and concentrations of the two colours. As in other animals, white pigeons have little to no pigment. [ citation needed ] Darker birds may be better able to store trace metals in their feathers due to their higher concentrations of melanin, which may help mitigate the negative effects of the metals, the concentrations of which are typically higher in urban areas. Pigeons, especially homing or carrier breeds, are well known for their ability to find their way home from long distances. Despite these demonstrated abilities, wild rock doves are sedentary and rarely leave their local areas. It is hypothesized that in their natural, arid habitat, they rely on this sense to navigate back home after foraging as deserts rarely possess navigational landmarks that may be used. A rock pigeon's lifespan ranges from 3–5 years in the wild to 15 years in captivity, though longer-lived specimens have been reported. The main causes of mortality in the wild are predators and persecution by humans. [ citation needed ] Some sources state the species was first introduced to North America in 1606 at Port Royal , Nova Scotia . Although other sources cite Plymouth and Jamestown settlements in the early 17th century as the first place for species introduction in North America. The call is a soft, slightly wavering, coo. Ornithologist David Sibley describes the display call as a whoo, hoo-witoo-hoo , whereas the Cornell Lab of Ornithology describes it as a Coo, roo-c'too-coo . Variations include an alarm call, a nest call, and noises made by juveniles. Sibley describes the nest call as a repeated hu-hu-hurrr . When displaying, songs are partly sexual, partly threatening. They are accompanied by an inflated throat, tail fanning, strutting, and bowing. The alarm call, given at sight of predators, is a grunt-like oorhh . Non-vocal sounds include a loud flapping noise at take-off, feet stomping, hisses, and beak snapping. Wings may also be clapped during flights, usually during display fights or after copulation. Juveniles particularly snap their bills, usually to respond to nest invasion. The foot stomping appears deliberate, though for what purpose is unclear. Foot stomping is done with a certain foot first, showing that rock doves have "footedness", similar to human handedness . The call is a soft, slightly wavering, coo. Ornithologist David Sibley describes the display call as a whoo, hoo-witoo-hoo , whereas the Cornell Lab of Ornithology describes it as a Coo, roo-c'too-coo . Variations include an alarm call, a nest call, and noises made by juveniles. Sibley describes the nest call as a repeated hu-hu-hurrr . When displaying, songs are partly sexual, partly threatening. They are accompanied by an inflated throat, tail fanning, strutting, and bowing. The alarm call, given at sight of predators, is a grunt-like oorhh . Non-vocal sounds include a loud flapping noise at take-off, feet stomping, hisses, and beak snapping. Wings may also be clapped during flights, usually during display fights or after copulation. Juveniles particularly snap their bills, usually to respond to nest invasion. The foot stomping appears deliberate, though for what purpose is unclear. Foot stomping is done with a certain foot first, showing that rock doves have "footedness", similar to human handedness . Before the Columbian Exchange , rock doves were restricted to a natural resident range in western and southern Europe , North Africa , and extending into South Asia . They were carried into the New World aboard European ships between 1603 and 1607. The species (including ferals) has a large range, with an estimated global extent of occurrence of 10,000,000 km 2 (3,900,000 sq mi) . It has a large global population, including an estimated 17 to 28 million individuals in Europe. Fossil evidence suggests the rock dove originated in southern Asia, and skeletal remains, unearthed in Israel , confirm its existence there for at least 300,000 years. However, this species has such a long history with humans that it is impossible to identify its original range exactly. Wild pigeons reside in rock formations and cliff faces, settling in crevices to nest. They nest communally, often forming large colonies of many hundreds of individuals. Wild nesting sites include caves, canyons, and sea cliffs. They will even live in the Sahara so long as an area has rocks, water, and some plant matter. They prefer to avoid dense vegetation. Rock doves have a commensal relationship with humans, gaining both ample access to food and nesting spots in civilized areas. Human structures provide an excellent imitation of cliff structures, making rock doves very common around human habitation. Skyscrapers, highway overpasses, farm buildings, abandoned buildings, and other human structures with ample crevices are conducive to rock dove nesting. Thus the modern range of the rock dove is due in large part to humans. Agricultural settlements are favoured over forested ones. Ideal human nesting attributes combine areas with tall buildings, green spaces, ample access to human food, and schools. Conversely, suburban areas which are far from city centers and have high street density are the least conducive to pigeons. Their versatility among human structures is evidenced by a population living inside a deep well in Tunisia. Feral pigeons are usually unable to find these accommodations, so they must nest on building ledges, walls or statues. They may damage these structures via their feces; starving birds can only excrete urates, which over time corrodes masonry and metal. In contrast, a well-fed bird passes mostly solid feces, containing only small amounts of uric acid. [ citation needed ]Pigeons are often found in pairs in the breeding season, but are usually gregarious. The rock dove breeds at any time of the year, but peak times are spring and summer. Nesting sites are along coastal cliff faces, as well as the artificial cliff faces created by apartment buildings with accessible ledges or roof spaces. Pigeons can compete with native birds for nest sites. For some avian species, such as seabirds, it could be a conservation issue. Current evidence suggests that wild, domestic and feral pigeons mate for life, although their long-term bonds are not unbreakable. They are socially monogamous, but extra-pair matings do occur, often initiated by males. Due to their ability to produce crop milk , pigeons can breed at any time of year. Pigeons breed when the food supply is abundant enough to support embryonic egg development, which in cities, can be any time of the year. Laying of eggs can take place up to six times per year. [ citation needed ] Pigeons are often found in pairs during the breeding season, but usually the pigeons are gregarious , living in flocks of 50 to 500 birds (dependent on the food supply). Courtship rituals can be observed in urban parks at any time of the year. The male on the ground or rooftops puffs up the feathers on his neck to appear larger and thereby impress or attract attention. He approaches the female at a rapid walking pace while emitting repetitive quiet notes, often bowing and turning as he comes closer. At first, the female invariably walks or flies a short distance away and the male follows her until she stops. At this point, he continues the bowing motion and very often makes full- or half- pirouettes in front of the female. The male then proceeds to feed the female by regurgitating food, as they do when feeding the young. [ citation needed ] The male then mounts the female, rearing backwards to be able to join their cloacae . The mating is very brief, with the male flapping his wings to maintain balance on top of the female. The nest is a flimsy platform of straw and sticks, laid on a ledge, under cover, often on the window ledges of buildings. Two white eggs are laid; incubation, shared by both parents, lasts 17 to 19 days. The newly hatched squab (nestling) has pale yellow down and a flesh-coloured bill with a dark band. For the first few days, the baby squabs are tended and fed (through regurgitation) exclusively on " crop milk " (also called "pigeon milk" or "pigeon's milk"). The pigeon milk is produced in the crops of both parents in all species of pigeon and dove. Pigeons are altricial and their fledging period is about 30 days. Rock doves are omnivorous, but prefer plant matter: chiefly fruits and grains. Studies of pigeons in a semi-rural part of Kansas found that their diet includes the following: 92% maize , 3.2% oats , 3.7% cherry , along with small amounts of knotweed , elm , poison ivy and barley . Feral pigeons can be seen eating grass seeds and berries in parks and gardens in the spring, but plentiful sources exist throughout the year from scavenging (e.g., food remnants left inside of dropped fast food cartons, in the form of popcorn , cake , peanuts , bread and currants ) and they also eat insects and spiders . Additional food is also usually available from waste bins, tourists or residents who feed bird seed to pigeons for reasons such as empathy, fun, tradition and as a means for social interaction. Pigeons tend to congregate in large, often thick flocks when feeding on discarded food, and may be observed flying skillfully around trees, buildings, telephone poles and cables and even through moving traffic just to reach a food source. [ citation needed ] Pigeons feed on the ground in flocks or individually. Pigeons are naturally granivorous, eating seeds that fit down their gullet. They may sometimes consume small invertebrates such as worms or insect larvae as a protein supplement. As they do not possess an enlarged cecum as in European wood pigeons, they cannot digest adult plant tissue; the various seeds they eat contain the appropriate nutrients they require. While most birds take small sips and tilt their heads backwards when drinking, pigeons are able to dip their bills into the water and drink continuously, without having to tilt their heads back. In cities they typically resort to scavenging human garbage, as unprocessed grain may be impossible to find. Pigeon groups typically consist of producers, which locate and obtain food, and scroungers, which feed on food obtained by the producers. Generally, groups of pigeons contain a greater proportion of scroungers than producers. Pigeons primarily use powder down feathers for preening, which gives a soft and silky feel to their plumage. They have no preen gland or at times have very rudimentary preen glands, so oil is not used for preening. Rather, powder down feathers are spread across the body. These have a tendency to disintegrate, and the powder, akin to talcum powder, helps maintain the plumage. Some varieties of domestic pigeon have modified feathers called "fat quills". These feathers contain yellow, oil-like fat that derives from the same cells as powder down. This is used while preening and helps reduce bacterial degradation of feathers by feather bacilli. With only their flying abilities protecting them from predation, rock pigeons are a favourite almost around the world for a wide range of raptors . In fact, with feral pigeons existing in almost every city in the world, they may form the majority of prey for several raptor species that live in urban areas. Peregrine falcons and Eurasian sparrowhawks are natural predators of pigeons and quite adept at catching and feeding upon this species. Up to 80% of the diet of peregrine falcons in several cities that have breeding falcons is composed of feral pigeons. Some common predators of feral pigeons in North America are raccoons , opossums , red-tailed hawks , great horned owls , eastern screech owls , and accipiters . The birds that prey on pigeons in North America can range in size from American kestrels to golden eagles and may even include crows , gulls and ravens . [ citation needed ] On the ground the adults, their young and their eggs are at risk from feral and domestic cats . Doves and pigeons are considered to be game birds , since many species are hunted and used for food in many of the countries in which they are native. The body feathers have dense, fluffy bases and are loosely attached to the skin, hence they drop out easily. When a predator catches a pigeon large numbers of feathers come out in the attacker's mouth and the pigeon may use this temporary distraction to make an escape. It also tends to drop the tail feathers when preyed upon or under traumatic conditions, probably as a distraction mechanism. Pigeons may harbour a diverse parasite fauna. They often host the intestinal helminths Capillaria columbae and Ascaridia columbae . Their ectoparasites include the ischnoceran lice Columbicola columbae , Campanulotes bidentatus compar , the amblyceran lice Bonomiella columbae , Hohorstiella lata , Colpocephalum turbinatum , the mites Tinaminyssus melloi , Dermanyssus gallinae , Dermoglyphus columbae , Falculifer rostratus and Diplaegidia columbae . The hippoboscid fly Pseudolynchia canariensis is a typical blood-sucking ectoparasite of pigeons in tropical and subtropical regions.The rock dove breeds at any time of the year, but peak times are spring and summer. Nesting sites are along coastal cliff faces, as well as the artificial cliff faces created by apartment buildings with accessible ledges or roof spaces. Pigeons can compete with native birds for nest sites. For some avian species, such as seabirds, it could be a conservation issue. Current evidence suggests that wild, domestic and feral pigeons mate for life, although their long-term bonds are not unbreakable. They are socially monogamous, but extra-pair matings do occur, often initiated by males. Due to their ability to produce crop milk , pigeons can breed at any time of year. Pigeons breed when the food supply is abundant enough to support embryonic egg development, which in cities, can be any time of the year. Laying of eggs can take place up to six times per year. [ citation needed ] Pigeons are often found in pairs during the breeding season, but usually the pigeons are gregarious , living in flocks of 50 to 500 birds (dependent on the food supply). Courtship rituals can be observed in urban parks at any time of the year. The male on the ground or rooftops puffs up the feathers on his neck to appear larger and thereby impress or attract attention. He approaches the female at a rapid walking pace while emitting repetitive quiet notes, often bowing and turning as he comes closer. At first, the female invariably walks or flies a short distance away and the male follows her until she stops. At this point, he continues the bowing motion and very often makes full- or half- pirouettes in front of the female. The male then proceeds to feed the female by regurgitating food, as they do when feeding the young. [ citation needed ] The male then mounts the female, rearing backwards to be able to join their cloacae . The mating is very brief, with the male flapping his wings to maintain balance on top of the female. The nest is a flimsy platform of straw and sticks, laid on a ledge, under cover, often on the window ledges of buildings. Two white eggs are laid; incubation, shared by both parents, lasts 17 to 19 days. The newly hatched squab (nestling) has pale yellow down and a flesh-coloured bill with a dark band. For the first few days, the baby squabs are tended and fed (through regurgitation) exclusively on " crop milk " (also called "pigeon milk" or "pigeon's milk"). The pigeon milk is produced in the crops of both parents in all species of pigeon and dove. Pigeons are altricial and their fledging period is about 30 days. Rock doves are omnivorous, but prefer plant matter: chiefly fruits and grains. Studies of pigeons in a semi-rural part of Kansas found that their diet includes the following: 92% maize , 3.2% oats , 3.7% cherry , along with small amounts of knotweed , elm , poison ivy and barley . Feral pigeons can be seen eating grass seeds and berries in parks and gardens in the spring, but plentiful sources exist throughout the year from scavenging (e.g., food remnants left inside of dropped fast food cartons, in the form of popcorn , cake , peanuts , bread and currants ) and they also eat insects and spiders . Additional food is also usually available from waste bins, tourists or residents who feed bird seed to pigeons for reasons such as empathy, fun, tradition and as a means for social interaction. Pigeons tend to congregate in large, often thick flocks when feeding on discarded food, and may be observed flying skillfully around trees, buildings, telephone poles and cables and even through moving traffic just to reach a food source. [ citation needed ] Pigeons feed on the ground in flocks or individually. Pigeons are naturally granivorous, eating seeds that fit down their gullet. They may sometimes consume small invertebrates such as worms or insect larvae as a protein supplement. As they do not possess an enlarged cecum as in European wood pigeons, they cannot digest adult plant tissue; the various seeds they eat contain the appropriate nutrients they require. While most birds take small sips and tilt their heads backwards when drinking, pigeons are able to dip their bills into the water and drink continuously, without having to tilt their heads back. In cities they typically resort to scavenging human garbage, as unprocessed grain may be impossible to find. Pigeon groups typically consist of producers, which locate and obtain food, and scroungers, which feed on food obtained by the producers. Generally, groups of pigeons contain a greater proportion of scroungers than producers. Pigeons primarily use powder down feathers for preening, which gives a soft and silky feel to their plumage. They have no preen gland or at times have very rudimentary preen glands, so oil is not used for preening. Rather, powder down feathers are spread across the body. These have a tendency to disintegrate, and the powder, akin to talcum powder, helps maintain the plumage. Some varieties of domestic pigeon have modified feathers called "fat quills". These feathers contain yellow, oil-like fat that derives from the same cells as powder down. This is used while preening and helps reduce bacterial degradation of feathers by feather bacilli. With only their flying abilities protecting them from predation, rock pigeons are a favourite almost around the world for a wide range of raptors . In fact, with feral pigeons existing in almost every city in the world, they may form the majority of prey for several raptor species that live in urban areas. Peregrine falcons and Eurasian sparrowhawks are natural predators of pigeons and quite adept at catching and feeding upon this species. Up to 80% of the diet of peregrine falcons in several cities that have breeding falcons is composed of feral pigeons. Some common predators of feral pigeons in North America are raccoons , opossums , red-tailed hawks , great horned owls , eastern screech owls , and accipiters . The birds that prey on pigeons in North America can range in size from American kestrels to golden eagles and may even include crows , gulls and ravens . [ citation needed ] On the ground the adults, their young and their eggs are at risk from feral and domestic cats . Doves and pigeons are considered to be game birds , since many species are hunted and used for food in many of the countries in which they are native. The body feathers have dense, fluffy bases and are loosely attached to the skin, hence they drop out easily. When a predator catches a pigeon large numbers of feathers come out in the attacker's mouth and the pigeon may use this temporary distraction to make an escape. It also tends to drop the tail feathers when preyed upon or under traumatic conditions, probably as a distraction mechanism. Pigeons may harbour a diverse parasite fauna. They often host the intestinal helminths Capillaria columbae and Ascaridia columbae . Their ectoparasites include the ischnoceran lice Columbicola columbae , Campanulotes bidentatus compar , the amblyceran lice Bonomiella columbae , Hohorstiella lata , Colpocephalum turbinatum , the mites Tinaminyssus melloi , Dermanyssus gallinae , Dermoglyphus columbae , Falculifer rostratus and Diplaegidia columbae . The hippoboscid fly Pseudolynchia canariensis is a typical blood-sucking ectoparasite of pigeons in tropical and subtropical regions.With only their flying abilities protecting them from predation, rock pigeons are a favourite almost around the world for a wide range of raptors . In fact, with feral pigeons existing in almost every city in the world, they may form the majority of prey for several raptor species that live in urban areas. Peregrine falcons and Eurasian sparrowhawks are natural predators of pigeons and quite adept at catching and feeding upon this species. Up to 80% of the diet of peregrine falcons in several cities that have breeding falcons is composed of feral pigeons. Some common predators of feral pigeons in North America are raccoons , opossums , red-tailed hawks , great horned owls , eastern screech owls , and accipiters . The birds that prey on pigeons in North America can range in size from American kestrels to golden eagles and may even include crows , gulls and ravens . [ citation needed ] On the ground the adults, their young and their eggs are at risk from feral and domestic cats . Doves and pigeons are considered to be game birds , since many species are hunted and used for food in many of the countries in which they are native. The body feathers have dense, fluffy bases and are loosely attached to the skin, hence they drop out easily. When a predator catches a pigeon large numbers of feathers come out in the attacker's mouth and the pigeon may use this temporary distraction to make an escape. It also tends to drop the tail feathers when preyed upon or under traumatic conditions, probably as a distraction mechanism. Pigeons may harbour a diverse parasite fauna. They often host the intestinal helminths Capillaria columbae and Ascaridia columbae . Their ectoparasites include the ischnoceran lice Columbicola columbae , Campanulotes bidentatus compar , the amblyceran lice Bonomiella columbae , Hohorstiella lata , Colpocephalum turbinatum , the mites Tinaminyssus melloi , Dermanyssus gallinae , Dermoglyphus columbae , Falculifer rostratus and Diplaegidia columbae . The hippoboscid fly Pseudolynchia canariensis is a typical blood-sucking ectoparasite of pigeons in tropical and subtropical regions.Rock doves have been domesticated for several thousand years, giving rise to the domestic pigeon ( Columba livia domestica ). They may have been domesticated as long as 5,000 years ago. Numerous breeds of fancy pigeons of all sizes, colours, and types have been bred. Domesticated pigeons are used as homing pigeons as well as food and pets. They were in the past also used as carrier pigeons . So-called war pigeons have played significant roles during wartime, and many pigeons have received awards and medals for their services in saving hundreds of human lives. Pigeons have notably been "employed" as medical imaging data sorters. They have been successfully trained under research conditions to examine data on a screen for the purposes of detecting breast cancer. They appear to use their innate visual navigation skills to do so. Many domestic birds have got lost, escaped or been released over the years and have given rise to feral pigeons. These show a variety of plumages, although many have the blue-barred pattern as does the pure rock dove. Feral pigeons are found in cities and towns all over the world. The scarcity of the pure wild species is partly due to interbreeding with feral birds. Contact with pigeon droppings poses a minor risk of contracting histoplasmosis , cryptococcosis and psittacosis , and long-term exposure to both droppings and feathers can induce an allergy known as bird fancier's lung . Pigeons are not a major concern in the spread of West Nile virus : though they can contract it, they apparently do not transmit it. Some contagions are transmitted by pigeons; for example, the bacteria Chlamydophila psittaci is endemic among pigeons and causes psittacosis in humans. It is generally transmitted from handling pigeons or their droppings (more commonly the latter). Psittacosis is a serious disease but rarely fatal (less than 1%). Pigeons are also important vectors for various species of the bacteria Salmonella , which causes diseases such as salmonellosis and paratyphoid fever. Pigeons are also known to host avian mites, which can infest human habitation and bite humans, a condition known as gamasoidosis . However, infesting mammals is relatively rare. Pigeons may, however, carry and spread avian influenza . One study has shown that adult pigeons are not clinically susceptible to the most dangerous strain of avian influenza, H5N1 , and that they do not transmit the virus to poultry. Other studies have presented evidence of clinical signs and neurological lesions resulting from infection but found that the pigeons did not transmit the disease to poultry reared in direct contact with them. Pigeons were found to be "resistant or minimally susceptible" to other strains of avian influenza, such as the H7N7 . Research into whether pigeons play a part in spreading bird flu have shown pigeons do not carry the deadly H5N1 strain. Three studies have been done since the late 1990s by the US Agriculture Department's Southeast Poultry Research Laboratory in Athens, Georgia, according to the center's director, David Swayne. The lab has been working on bird flu since the 1970s. In one experiment, researchers squirted into pigeons' mouths liquid drops that contained the highly pathogenic H5N1 virus from a Hong Kong sample. The birds received 100 to 1,000 times the concentration that wild birds would encounter in nature. "We couldn't infect the pigeons", Swayne said. "So that's good news." Rock doves have been domesticated for several thousand years, giving rise to the domestic pigeon ( Columba livia domestica ). They may have been domesticated as long as 5,000 years ago. Numerous breeds of fancy pigeons of all sizes, colours, and types have been bred. Domesticated pigeons are used as homing pigeons as well as food and pets. They were in the past also used as carrier pigeons . So-called war pigeons have played significant roles during wartime, and many pigeons have received awards and medals for their services in saving hundreds of human lives. Pigeons have notably been "employed" as medical imaging data sorters. They have been successfully trained under research conditions to examine data on a screen for the purposes of detecting breast cancer. They appear to use their innate visual navigation skills to do so. Many domestic birds have got lost, escaped or been released over the years and have given rise to feral pigeons. These show a variety of plumages, although many have the blue-barred pattern as does the pure rock dove. Feral pigeons are found in cities and towns all over the world. The scarcity of the pure wild species is partly due to interbreeding with feral birds. So-called war pigeons have played significant roles during wartime, and many pigeons have received awards and medals for their services in saving hundreds of human lives.Pigeons have notably been "employed" as medical imaging data sorters. They have been successfully trained under research conditions to examine data on a screen for the purposes of detecting breast cancer. They appear to use their innate visual navigation skills to do so. Many domestic birds have got lost, escaped or been released over the years and have given rise to feral pigeons. These show a variety of plumages, although many have the blue-barred pattern as does the pure rock dove. Feral pigeons are found in cities and towns all over the world. The scarcity of the pure wild species is partly due to interbreeding with feral birds. Contact with pigeon droppings poses a minor risk of contracting histoplasmosis , cryptococcosis and psittacosis , and long-term exposure to both droppings and feathers can induce an allergy known as bird fancier's lung . Pigeons are not a major concern in the spread of West Nile virus : though they can contract it, they apparently do not transmit it. Some contagions are transmitted by pigeons; for example, the bacteria Chlamydophila psittaci is endemic among pigeons and causes psittacosis in humans. It is generally transmitted from handling pigeons or their droppings (more commonly the latter). Psittacosis is a serious disease but rarely fatal (less than 1%). Pigeons are also important vectors for various species of the bacteria Salmonella , which causes diseases such as salmonellosis and paratyphoid fever. Pigeons are also known to host avian mites, which can infest human habitation and bite humans, a condition known as gamasoidosis . However, infesting mammals is relatively rare. Pigeons may, however, carry and spread avian influenza . One study has shown that adult pigeons are not clinically susceptible to the most dangerous strain of avian influenza, H5N1 , and that they do not transmit the virus to poultry. Other studies have presented evidence of clinical signs and neurological lesions resulting from infection but found that the pigeons did not transmit the disease to poultry reared in direct contact with them. Pigeons were found to be "resistant or minimally susceptible" to other strains of avian influenza, such as the H7N7 . Research into whether pigeons play a part in spreading bird flu have shown pigeons do not carry the deadly H5N1 strain. Three studies have been done since the late 1990s by the US Agriculture Department's Southeast Poultry Research Laboratory in Athens, Georgia, according to the center's director, David Swayne. The lab has been working on bird flu since the 1970s. In one experiment, researchers squirted into pigeons' mouths liquid drops that contained the highly pathogenic H5N1 virus from a Hong Kong sample. The birds received 100 to 1,000 times the concentration that wild birds would encounter in nature. "We couldn't infect the pigeons", Swayne said. "So that's good news."

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West Nile

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Culex quinquefasciatus

Culex quinquefasciatus (originally named Culex fatigans ), commonly known as the southern house mosquito , is a medium-sized mosquito found in tropical and subtropical regions of the world. It is a vector of Wuchereria bancrofti , avian malaria , and arboviruses including St. Louis encephalitis virus , Western equine encephalitis virus , Zika virus and West Nile virus . It is taxonomically regarded as a member of the Culex pipiens species complex . Its genome was sequenced in 2010, and was shown to have 18,883 protein-coding genes. American entomologist Thomas Say described Culex quinquefasciatus , which he collected along the Mississippi River , in 1823. Originally written as "C. 5-fasciatus", the name refers to 5 ( quinque ) black, broad, transverse bands ("fasciatus" or "fasciae") on the mosquito's dorsal abdomen. The name remains despite later revelations of more than 5 fasciae, thanks to improved microscopy. Although quinquefasciatus is the official scientific name, there are at least 5 synonymous names for this species. Cx. quinquefasciatus is a member of the Culex pipiens species complex . Smith et al. 2004 develop an assay specifically for this complex and use it to confirm that it does encompass this species. The adult C. quinquefasciatus is a medium-sized mosquito and is brown in colour. The body is about 3.96 to 4.25 mm long. While the main body is brown, the proboscis , thorax , wings , and tarsi are darker than the rest of the body. The head is light brown, with the lightest portion in the center. The antennae and the proboscis are about the same length, but in some cases, the antennae are slightly shorter than the proboscis. The flagellum has 13 segments that may have few or no scales . The scales of the thorax are narrow and curved. The abdomen has pale, narrow, rounded bands on the basal side of each tergite . Males can be differentiated from females in having large palps and feathery antennae. The larva has a short and stout head. The mouth brushes have long yellow filaments used for filtering organic materials. The abdomen consists of eight segments, the siphon , and the saddle . Each segment has a unique setae pattern. The siphon is on the dorsal side of the abdomen, and is four times longer than its breadth. The siphon has multiple setae tufts. The saddle is barrel-shaped and located on the ventral side of the abdomen, with four long anal papillae protruding from the posterior end. Mature C. quinquefasciatus females fly at night to nutrient-rich standing water to lay eggs. They breed profusely in dirty water collections, including stagnant drains, cesspools, septic tanks with leaks, burrow pits, and almost all organic polluted water collections. A single female can lay up to five rafts of eggs in a lifetime, with each raft containing 100 to 300 eggs. The exact number varies depending on climatic conditions. The larvae feed on organic material in the water and require between five and eight days to complete their development at 30 °C (86 °F) . The larvae pass through four larval instars , and towards the end of the fourth instar, they stop eating and undergo moulting to give rise to pupae . After 36 hours at 27 °C (81 °F) , adults emerge. The exact timing of development can vary depending on temperature. In optimum temperature and humidity, the lifecycle will be completed in seven days, passing through the egg, larval, pupal, and adult stages. [ citation needed ] Both male and female adults take sugar meals from plants. After mating, the female seeks a blood meal from a mammal or bird, as ingested blood is necessary for egg development. C. quinquefasciatus shows a preference for the blood of birds, but will also commonly bite humans. Known hosts include birds (Aves), cattle ( Bos taurus) , dogs ( Canis familiaris) , Equus including donkeys ( E. asinus) , cats ( Felis) , mice ( Mus musculus) , house sparrows ( Passer domesticus) , rats ( Rattus) and boars ( Sus scrofa) . "Quinx" are among the world's most abundant peridomestic mosquitoes, earning the nickname "southern house mosquito". The species' place of origin is uncertain. It may have been native to the lowlands of West Africa, or to Southeast Asia. Cx. quinquefasciatus is now found throughout subtropical and tropical areas worldwide, including the Americas, Australia and New Zealand, except for exceedingly dry or cold regions. Thomas Say described the species as "exceedingly numerous and troublesome". It rests in trees and high places. The southern house mosquito is a principal vector of numerous pathogens, transmitting the phlebovirus Rift Valley fever virus, and the two flaviviruses St. Louis encephalitis virus and West Nile virus, plus filarial worms and avian malarial parasites. It transmits zoonotic diseases that affect humans and wild and domestic animals, such as lymphatic filariasis , avian malaria , St. Louis encephalitis , Western equine encephalitis , and West Nile fever , and may be a vector of the Zika virus . It causes infection through biting during blood meal. In the southern U.S., it is the primary vector of St. Louis encephalitis virus. In India and Southeast Asia, it is the primary vector of Wuchereria bancrofti , a nematode that causes lymphatic filariasis . It acts as an intermediate host for the helminth parasite by harbouring the larval stages. In Hawaii , it is the principal vector of avian malaria ( Plasmodium relictum ), to which historic extinctions and significant contemporary population declines in Hawaii's native honeycreeper species are attributed. It is the definitive host for the malarial parasite as it harbours the sexual cycle. In 2013 West Nile Virus positive specimens were collected in Southern California. Now, people have to stop the invasive spread to save the native birds. [ failed verification ]

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Black-necked grebe

The black-necked grebe or eared grebe ( Podiceps nigricollis ) is a member of the grebe family of water birds. It was described in 1831 by Christian Ludwig Brehm . There are currently three accepted subspecies, including the nominate subspecies . Its breeding plumage features distinctive ochre-coloured feathers which extend behind its eye and over its ear coverts. The rest of the upper parts, including the head, neck, and breast, are coloured black to blackish brown. The flanks are tawny rufous to maroon-chestnut, and the abdomen is white. In its non-breeding plumage, this bird has greyish-black upper parts, including the top of the head and a vertical stripe on the back of the neck. The flanks are also greyish-black. The rest of the body is a white or whitish colour. The juvenile has more brown in its darker areas. The subspecies californicus can be distinguished from the nominate by the former's usually longer bill. The other subspecies, P. n. gurneyi , can be differentiated by its greyer head and upper parts and by its smaller size. P. n. gurneyi can also be told apart by its lack of a non-breeding plumage. This species is present in parts of Africa , Eurasia , and the Americas . The black-necked grebe uses multiple foraging techniques. Insects, which make up the majority of this bird's diet, are caught either on the surface of the water or when they are in flight; this species occasionally practices foliage gleaning . This grebe dives to catch crustaceans , molluscs , tadpoles, and small frogs and fish. When moulting at saline lakes, this bird feeds mostly on brine shrimp . The black-necked grebe makes a floating cup nest on an open lake. The nest cup is covered with a disc. This nest is located both in colonies and by itself. During the breeding season, which varies depending on location, this species will lay one (sometimes two) clutch of three to four eggs. The number of eggs is sometimes larger due to conspecific brood parasitism . After a 21-day incubation period, the eggs hatch, and then the nest is deserted. After about 10 days, the parents split up the chicks between themselves. After this, the chicks become independent in about 10 days, and fledge in about three weeks. Although it generally avoids flight, the black-necked grebe travels as far as 6,000 kilometres (3,700 mi) during migration . In addition, it becomes flightless for at least a month after completing a migration to reach an area where it can safely moult. During this moult, the grebe can double in weight. The migrations to reach these areas are dangerous, sometimes with thousands of grebe deaths. In spite of this, it is classified as a least concern species by the International Union for Conservation of Nature (IUCN). It is likely that this is the most numerous grebe in the world. There are potential threats to it, such as oil spills, but these are not likely to present a major risk to the overall population.This species was first described by Carl Ludwig Hablitz in 1783 as Colymbus caspicus , from a bird in Bandar-e Anzali . This was originally thought to be a synonym for the horned grebe , until Erwin Stresemann discovered that the description applied more to the black-necked grebe in 1948. Before this, the earliest description was thought to be by Christian Ludwig Brehm in 1831, who gave this bird its current scientific name of Podiceps nigricollis from a German bird. To resolve this, the International Commission on Zoological Nomenclature suppressed the name C. caspicus . The genus name Dytes is sometimes used for this species, a placement which was formalized by Robert Ridgway in 1881. This bird is closely related to the silvery grebe and the Junin grebe . The extinct Colombian grebe is sometimes considered to be a subspecies of this species, in addition to three other extant subspecies: The generic name, Podiceps , comes from two Latin words: podicis , meaning ' vent ' or ' anus ' , and pes meaning ' foot ' . This is a reference to the attachment point of the bird's legs—at the extreme back end of its body. The specific epithet nigricollis is Latin for ' black-necked ' : niger means ' black ' and collis means ' neck ' . The subspecies epithet californicus comes from "California", while gurneyi comes from the name of British ornithologist John Henry Gurney Sr. "Black-necked grebe" has been designated the official name by the International Ornithological Committee (IOC). Both common names for this species refer to features visible when the bird is in its breeding plumage; in such plumage, it has an all-black neck and a spray of golden plumes on each side of its head. The name "eared grebe" is nearly a century older than the name "black-necked grebe". The latter was first used in 1912 by Ernst Hartert, in an effort to bring the common name of the species in line with its scientific name. The name "eared grebe" is still used in North America to refer to this bird. The black-necked grebe usually measures between 28 and 34 centimetres (11 and 13 in) in length and weighs 265 to 450 grams (9.3 to 15.9 oz) . The bird has a wingspan range of 20.5–21.6 in (52–55 cm). The nominate subspecies in breeding plumage has the head, neck, breast, and upper parts coloured black to blackish brown, with the exception of the ochre -coloured fan of feathers extending behind the eye over the eye-coverts and sides of the nape. This eye is mostly red, with a narrow and paler yellow ring on the inner parts of the eye and an orange-yellow to pinkish-red orbital ring . The thin, upturned bill, on the other hand, is black, and is connected to the eye by a blackish line starting at the gape . Sometimes, the foreneck can be found to be mostly tinged brown. The upperwing is blackish to drab brown in colour and has a white patch formed by the secondaries and part of the inner primaries. The flanks are coloured tawny rufous to maroon-chestnut and have the occasional blackish fleck. The underwing and abdomen is white, with an exception to the former being the dark tertials and the mostly pale grey-brown outer primaries. The legs are a dark greenish grey. The sexes are similar. In non-breeding plumage, the nominate has greyish-black upper parts, cap, nape, and hindneck, with the colour on the upper portion of the latter being contained in a vertical stripe. The dark colour of the cap reaches below the eye and can be seen, diffused, to the ear-coverts. Behind the ear-coverts on the sides of the neck, there are white ovals. The rest of the neck is grey to brownish-grey in colour and has white that varies in amount. The breast is white, and the abdomen is whitish. The flanks are coloured in a mix of blackish-grey with white flecks. The colour of the bill when not breeding differs from that of the breeding plumage, with the former being significantly more grey. The juvenile black-necked grebe is similar to the non-breeding adult. There are differences, however, including the fact that the dark areas are usually more brownish in the juvenile, with less black. The lores are often tinged pale grey, with whitish marks behind the eye. On the sides of the head and upper neck, there is a buffy or tawny tinge. The chick is downy and has a blackish-grey head with stripes and spots that are white or pale buff-grey. The throat and foreneck are largely pale. The upper parts are mostly dark grey in colour, and the abdomen is white. The subspecies californicus usually has a longer bill compared to the nominate, and has brown-grey inner primaries during the breeding season. When not breeding, the nominate has diffuse and pale lores less often than Podiceps nigricollis californicus . The other subspecies, P. n. gurneyi , is the smallest of the three subspecies, in addition to having a greyer head and upper parts. The adult of this subspecies also has a rufous-brown tinge on its lesser wing-coverts. It also lacks a non-breeding plumage, in addition to the tufts on the side of its head being paler. When breeding, the black-necked grebe gives a quiet "ooeek" [ needs IPA ] that ascends in pitch from an already high pitch. This call is also used as a territorial call, in addition to a low and fast trill, which itself is also used during courtship. Another call is a short "puuii" or "wit". [ needs IPA ] This grebe is silent when it is not the breeding season and when it is feeding or resting. When breeding, the black-necked grebe gives a quiet "ooeek" [ needs IPA ] that ascends in pitch from an already high pitch. This call is also used as a territorial call, in addition to a low and fast trill, which itself is also used during courtship. Another call is a short "puuii" or "wit". [ needs IPA ] This grebe is silent when it is not the breeding season and when it is feeding or resting. This species breeds in vegetated areas of freshwater lakes across Europe, Asia , Africa, northern South America and the southwest and western United States. After breeding, this bird migrates to saline lakes to moult. Then, after completing the moult and waiting for sometimes several months, it migrates to winter in places such as the south-western Palearctic and the eastern parts of both Africa and Asia. It also winters in southern Africa, another place where it breeds. In the Americas , it winters as far south as Guatemala , although the wintering population there is mainly restricted to islands in the Gulf of California , the Salton Sea , and Baja California . When not breeding, its habitat is primarily saline lakes and coastal estuaries . This grebe is highly gregarious , usually forming large colonies when breeding and large flocks when not. This species builds its floating nest in the usually shallow water of open lakes. The nest itself is anchored to the lake by plants. It is built by both the male and the female and made out of plant matter. Most of it is submerged, with the bottom of the shallow cup usually being level with the water. Above the cup, there is a flat disc. This grebe nests both in colonies and by itself. When it does not nest by itself, it will often nest in mixed-species colonies made up of black-headed gulls , ducks , and various other waterbirds . The space between the nests in these colonies is often 1 to 2 metres (3.3 to 6.6 ft) . Whether it nests in colonies or not has an effect on the dimensions of the nest. When the bird is not in a colony, the nest has an average diameter of 28 centimetres (11 in) , although this can vary, with nests ranging from about 20 centimetres (8 in) to over 30 centimetres (12 in) . This is compared to nests in colonies, which have an average diameter of about 25.5 centimetres (10 in) . It is suggested that rarely some pairs of this grebe will steward over multiple nests when in colonies. Pair formation in the black-necked grebe usually starts during pauses in the migration to the breeding grounds, although it occasionally occurs before, in wintering pairs. This pair formation continues after this grebe has arrived to its breeding grounds. Courtship occurs when it arrives at the breeding lake. The displays are performed in the middle of the lake. There is no territory involved in courting; individuals use the whole area of the lake. When advertising for a mate, a black-necked grebe will approach others of its species with its body fluffed out and its neck erect. It closes its beak to perform a call, poo-eee-chk , with the last note only barely audible. Courtship generally stops at the start of nesting. In the Northern Hemisphere, this bird breeds from April to August. In east Africa, the breeding season is at least from January to February, while in southern Africa, the breeding season is from October to April. The black-necked grebe is socially monogamous . Conspecific or intraspecific brood parasitism , where the female lays eggs in the nest of others of their own species is common with nearly 40% of nests being parasitized on average. In terms of territory, this grebe will defend only its nest site. This grebe lays a clutch , sometimes two, of three to four chalky greenish or bluish eggs. Nests that have been parasitized, however, will have two more eggs on average, even though the number the host lays is about the same no matter if it has been parasitized or not. The eggs, although initially immaculate, do get stained by plant matter that the nest is built out of. The eggs measure 45 by 30 millimetres (1.8 by 1.2 in) on average and are incubated by both parents for about 21 days. The laying date of the eggs is somewhat synchronized, with birds in small colonies having the laying dates spread out by just a few days, compared to large colonies, where the laying date is spread out over more than 10 days. After the chicks hatch, the birds will desert their nest. Even though the young can swim and dive during this time, they rarely do, instead staying on the parents' backs for four days after hatching. This behaviour is present in all grebes, and is likely to have evolved because it reduces travel costs, specifically those back to the nest to brood the chicks and give them food. After about 10 days, the parents split the chicks up, with each parent taking care of about half of the brood. After this split, the chicks are independent in about 10 days, and fledge in about three weeks. When disturbed while incubating, this bird usually (just under 50% of the time) partly covers its eggs with nest material when the disruption is not sudden, but a bird with an incomplete clutch usually does not attempt to cover the eggs. When the disruption is sudden, on the other hand, the black-necked grebe usually (just under 50% of the time) does not cover its eggs. In comparison, other species of grebes cover up their eggs when leaving the nest. Predation is usually not the primary cause of egg loss, with most nesting failures occurring after the chicks have hatched. A major cause of this is the chilling of the young. The black-necked grebe forages mainly by diving from the water, with dives usually lasting less than 30 seconds. These dives are usually shorter in time when in more shallow water. In between dives, this grebe rests for an average of 15 seconds. When feeding on brine shrimp at hypersaline lakes, it likely uses its large tongue to block the oral cavity. It is hypothesized that it then crushes prey against its palate to remove excess water. It also forages by gleaning foliage, plucking objects off of the surface of water, having its head submerged while swimming, and sometimes capturing flying insects. This grebe eats mostly insects, of both adult and larval stages, as well as crustaceans , molluscs , tadpoles, and small frogs and fish. When moulting at lakes with high salinity, however, this bird feeds mostly on brine shrimp. The behaviour of black-necked grebes changes in response to the availability of brine shrimp; bodies of water with more shrimp have more grebes, and grebes spend more time foraging when the number of shrimp and the water temperature decrease. The young are fed one at a time by the parents, with one bird carrying the young while the other feeds it. The young take food by grabbing it, with their beaks, from their parents, or by grabbing food dropped into the water. When a young bird cannot grab the food, then the adults submerge their bill into the water and shake their bill to break up the food. When breeding is over, some black-necked grebes moult while still on the breeding grounds, but most do so only after a moult migration. This migration is to saline lakes, especially lakes with large numbers of invertebrate prey, so that birds can fatten up while moulting before continuing on the winter migration. The moult migration is dangerous, with hundreds and sometimes thousands of birds being killed by snowstorms when traveling to places such as Mono Lake . After the moult migration, birds moult their remiges between August and September, which makes them unable to fly. The moult is preceded by an increase in weight. During the moult, the breast muscles atrophy. When the moult is completed, birds continue to gain weight, often more than doubling their original weight. This additional fat is used to power the black-necked grebe's overnight fall migration to its wintering grounds. The fat is most concentrated in the abdomen, second most in the thorax, and least in the chest. Migration usually starts earlier when shrimp are more abundant and when the moulting lake is at a higher than average temperature. Birds generally leave on a clear night with lower than average surface temperatures. This grebe is one of the most inefficient fliers among birds. Generally, it avoids flying at all costs and reserves long-distance flight exclusively for migration. This is combined with the fact that this bird is flightless for 35–40 days during its moult. However, when migrating, it travels as much as 6,000 kilometres (3,700 miles) to reach rich feeding areas that are exploited by few other species. In flight, the shape of this grebe is like a loon : straight neck, legs trailing, and wings beating often. When diving, this bird pulls its head back and then arches it forward into the water, with the body following and a slight springing. The legs start moving only after they are underwater. When swimming on the surface of the water, the body of this grebe is relatively high, although none of the underparts are seen. The neck is held straight up in a relaxed manner, with the bill being held forward and parallel to the water. Each of the feet perform strong alternating strokes. This species builds its floating nest in the usually shallow water of open lakes. The nest itself is anchored to the lake by plants. It is built by both the male and the female and made out of plant matter. Most of it is submerged, with the bottom of the shallow cup usually being level with the water. Above the cup, there is a flat disc. This grebe nests both in colonies and by itself. When it does not nest by itself, it will often nest in mixed-species colonies made up of black-headed gulls , ducks , and various other waterbirds . The space between the nests in these colonies is often 1 to 2 metres (3.3 to 6.6 ft) . Whether it nests in colonies or not has an effect on the dimensions of the nest. When the bird is not in a colony, the nest has an average diameter of 28 centimetres (11 in) , although this can vary, with nests ranging from about 20 centimetres (8 in) to over 30 centimetres (12 in) . This is compared to nests in colonies, which have an average diameter of about 25.5 centimetres (10 in) . It is suggested that rarely some pairs of this grebe will steward over multiple nests when in colonies. Pair formation in the black-necked grebe usually starts during pauses in the migration to the breeding grounds, although it occasionally occurs before, in wintering pairs. This pair formation continues after this grebe has arrived to its breeding grounds. Courtship occurs when it arrives at the breeding lake. The displays are performed in the middle of the lake. There is no territory involved in courting; individuals use the whole area of the lake. When advertising for a mate, a black-necked grebe will approach others of its species with its body fluffed out and its neck erect. It closes its beak to perform a call, poo-eee-chk , with the last note only barely audible. Courtship generally stops at the start of nesting. In the Northern Hemisphere, this bird breeds from April to August. In east Africa, the breeding season is at least from January to February, while in southern Africa, the breeding season is from October to April. The black-necked grebe is socially monogamous . Conspecific or intraspecific brood parasitism , where the female lays eggs in the nest of others of their own species is common with nearly 40% of nests being parasitized on average. In terms of territory, this grebe will defend only its nest site. This grebe lays a clutch , sometimes two, of three to four chalky greenish or bluish eggs. Nests that have been parasitized, however, will have two more eggs on average, even though the number the host lays is about the same no matter if it has been parasitized or not. The eggs, although initially immaculate, do get stained by plant matter that the nest is built out of. The eggs measure 45 by 30 millimetres (1.8 by 1.2 in) on average and are incubated by both parents for about 21 days. The laying date of the eggs is somewhat synchronized, with birds in small colonies having the laying dates spread out by just a few days, compared to large colonies, where the laying date is spread out over more than 10 days. After the chicks hatch, the birds will desert their nest. Even though the young can swim and dive during this time, they rarely do, instead staying on the parents' backs for four days after hatching. This behaviour is present in all grebes, and is likely to have evolved because it reduces travel costs, specifically those back to the nest to brood the chicks and give them food. After about 10 days, the parents split the chicks up, with each parent taking care of about half of the brood. After this split, the chicks are independent in about 10 days, and fledge in about three weeks. When disturbed while incubating, this bird usually (just under 50% of the time) partly covers its eggs with nest material when the disruption is not sudden, but a bird with an incomplete clutch usually does not attempt to cover the eggs. When the disruption is sudden, on the other hand, the black-necked grebe usually (just under 50% of the time) does not cover its eggs. In comparison, other species of grebes cover up their eggs when leaving the nest. Predation is usually not the primary cause of egg loss, with most nesting failures occurring after the chicks have hatched. A major cause of this is the chilling of the young. The black-necked grebe forages mainly by diving from the water, with dives usually lasting less than 30 seconds. These dives are usually shorter in time when in more shallow water. In between dives, this grebe rests for an average of 15 seconds. When feeding on brine shrimp at hypersaline lakes, it likely uses its large tongue to block the oral cavity. It is hypothesized that it then crushes prey against its palate to remove excess water. It also forages by gleaning foliage, plucking objects off of the surface of water, having its head submerged while swimming, and sometimes capturing flying insects. This grebe eats mostly insects, of both adult and larval stages, as well as crustaceans , molluscs , tadpoles, and small frogs and fish. When moulting at lakes with high salinity, however, this bird feeds mostly on brine shrimp. The behaviour of black-necked grebes changes in response to the availability of brine shrimp; bodies of water with more shrimp have more grebes, and grebes spend more time foraging when the number of shrimp and the water temperature decrease. The young are fed one at a time by the parents, with one bird carrying the young while the other feeds it. The young take food by grabbing it, with their beaks, from their parents, or by grabbing food dropped into the water. When a young bird cannot grab the food, then the adults submerge their bill into the water and shake their bill to break up the food. When breeding is over, some black-necked grebes moult while still on the breeding grounds, but most do so only after a moult migration. This migration is to saline lakes, especially lakes with large numbers of invertebrate prey, so that birds can fatten up while moulting before continuing on the winter migration. The moult migration is dangerous, with hundreds and sometimes thousands of birds being killed by snowstorms when traveling to places such as Mono Lake . After the moult migration, birds moult their remiges between August and September, which makes them unable to fly. The moult is preceded by an increase in weight. During the moult, the breast muscles atrophy. When the moult is completed, birds continue to gain weight, often more than doubling their original weight. This additional fat is used to power the black-necked grebe's overnight fall migration to its wintering grounds. The fat is most concentrated in the abdomen, second most in the thorax, and least in the chest. Migration usually starts earlier when shrimp are more abundant and when the moulting lake is at a higher than average temperature. Birds generally leave on a clear night with lower than average surface temperatures. This grebe is one of the most inefficient fliers among birds. Generally, it avoids flying at all costs and reserves long-distance flight exclusively for migration. This is combined with the fact that this bird is flightless for 35–40 days during its moult. However, when migrating, it travels as much as 6,000 kilometres (3,700 miles) to reach rich feeding areas that are exploited by few other species. In flight, the shape of this grebe is like a loon : straight neck, legs trailing, and wings beating often. When diving, this bird pulls its head back and then arches it forward into the water, with the body following and a slight springing. The legs start moving only after they are underwater. When swimming on the surface of the water, the body of this grebe is relatively high, although none of the underparts are seen. The neck is held straight up in a relaxed manner, with the bill being held forward and parallel to the water. Each of the feet perform strong alternating strokes. Large-scale deaths (such as 150,000 birds on the Salton Sea in 1992) from erysipelas , avian cholera, avian botulism , and West Nile virus have been recorded in the past. In 2013 at the Great Salt Lake, for example, there was an outbreak of West Nile virus which caused one of the largest recorded avian die-offs in the US. The cause of the outbreak and modes of transmission are unknown, but there has been speculation about the latter. Since West Nile virus is able to survive in brine shrimp (and, for a temporary time, water at specific temperatures), it is likely that grebes could have become infected by eating diseased shrimp and/or swimming in the contaminated water. It is also theorized that West Nile virus could be transmitted among grebes through contact with the excrement of an infected bird, possibly around bodies of water, communal nest sites, areas of cohabitating birds, etc. Avian cholera, another disease that can cause massive die-offs in this species, is transmitted by currently-unknown biotoxins and/or pathogens, as well as problems with feather waterproofing putting birds at risk. As of 2016, the black-necked grebe is classified as least concern by the International Union for Conservation of Nature (IUCN). The trend of the population is uncertain, as some populations are decreasing, whereas others are stable, have an uncertain trend, or are increasing. The justification for the current classification of this species is its very large population (estimated around 3.9–4.2 million individuals) combined with a large estimated extent of occurrence (about 155 million km 2 (60 million sq mi)). This grebe is probably the most numerous grebe in the world. Unknown biotoxins , pathogens, and the impairment of feather waterproofing can lead to hypothermia and avian cholera . Since this grebe usually winters on the coast, it is also vulnerable to oil pollution. Large-scale disease, such as avian cholera, could threaten the species. These and other factors, such as human disturbance, including collisions with power transmission lines, contribute to declining populations in certain areas. This species used to be threatened in North America by the millinery industry, which helped facilitate the hunting of the birds, and egg collectors. Although this is true, this grebe is hunted in the Gilan Province in Iran, for both commercial and recreational purposes. However, there is no evidence suggesting that these threats could result in a significant risk for the overall population.

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DEET

InChI=1S/C12H17NO/c1-4-13(5-2)12(14)11-8-6-7-10(3)9-11/h6-9H,4-5H2,1-3H3 Y Key: MMOXZBCLCQITDF-UHFFFAOYSA-N Y InChI=1S/C12H17NO/c1-4-13(5-2)12(14)11-8-6-7-10(3)9-11/h6-9H,4-5H2,1-3H3 Key: MMOXZBCLCQITDF-UHFFFAOYAE O=C(c1cc(ccc1)C)N(CC)CC N , N -Diethyl- meta -toluamide , also called diethyltoluamide or DEET ( / d iː t / , from DET, the initials of di- + ethyl + toluamide), is the oldest, most effective and most common active ingredient in commercial insect repellents . It is a slightly yellow oil intended to be applied to the skin or to clothing and provides protection against mosquitoes , flies, ticks , fleas , chiggers , leeches , and many other biting insects. Unlike Icaridin , DEET emits an odor that many find unpleasant, leaves skin greasy, dissolves plastics and synthetic fabrics and interacts negatively with sunscreen. DEET and icaridin are the most effective insect repellents available. DEET is effective against a variety of invertebrates, including ticks, flies, mosquitos, and some parasitic worms. A 2018 systematic review found no consistent performance difference between DEET and icaridin in field studies and concluded that they are equally preferred mosquito repellents, noting that 50% DEET offers longer protection but is not available in some countries. The concentration of DEET in products may range from less than 10% to nearly 100%, but concentrations greater than 50% do not increase the duration of protection. Higher concentrations can be safely applied to clothing, although it may damage some types of synthetic fibers. In the United Kingdom, the publicly-funded healthcare system, the National Health Service (NHS), recommends that UK citizens should use a concentration of 50% when visiting areas of the world with malaria. A lower concentration of 10% is recommended for infants and children. Health Canada decided to limit DEET concentration to 30% in the country since 2002 due to an increased long-term risk observed with repeated applications. DEET is often sold and used in spray or lotion in concentrations up to 100%. Consumer Reports found a direct correlation between DEET concentration and hours of protection against insect bites. 100% DEET was found to offer up to 12 hours of protection while several lower concentration DEET formulations (20–34%) offered 3–6 hours of protection. [ citation needed ] Other research has corroborated the effectiveness of DEET. The Centers for Disease Control and Prevention recommends 30–50% DEET to prevent the spread of pathogens carried by insects. A 2008 study found that higher concentrations of DEET have an improved ability to repel insects through fabric. The concentration of DEET in products may range from less than 10% to nearly 100%, but concentrations greater than 50% do not increase the duration of protection. Higher concentrations can be safely applied to clothing, although it may damage some types of synthetic fibers. In the United Kingdom, the publicly-funded healthcare system, the National Health Service (NHS), recommends that UK citizens should use a concentration of 50% when visiting areas of the world with malaria. A lower concentration of 10% is recommended for infants and children. Health Canada decided to limit DEET concentration to 30% in the country since 2002 due to an increased long-term risk observed with repeated applications. DEET is often sold and used in spray or lotion in concentrations up to 100%. Consumer Reports found a direct correlation between DEET concentration and hours of protection against insect bites. 100% DEET was found to offer up to 12 hours of protection while several lower concentration DEET formulations (20–34%) offered 3–6 hours of protection. [ citation needed ] Other research has corroborated the effectiveness of DEET. The Centers for Disease Control and Prevention recommends 30–50% DEET to prevent the spread of pathogens carried by insects. A 2008 study found that higher concentrations of DEET have an improved ability to repel insects through fabric. DEET should not be used on children younger than 2 months of age. When used as directed, products containing between 10% and 30% DEET have been found by the American Academy of Pediatrics to be safe to use on children as well as adults. As a precaution, manufacturers advise that DEET products should not be used under clothing or on damaged skin, and that preparations be washed off after they are no longer needed or between applications. DEET can irritate the eyes and, unlike icaridin , it can cause breathing difficulty, headaches , or, in rare cases, it may cause severe epidermal reactions. The authors of a 2002 study published in The New England Journal of Medicine wrote: ... this repellent has been subjected to more scientific and toxicologic scrutiny than any other repellent substance. ... DEET has a remarkable safety profile after 40 years of use and nearly 8 billion human applications. Fewer than 50 cases of serious toxic effects have been documented in ... medical literature since 1960 ... Many of these cases of toxic effects involved long-term, heavy, frequent, or whole-body application of DEET. No correlation has been found between the concentration of DEET used and the risk of toxic effects. ... When applied with common sense, DEET-based repellents can be expected to provide a safe as well as a long-lasting repellent effect ... under circumstances in which it is crucial to be protected against arthropod bites that might transmit disease. In the DEET Reregistration Eligibility Decision (RED) in 1998, the United States Environmental Protection Agency (EPA) reported 14 to 46 cases of potential DEET-associated seizures , including four deaths. The EPA states: "... it does appear that some cases are likely related to DEET toxicity ," which may underreport the risk as physicians may fail to check for history of DEET use or fail to report cases of seizure subsequent to DEET use. In 1997, the Pesticide Information Project of Cooperative Extension Offices of Cornell University stated that " Everglades National Park employees having extensive DEET exposure were more likely to have insomnia , mood disturbances and impaired cognitive function than lesser exposed co-workers". Citing human health reasons, Health Canada barred the sale of insect repellents for human use that contained more than 30% DEET in a 2002 re-evaluation "based on a human health risk assessment that considered daily application of DEET over a prolonged period of time". The agency recommended that DEET-based products be used on children between the ages of 2 and 12 only if the concentration of DEET is 10% or less and that repellents be applied no more than 3 times a day, children under 2 should not receive more than 1 application of repellent in a day and DEET-based products of any concentration should not be used on infants under 6 months. A 2020 study performed by students within the University of Florida 's College of Public Health and Health Professions analyzed data from the National Health and Nutrition Examination Survey and identified 1,205 participants who had "DEET metabolic levels recorded at or above detection limits". They analyzed biomarkers related to systemic inflammation, immune, liver, and kidney functions, and found no "evidence that DEET exposure has any impact on the biomarkers identified." DEET may be measured in blood, plasma, or urine by gas or liquid chromatography-mass spectrometry to confirm a diagnosis of poisoning in hospitalized patients or to provide evidence in a medicolegal death investigation. Blood or plasma DEET concentrations are expected to be in a range of 0.3–3.0 mg/L during the first 8 hours after dermal application in persons using the chemical appropriately, >6 mg/L in intoxicated patients and >100 mg/L in victims of acute intentional oral overdose. DEET may be measured in blood, plasma, or urine by gas or liquid chromatography-mass spectrometry to confirm a diagnosis of poisoning in hospitalized patients or to provide evidence in a medicolegal death investigation. Blood or plasma DEET concentrations are expected to be in a range of 0.3–3.0 mg/L during the first 8 hours after dermal application in persons using the chemical appropriately, >6 mg/L in intoxicated patients and >100 mg/L in victims of acute intentional oral overdose. Applying DEET to the skin is safe if done as directed. Adverse reactions are very rare, about 1 in 100 million people. However, repeated use of DEET in very high concentrations can lead to toxic encephalopathy with severe neurological symptoms including seizures, tremors and slurred speech. The risk is higher for children since they have a greater surface area to body weight ratio. Limited data indicates that combining insect repellents with DEET and sunscreen decreases the sun protection factor of the sunscreen by about a third. Unlike icaridin , the combination also increases the absorption of both significantly. When the two need to be used together, the repellent should be applied after the sunscreen has been absorbed, about 30 or more minutes later. When DEET is used in combination with insecticides for cockroaches it can strengthen the toxicity of carbamate , an acetylcholinesterase inhibitor. These 1996 findings indicate that DEET has neurological effects on insects in addition to known olfactory effects, and that its toxicity is strengthened in combination with other insecticides. Unlike icaridin , DEET is an effective solvent and may dissolve some watch crystals, plastics, rayon , spandex , other synthetic fabrics , and painted or varnished surfaces including nail polish. It also may act as a plasticizer by remaining inside some formerly hard plastics, leaving them softened and more flexible. DEET is incompatible with rayon, acetate , or dynel clothing. Though DEET is not expected to bioaccumulate , it has been found to have a slight toxicity for fresh-water fish such as rainbow trout and tilapia , and it also has been shown to be toxic for some species of freshwater zooplankton . DEET has been detected at low concentrations in water bodies as a result of production and use, such as in the Mississippi River and its tributaries, where a 1991 study detected levels varying from 5 to 201 ng /L. A 1975 study analyzed the effects of DEET on communities of freshwater organisms native to Chinese waterways and found that DEET was moderately toxic to aquatic organisms compared to other commercial insect repellants. The most-at-risk organisms were algae colonies which often experienced "significant biomass decline and community composition shift[s]" when exposed to DEET at 500 ng/L. DEET is biodegraded by fungi into products less toxic to zooplankton. It degrades well under aerobic conditions, but poorly and slowly under anaerobic conditions. DEET is thought to provide protection from mosquitos via two pathways, both by negatively impacting mosquito odorant receptors at a distance, and by negatively impacting mosquito chemoreceptors upon contact. The exact mechanisms are still being researched, but the two most likely hypotheses are the "smell and avoid hypothesis" (that DEET has an unpleasant odor to insects), and the "bewilderment hypothesis" (that smelling DEET confuses insects). A slightly yellow liquid at room temperature , it can be prepared by converting m -toluic acid (3-methylbenzoic acid) to the corresponding acyl chloride using thionyl chloride (SOCl 2 ), and then allowing that product to react with diethylamine : DEET was developed in 1944 by Samuel Gertler of the United States Department of Agriculture for use by the United States Army , following its experience of jungle warfare during World War II . It was originally tested as a pesticide on farm fields, and entered military use in 1946 and civilian use in 1957. It was used in Vietnam and Southeast Asia. In its original form, known as "bug juice", the application solution was composed of 75% DEET and 25% ethanol. Later, a new version of the repellent was developed by the U.S. Army and the USDA. This formulation consisted of DEET and a mixture of polymers that extended its release and reduced its evaporation rate. This extended-release application was registered by the Environmental Protection Agency in 1991.

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West Nile

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London Underground mosquito

The London Underground mosquito is a form of mosquito in the genus Culex . It is found in the London Underground railway system as its name suggests, but has a worldwide distribution and long predates the existence of the London Underground. It was first described as a distinct species from Egyptian specimens by the biologist Peter Forsskål (1732–1763). He named this mosquito Culex molestus due to its voracious biting, but later biologists renamed it Culex pipiens f. molestus because there were no morphological differences between it and Culex pipiens . Notably, this mosquito assaulted Londoners sleeping in the Underground during the Blitz , although similar populations were long known. A study from 2004 analyzing DNA microsatellites suggested that Culex molestus is likely a distinct species from Culex pipiens . However, a more recent paper from 2012 argues that it is more accurately "a physiological and ecological variant of Cx. pipiens " and should not be considered a distinct species. This mosquito, first identified in Egypt in the late 18th century, has been found in underground systems around the world. Some authors suggested that it adapted to human-made underground systems since the last century from local above-ground Culex pipiens , but the more recent evidence suggests it is a southern mosquito variety related to C. pipiens that has adapted to the warm underground spaces of northern cities. Behavioral evidence for this mosquito being a different species from C. pipiens comes from research by Kate Byrne and Richard Nichols. The species have very different behaviours, are extremely difficult to mate, and with different allele frequencies consistent with genetic drift during a founder event . More specifically, this mosquito, C. molestus , breeds all-year round, is cold intolerant, and bites rats, mice, and humans, in contrast to the above-ground species, which is cold tolerant, hibernates in the winter, and is considered to mostly feed on bird hosts. When the two varieties were crossbred, the eggs were infertile, suggesting reproductive isolation. The mosquito has been documented to feed upon birds. For decades Cx. molestus was known only as a fully competent host of one kind of malaria, Plasmodium garnhami . Only this Plasmodium had been demonstrated to complete sporogony by Garnham 1966. Due to this lack of study a team investigated whether a more common kind of malaria could also go through the life cycle. Žiegytė et al. 2014 find that P. relictum also completes sporogony in Cx. molestus . They also discovered that two P. relictum strains differing only by one base pair produced markedly different parasitemia of the insect; pGRW11 much more than pSGS1 . Genetic data indicate the molestus form in the London Underground appear to have a common ancestry, rather than the population at each station being related to the nearest above-ground population. Byrne and Nichols' working hypothesis was that adaptation to the underground environment had occurred locally in London once only – many hurdles must be overcome to become adapted to the subterranean environment, and understandably it would occur rarely. This hypothesis implies that local adaptation would be expected in different locations around Europe and beyond, as each local population evolved an offshoot that overcame the problems of living underground. However, more recently collected genetic evidence reported by Fonseca and others suggests a single C. molestus form has spread throughout Europe and beyond, since populations over a large area share a common genetic heritage. These widely separated populations are distinguished by very minor genetic differences, which suggest the underground form developed recently; a single mtDNA difference is shared among the underground populations of 10 Russian cities, and a single fixed microsatellite difference occurs in populations spanning Europe, Japan, Australia, the Middle East, and the Atlantic islands. This worldwide spread might have occurred after the last glaciations or may be even more recent, due to the insects hitchhiking on world trade routes; one possibility is the international secondhand tire trade. The tires retain water in which the larvae can survive, and completely removing water from an old tire can be difficult. Also, the Fonseca paper obtained genetic evidence that the recent colonization of America by Culex mosquitoes actually involves a strain derived from a rare successful hybridization between C. pipiens and C. molestus . They suggest hybridization may explain why the American form bites both birds and humans (this interpretation is controversial, see letter from Spielman et al. and the response that follows it in Science ). The consequences of this more indiscriminate feeding hit the news in 1999 with the outbreak of human encephalitis in New York, caused by West Nile virus. It was the first documented introduction of this virus into the Western Hemisphere; perhaps because in the longer established populations, the Old World northern above-ground C. pipiens almost exclusively bites birds, with the human-biting ones being incarcerated below ground.Culex molestus has been observed in North and South America, Europe, Asia, Africa, and Australasia. It was first described in Egypt in the late 1700s, and has likely spread via trade and colonial passages over the past centuries. In the summer of 2011, an invasion of Culex molestus appeared on the Upper West Side in Manhattan , New York City . The mosquito is well known for being commonly found in sewers of New York and thriving throughout the year feeding on humans. Residents of older brownstones found the mosquitoes coming into basements and then through air vents and other openings into their homes. The city government did not make this infestation of the pest a top priority because they tested negative for West Nile virus and because of the high cost of mosquito control. In Australia , Culex molestus was first recorded in the 1940s, and has since spread across all southern states, causing a significant biting nuisance in urban areas. Unlike most Australian urban mosquitos, molestus is active through all 12 months of the year. Its introduction was likely through military movements into Melbourne during World War II, and genetic studies have indicated its most likely passage was from eastern Asia and Japan. It has also been identified as a potential vector for several Australian blood-borne diseases, such as Ross River virus .

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Japanese encephalitis

Japanese encephalitis ( JE ) is an infection of the brain caused by the Japanese encephalitis virus (JEV). While most infections result in little or no symptoms, occasional inflammation of the brain occurs . In these cases, symptoms may include headache, vomiting, fever, confusion and seizures . This occurs about 5 to 15 days after infection. JEV is generally spread by mosquitoes , specifically those of the Culex type. Pigs and wild birds serve as a reservoir for the virus. The disease occurs mostly outside of cities. Diagnosis is based on blood or cerebrospinal fluid testing. Prevention is generally achieved with the Japanese encephalitis vaccine , which is both safe and effective. Other measures include avoiding mosquito bites. Once infected, there is no specific treatment, with care being supportive . This is generally carried out in a hospital. Permanent problems occur in up to half of people who recover from JE. The disease primarily occurs in East and Southeast Asia as well as the Western Pacific . About 3 billion people live in areas where the disease occurs. About 68,000 symptomatic cases occur a year, with about 17,000 deaths. Often, cases occur in outbreaks . The disease was first described in Japan in 1871 . The Japanese encephalitis virus (JEV) has an incubation period of 2 to 26 days. The vast majority of infections are asymptomatic : only 1 in 250 infections develop into encephalitis. Severe rigors may mark the onset of this disease in humans. Fever, headache and malaise are other non-specific symptoms of this disease which may last for a period of between 1 and 6 days. Signs which develop during the acute encephalitic stage include neck rigidity, cachexia , hemiparesis , convulsions and a raised body temperature between 38–41 °C (100.4–105.8 °F) . The mortality rate of the disease is around 25% and is generally higher in children under five, the immuno-suppressed and the elderly. Transplacental spread has been noted. Neurological disorders develop in 40% of those who survive with lifelong neurological defects such as deafness, emotional lability and hemiparesis occurring in those who had central nervous system involvement. Increased microglial activation following Japanese encephalitis infection has been found to influence the outcome of viral pathogenesis. Microglia are the resident immune cells of the central nervous system (CNS) and have a critical role in host defense against invading microorganisms. Activated microglia secrete cytokines, such as interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF-α) , which can cause toxic effects in the brain. Additionally, other soluble factors such as neurotoxins , excitatory neurotransmitters , prostaglandin , reactive oxygen , and nitrogen species are secreted by activated microglia. [ citation needed ] In a murine model of JE, it was found that in the hippocampus and the striatum , the number of activated microglia was more than anywhere else in the brain, closely followed by that in the thalamus . In the cortex, the number of activated microglia was significantly less when compared to other regions of the mouse brain . An overall induction of differential expression of proinflammatory cytokines and chemokines from different brain regions during a progressive Japanese encephalitis infection was also observed. [ citation needed ] Although the net effect of the proinflammatory mediators is to kill infectious organisms and infected cells as well as to stimulate the production of molecules that amplify the mounting response to damage, it is also evident that in a nonregenerating organ such as the brain, a dysregulated innate immune response would be deleterious. In JE the tight regulation of microglial activation appears to be disturbed, resulting in an autotoxic loop of microglial activation that possibly leads to bystander neuronal damage. In animals, key signs include infertility and abortion in pigs, neurological disease in horses, and systemic signs including fever, lethargy and anorexia. It is a disease caused by the mosquito -borne Japanese encephalitis virus (JEV). JEV is a virus from the family Flaviviridae , part of the Japanese encephalitis serocomplex of 9 genetically and antigenically related viruses, some which are particularly severe in horses , and four known to infect humans including West Nile virus . The enveloped virus is closely related to the West Nile virus and the St. Louis encephalitis virus. The positive sense single-stranded RNA genome is packaged in the capsid which is formed by the capsid protein. The outer envelope is formed by envelope protein and is the protective antigen. It aids in entry of the virus into the cell. The genome also encodes several nonstructural proteins (NS1, NS2a, NS2b, NS3, N4a, NS4b, NS5). NS1 is produced as a secretory form also. NS3 is a putative helicase , and NS5 is the viral polymerase . It has been noted that Japanese encephalitis infects the lumen of the endoplasmic reticulum (ER) and rapidly accumulates substantial amounts of viral proteins. Based on the envelope gene, there are five genotypes (I–V). The Muar strain, isolated from a patient in Malaya in 1952, is the prototype strain of genotype V. Genotype V is the earliest recognized ancestral strain. The first clinical reports date from 1870, but the virus appears to have evolved in the mid-16th century. Over sixty complete genomes of this virus had been sequenced by 2010. [ citation needed ]JEV is a virus from the family Flaviviridae , part of the Japanese encephalitis serocomplex of 9 genetically and antigenically related viruses, some which are particularly severe in horses , and four known to infect humans including West Nile virus . The enveloped virus is closely related to the West Nile virus and the St. Louis encephalitis virus. The positive sense single-stranded RNA genome is packaged in the capsid which is formed by the capsid protein. The outer envelope is formed by envelope protein and is the protective antigen. It aids in entry of the virus into the cell. The genome also encodes several nonstructural proteins (NS1, NS2a, NS2b, NS3, N4a, NS4b, NS5). NS1 is produced as a secretory form also. NS3 is a putative helicase , and NS5 is the viral polymerase . It has been noted that Japanese encephalitis infects the lumen of the endoplasmic reticulum (ER) and rapidly accumulates substantial amounts of viral proteins. Based on the envelope gene, there are five genotypes (I–V). The Muar strain, isolated from a patient in Malaya in 1952, is the prototype strain of genotype V. Genotype V is the earliest recognized ancestral strain. The first clinical reports date from 1870, but the virus appears to have evolved in the mid-16th century. Over sixty complete genomes of this virus had been sequenced by 2010. [ citation needed ]Japanese encephalitis is diagnosed by commercially available tests detecting JE virus-specific IgM antibodies in serum and/or cerebrospinal fluid , for example by IgM capture ELISA . JE virus IgM antibodies are usually detectable 3 to 8 days after onset of illness and persist for 30 to 90 days, but longer persistence has been documented. Therefore, positive IgM antibodies occasionally may reflect a past infection or vaccination. Serum collected within 10 days of illness onset may not have detectable IgM, and the test should be repeated on a convalescent sample. For patients with JE virus IgM antibodies, confirmatory neutralizing antibody testing should be performed. Confirmatory testing in the US is available only at the CDC and a few specialized reference laboratories. In fatal cases, nucleic acid amplification and virus culture of autopsy tissues can be useful. Viral antigen can be shown in tissues by indirect fluorescent antibody staining . Infection with Japanese encephalitis confers lifelong immunity . There are currently three vaccines available: SA14-14-2, IXIARO (IC51, also marketed in Australia, New Zealand as JESPECT and India as JEEV ) and ChimeriVax-JE (marketed as IMOJEV). All current vaccines are based on the genotype III virus. [ citation needed ] A formalin -inactivated mouse-brain-derived vaccine was first produced in Japan in the 1930s and was validated for use in Taiwan in the 1960s and in Thailand in the 1980s. The widespread use of vaccine and urbanization has led to control of the disease in Japan and Singapore. The high cost of this vaccine, which is grown in live mice, means that poorer countries have not been able to afford to give it as part of a routine immunization program. The most common adverse effects are redness and pain at the injection site. Uncommonly, an urticarial reaction can develop about four days after injection. Vaccines produced from mouse brain have a risk of autoimmune neurological complications of around 1 per million vaccinations. However where the vaccine is not produced in mouse brains but in vitro using cell culture there are few adverse effects compared to placebo , the main side effects being headache and myalgia . The neutralizing antibody persists in the circulation for at least two to three years, and perhaps longer. The total duration of protection is unknown, but because there is no firm evidence for protection beyond three years, boosters are recommended every three years for people who remain at risk. Furthermore, there are no data available regarding the interchangeability of other JE vaccines and IXIARO. [ citation needed ]There is no specific treatment for Japanese encephalitis and treatment is supportive, with assistance given for feeding , breathing or seizure control as required. Raised intracranial pressure may be managed with mannitol . There is no transmission from person to person and therefore patients do not need to be isolated. [ citation needed ] A breakthrough in the field of Japanese encephalitis therapeutics is the identification of macrophage receptor involvement in the disease severity. A recent report of an Indian group demonstrates the involvement of monocyte and macrophage receptor CLEC5A in severe inflammatory response in Japanese encephalitis infection of the brain. This transcriptomic study provides a hypothesis of neuroinflammation and a new lead in development of appropriate therapies for Japanese encephalitis. The effectiveness of intravenous immunoglobulin for the management of encephalitis is unclear due to a lack of evidence. Intravenous immunoglobulin for Japanese encephalitis appeared to have no benefit. Japanese encephalitis (JE) is the leading cause of viral encephalitis in Asia , with up to 70,000 cases reported annually. Case-fatality rates range from 0.3% to 60% and depend on the population and age. Rare outbreaks in U.S. territories in the Western Pacific have also occurred. Residents of rural areas in endemic locations are at highest risk; Japanese encephalitis does not usually occur in urban areas. [ citation needed ] Countries which have had major epidemics in the past, but which have controlled the disease primarily by vaccination, include China , South Korea , Singapore , Japan , Taiwan and Thailand . Other countries that still have periodic epidemics include Vietnam , Cambodia , Myanmar , India , Nepal , and Malaysia . Japanese encephalitis has been reported in the Torres Strait Islands , and two fatal cases were reported in mainland northern Australia in 1998. There were reported cases in Kachin State , Myanmar in 2013. There were 116 deaths reported in Odisha's Malkangiri district of India in 2016. [ citation needed ] In 2022, the notable increase in distribution of the virus in Australia due to climate change became a concern to health officials as the population has limited immunity to the disease and the presence of large numbers of farmed and feral pigs could act as reservoirs for the virus. In February 2022, Japanese encephalitis was detected and confirmed in piggeries in Victoria, Queensland and New South Wales. On 4 March, cases were detected in South Australia. By October 2022, the outbreak in eastern mainland Australia had caused 42 symptomatic human cases of the disease, resulting in seven deaths. Humans, cattle, and horses are dead-end hosts as the disease manifests as fatal encephalitis. Pigs act as an amplifying host and have a very important role in the epidemiology of the disease. Infection in swine is asymptomatic, except in pregnant sows, when abortion and fetal abnormalities are common sequelae. The most important vector is Culex tritaeniorhynchus , which feeds on cattle in preference to humans. The natural hosts of the Japanese encephalitis virus are birds, not humans, and many believe the virus will therefore never be eliminated. In November 2011, the Japanese encephalitis virus was reported in Culex bitaeniorhynchus in South Korea . Recently, whole genome microarray research of neurons infected with the Japanese encephalitis virus has shown that neurons play an important role in their own defense against Japanese encephalitis infection. Although this challenges the long-held belief that neurons are immunologically quiescent, an improved understanding of the proinflammatory effects responsible for immune-mediated control of viral infection and neuronal injury during Japanese encephalitis infection is an essential step for developing strategies for limiting the severity of CNS disease. A number of drugs have been investigated to either reduce viral replication or provide neuroprotection in cell lines or studies upon mice. None are currently advocated in treating human patients.It is theorized that the virus may have originated from an ancestral virus in the mid-1500s in the Malay Archipelago region and evolved there into five different genotypes which spread across Asia. The mean evolutionary rate has been estimated to be 4.35 × 10 −4 (range: 3.49 × 10 −4 to 5.30 × 10 −4 ) nucleotide substitutions per site per year.

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Fish crow

The fish crow ( Corvus ossifragus ) is a species of crow associated with wetland habitats in the eastern and southeastern United States.The fish crow was given its binomial name by the Scottish ornithologist Alexander Wilson in 1812, in the fifth volume of his American Ornithology . The binomial is from Latin ; Corvus means "raven", while ossifragus means "bone-breaker". It is derived from os or ossis , meaning "bone", and frangere , meaning "to break". The English-language common name fish crow also derives from Wilson, who ascribed the name to the crow's aquatic diet, as described to him by local fishermen. He distinguished the fish crow from John Bartram 's great seaside crow by the former's diminutive size when compared to the American crow . The fish crow's taxonomic relation to other species of the Corvus genus is still poorly understood, but DNA sequencing indicates that it is most closely related to the palm crow ( C. palmarum ) and the Jamaican crow ( C. jamaicensis ), with the three species forming a Nearctic clade . The Sinaloa crow ( C. sinaloae ) and Tamaulipas crow ( C. imparatus ) bear morphological similarities to and were once considered conspecific subspecies of the fish crow, but have since been recognized as distinct species. The fish crow is a small bird, with an average adult weight of 280–320 grams (9.9–11.3 oz) in males and 247–293 grams (8.7–10.3 oz) in females. The average male wingspan is similarly larger at 278–292 millimetres (10.9–11.5 in) , compared to 264–277 millimetres (10.4–10.9 in) in females. The total body length is between 36–40 centimetres (14–16 in) . The fish crow is superficially similar to the American crow, but is smaller and has a silkier, smoother plumage by comparison. The upperparts have a blue or blue-green sheen, while the underparts have a more greenish tint to the black. The eyes are dark brown. The differences are often only really apparent between the two species when seen side by side or when heard calling. The bill is usually somewhat slimmer than the American crow, but is only readily distinguishable if both species are seen together. Visual differentiation from the American crow is extremely difficult and often inaccurate. Nonetheless, differences apart from size do exist. Fish crows tend to have more slender bills and feet. There may also be a small sharp hook at the end of the upper bill. Fish crows also appear as if they have shorter legs when walking. More dramatically, when calling, fish crows tend to hunch and fluff their throat feathers. The voice is the most outwardly differing characteristic for this species and other American crow species. The call of the fish crow has been described as a nasal "ark-ark-ark" or a begging "waw-waw". Birders often distinguish the two species (in areas where their range overlaps) with the mnemonic aid "Just ask him if he is an American crow. If he says "no", he is a fish crow." referring to the fact that the most common call of the American crow is a distinct "caw caw", while that of the fish crow is a nasal "nyuh unh". The fish crow also has a single call sounding like "cahrrr". This species occurs on the eastern seaboard of the United States from Rhode Island south to Key West , and west along the northern coastline of the Gulf of Mexico . Coastal marshes and beaches, rivers, inland lakes and marshes, river banks, and the land immediately surrounding all are frequented. Fish crows are also found along many river systems inland for quite some distance, having expanded their range along rivers since the early 1900s. Since 2012, fish crows have rapidly expanded into Canada , with breeding populations along Lake Ontario . Food is taken mainly from the ground or shallow water where the bird hovers and plucks food items out of the water with its feet. The fish crow is omnivorous. It feeds on small crustaceans , such as crabs and shrimps , other invertebrates, stranded fish, and live fish if the situation favors their capture, eggs and nestlings of birds, small reptiles, the fruits of many trees, peanuts, and grains, as well as human scraps where available. The nest is usually built high in a tree and is often accompanied in nearby trees with other nests of the same species forming small, loose colonies. Usually, four or five eggs are laid. Pale blue-green in colour, they bear blotches of olive-brown. Fish crows build a new nest for each breeding attempt. A pair of fish crows were reported to have raised a young blue jay for multiple weeks. Food is taken mainly from the ground or shallow water where the bird hovers and plucks food items out of the water with its feet. The fish crow is omnivorous. It feeds on small crustaceans , such as crabs and shrimps , other invertebrates, stranded fish, and live fish if the situation favors their capture, eggs and nestlings of birds, small reptiles, the fruits of many trees, peanuts, and grains, as well as human scraps where available. The nest is usually built high in a tree and is often accompanied in nearby trees with other nests of the same species forming small, loose colonies. Usually, four or five eggs are laid. Pale blue-green in colour, they bear blotches of olive-brown. Fish crows build a new nest for each breeding attempt. A pair of fish crows were reported to have raised a young blue jay for multiple weeks. This species appears to be somewhat more resistant to West Nile virus than the American crow. Survival rates of up to 45% have been reported for fish crows, compared with near zero for American crows.

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Arua

Arua is a city and commercial centre within the Arua District in the Northern Region of Uganda . Arua is approximately 475 kilometres (295 mi) north-west of Kampala , the capital and largest city of Uganda, Arua is about 228 kilometres (142 mi) , by road, west of Gulu , the largest city in Uganda's Northern Region. The geographical coordinates of the city of Arua are 03°02'07.0"N, 30°54'39.0"E (Latitude:3.035278; Longitude:30.910833). Arua sits at an average elevation of 1,310 metres (4,298 ft) above sea level. Arua is closely bordered to the Democratic Republic of Congo in the west and South Sudan in the north, which makes it a strategic location for business between Uganda and her two neighbors to the west and north. Due to its strategic location, Arua is also part of the refugee program of hosting up to 20% of the refugees entering Uganda annually. Arua is an important base for non-governmental organizations working in the West Nile sub-region or serving Western Equatoria in South Sudan and the northeastern Democratic Republic of the Congo . It became an important commercial supply centre and transport route when the Juba - Yei - Morobo - Kaya Road opened, enabling supplies to come into Juba from the south on the Kaya Highway instead of through Khartoum from the north. A branch of the Uganda Railways was to be extended to Arua sometime after 1964, but there has been no passenger rail service in Uganda for many years. The Vurra–Arua–Koboko–Oraba Road passes through town, in a south–north direction. Arua is connected to the other towns in West Nile by road. These are: Nebbi, Pakwach, Paidha, Koboko, Yumbe, Moyo, Obongi, Adjumani and other smaller towns. There is regular road transport between Arua and Kampala, Gulu, Masindi and Hoima The city is served by Arua Airport , which has scheduled air service. Arua airport has been the second busiest in Uganda after Entebbe. It was due to be upgraded to an international airport.The 1969 national census enumerated the population of Arua Town at 10,837. In 1991, the census enumerated 22,217 people in the town. In 2002, the population had increased to 43,929. The August 2014 national census and household survey enumerated the population of Arua Town Council at 61,962. In 2020, the Uganda Bureau of Statistics (UBOS) estimated the mid-year population to be 72,400. UBOS calculated that the population of Arua Municipality grew at an average rate of 2.7 percent annually, between 2014 and 2020. Arua has a tropical savanna climate ( Köppen climate classification Aw ).The following administrations are seated in Arua: Analog broadcasts, which originate from Kampala, include WBS TV (which is currently closed), UBC TV , and NTV . In early 2014, MBC 2 was aired in Arua as a test broadcast to pave way for Vision Group's Urban TV. Voice of Life, a Church of Uganda -founded radio station, has pioneered FM broadcasting in Arua since 1997. The following administrations are seated in Arua:Analog broadcasts, which originate from Kampala, include WBS TV (which is currently closed), UBC TV , and NTV . In early 2014, MBC 2 was aired in Arua as a test broadcast to pave way for Vision Group's Urban TV. Voice of Life, a Church of Uganda -founded radio station, has pioneered FM broadcasting in Arua since 1997.

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Shooting Star (band)

Shooting Star is an American rock band from Kansas City , Missouri . The band was formed in the late 1970s. After gaining popularity in the Kansas City area, Shooting Star became the first American group to sign with Virgin Records . They recorded their 1979 debut album in England with producer Gus Dudgeon . The band gained national exposure when a number of songs garnered moderate airplay on album-oriented rock radio stations in the US. Shooting Star initially consisted of Van McLain (guitars, vocals), Bill Guffey (keyboards), Steve Thomas (drums), Ron Verlin (bass), Charles Waltz (violin, keyboards, vocals), and Gary West (lead vocals, guitars, keyboards).Shooting Star was formed in suburban Kansas City by childhood friends Ron Verlin and Van McLain (born Van Allen McElvain on May 3, 1955, in Kansas City, Missouri; died March 2, 2018). They were next-door neighbors and good friends. They created a band with their brothers, Craig McLain and John Verlin, and played Beatles records in Ron's grandmother's garage. Two years later, Van and Craig had moved to different school districts and the band split up. Upon entering Shawnee Mission South High School , Van and Ron met up again. With the 1950s nostalgia craze of 1971 brewing, they played classic 1950s hits. After seeing Sha Na Na in the movie Woodstock , they added three dancers to the act and called the band The Shooting Stars featuring The Galaxies, the name inspired by Bill Haley & His Comets .By 1974, Van began serious songwriting. The band decided to stop playing cover songs and perform their own music. Later that year, they recorded a four-song demo tape and planned a trip to London , England to shop their songs for a record deal. They left on January 6, 1975, and after three weeks of shopping their music to different record labels, they were offered a recording contract with Arista Records . Upon signing, The Shooting Stars were then given the opportunity to play a showcase performance at the legendary Marquee Club in London. The band then made their way to Morgan Studios to record their first single, Take the Money & Run . Shortly after this record was cut, Steve Miller released his song Take the Money & Run , which became a huge hit. Arista Records then released The Shooting Stars from their contract, and they returned to Kansas City. In 1977 Van persuaded fellow musician Gary West (born Gary Hodgden) to join them as a singer and songwriting partner. Gary, with his brother Ron West, had been a member of the premier Kansas City rock band of the 1960s, The Chesmann Square. After The Chesmann dissolved in 1974, Ron West formed the band Missouri and Gary West moved with the Chesmann's lead guitarist Jim McAllister to New York City. There they formed the group The Beckies with songwriter Michael Brown , formerly of the group The Left Banke , and former Kansas Citian Scott Trusty. The Beckies released one album on Sire Records . Upon Gary's return to Kansas City, he and Van began songwriting in earnest. Later on, in 1977, they added Ron Verlin on bass, Steve Thomas on drums, and Bill Guffey on keyboards for a new lineup of The Shooting Stars. With the addition of Charles Waltz on violin, keyboards, and vocals in early 1978, the name was shortened to Shooting Star and they started recording demos in Gary's garage, all the while playing gigs around the Midwest. After saving enough money and putting a press kit together they tried to secure another record deal in New York City. Through connections that Gary had made while a member of The Beckies, the band booked a showcase at the punk rock club CBGB . The representative for a New York management firm was in the crowd that night and offered them a contract. With a management deal secured, Shooting Star returned to Kansas City to continue writing new material. Six months later, the band's management arranged for them to play another showcase at the New York City club Tracks. Three record companies, Atlantic Records , Virgin Records , and A&M Records , made offers to sign the band. Virgin, then a small British record label, succeeded. The label was looking for a rock group to break into the US market, and Shooting Star became the first American band on their roster. In May 1979 Shooting Star returned to London to record their eponymous debut album with producer Gus Dudgeon of Elton John fame. The album Shooting Star was released in January 1980, and the band embarked on a national tour opening for Robin Trower and Triumph . With their debut, the band gained popularity with the songs "You Got What I Need," "Tonight," "Bring It On," and "Last Chance." "Wild In the Streets", a B-side release, was a staple of live show encores; the song was eventually released on CD as a bonus track. "You Got What I Need" ended up peaking at #76 on the Billboard Hot 100 . The debut album stalled out at #147 on the Billboard Top 200 and Van McLain explained his version as to why: "We had the number one most played AOR song in the country with 'Last Chance' and our record company, Virgin, had gotten into a fight with Atlantic Records , who was their distribution. We ended up not being able to get our album in the stores for six months. We should have sold a ton of albums from having that popular of a song on the radio, but when people went to the stores, they couldn't buy the album because it was not in the stores." With the radio success, and Virgin switching over to Epic Records for their distribution, Shooting Star returned to the studio in 1981 to record Hang On for Your Life (July 1981) with producer Dennis McKay. The album generated FM airplay with the songs "Flesh and Blood," "Breakout" and the title track. "Hollywood" was released as a single and climbed the Billboard Hot 100 , topping out at #70. In support of the album, the band toured with ZZ Top , Cheap Trick , Todd Rundgren , Jefferson Starship , and Journey . They appeared on the radio shows Rock Line, King Biscuit Flower Hour (KBFH), The Source , and Westwood One . [ citation needed ] Keyboardist Bill Guffey left the group after the recording of Hang On for Your Life . In 1982 Shooting Star began recording their third album, III Wishes (July 1982), at the legendary Caribou Ranch studio near Boulder, Colorado . At the helm was Journey producer Kevin Elson. Without missing a beat, they returned to touring with such acts as REO Speedwagon , John Mellencamp , Jefferson Starship , Kansas , and others. 1983 saw their continued collaboration with Kevin Elson on their fourth album, Burning (June 1983). This record produced the songs "Straight Ahead," "Winner" and "Train Rolls On." In 1984 the band experienced the departure of bassist Ron Verlin, who had become disenchanted with the music industry. Bassist Norm Dahlor was recruited to take over for Ron. That same year the band was asked to record two songs for the movie soundtrack Up the Creek . The songs were "Get Ready Boy" and "Take It." Virgin Records then picked up Geffen Records as their distributor and the group began to record their fifth album, Silent Scream , with producer Ron Nevison . It was released in April 1985 and produced the radio hit "Summer Sun." The band's accompanying music video was popular on MTV and other video channels. Van, Norm, and Steve were also the backing band on Ian Hunter 's single "Great Expectations." The band then toured with Heart , Bryan Adams , and ZZ Top . In 1986, after almost a decade of touring and five albums, Shooting Star decided to go on hiatus. A farewell show was played on December 27, 1986, at Memorial Hall in Kansas City, Kansas and after a few more concerts, Shooting Star went their separate ways in late spring of 1987. Gary West, with Van McLain's help, began work on demos that were more in a pop/rhythm and blues direction. CBS Records signed West but then lost interest. Guitarist McLain, in a 2013 interview with Goldmine Magazine , explained why the group disbanded: "We signed with Geffen, and we put out Silent Scream . Geffen got into a fight with all the radio promo guys, and they fired them the week our album came out. We had 200 ads on the radio, out of 300 reporting stations, in the first week. 'Summer Sun' was being added everywhere, and it looked like the album would be a smash. After the fight with the promo guys, it dropped to 40 stations. What do you do? We really worked hard on that record, and it was the one. It just crushed Gary when it all fell apart over something that ridiculous; It literally drove him out of the music business. You put your heart and soul into this stuff, and you expect these business guys to come through for you. We got hosed four or five times. Over the next several years fans from around the world were frustrated by not being able to find Shooting Star records, which all went out of print, while the band continued to receive radio airplay". Being dropped by CBS further discouraged Gary, and he left the music business. In July 1989 V&R Records, the band's own label, acquired the rights to release The Best of Shooting Star . This release marked the first time that any Shooting Star record appeared on CD and included two previously unreleased songs, "Christmas Together," a 1985 single which had been played on Kansas City radio, and "Touch Me Tonight," a new song by Van which peaked on the Billboard Hot 100 at #67. Enigma Records, a heavy metal label that was starting to acquire more mainstream artists, bought the rights to the album and retitled it Touch Me Tonight – The Best Of Shooting Star . In the November 4, 1989, issue of Billboard, the album was the first album to reach that magazine's pop albums chart without being available as a vinyl record. The band also released the first two albums on one CD called Shooting Star/Hang on for Your Life ; it omitted two songs from the albums ("Stranger" and "Sweet Elatia"). This CD became a collectible until the release of the band's entire catalog on CD. With the success of The Best Of and fans' desire for new material, Shooting Star was offered a new recording contract with Enigma Records . Returning to the group were original members Ron Verlin, Van McLain, and Steve Thomas. The other members were Dennis Laffoon on keyboards and vocalist Keith Mitchell. Charles Waltz was originally slated to rejoin but had moved to California and was busy with another band, Toledo Waltz, while Gary West had left the music business entirely. Thomas played drums on "Touch Me Tonight" but departed shortly afterward as he was unable to commit to music full-time during this period. He was subsequently replaced by Rod Lincoln. In Los Angeles, the band made a video for "Touch Me Tonight." It received extensive airplay on MTV , making their request chart and rose to #67 on the Billboard Hot 100 . This was the highest-charting single of the band's career. The song also appeared in the Dolph Lundgren movie I Come in Peace . In February 1991 the band released their sixth effort, It's Not Over . During the recording of this project, Enigma Records went bankrupt, and the group decided to finish it on their own. Released on their own V & R label, the album received critical acclaim throughout Europe and helped broaden the Shooting Star audience. After the album's release, Ron Verlin was replaced on bass by Eric Johnson (not the famous guitarist) and the band toured with Bad English , Bryan Adams , and 38 Special . After selling about 10,000 copies of It's Not Over , the group was contacted by JRS Records (whose parent company was SCS Music), which agreed to take over distribution of the album nationally. But the group became dissatisfied with JRS, claiming they did very little to promote the album, and filed a lawsuit against them on October 14, 1992, in Johnson County, Kansas District Court. By 1993, disappointed over the collapse of Enigma, the JRS fiasco and the general decline in popularity of classic rock music, the band went into semi-retirement but resurfaced each year to play occasional concerts with Verlin back on bass. In 1997 the violin became a part of their sound again with the addition of violinist Terry Brock (not the same guy who performed as a background vocalist with Kansas on their Drastic Measures tour). In 1998, after recovering from a battle with esophageal cancer, Van was asked to perform at a cancer benefit concert in Chicago. On stage were members of Night Ranger , Cheap Trick , Survivor and 38 Special. Van received a heartfelt response from the fans and his friends on stage, which rekindled interest in playing again. Upon returning home from the show, he began writing songs and contemplated recording them. In the summer of 1999, while vacationing in Nashville , Tennessee , Van was reunited with producer/engineer Kevin Beamish . Kevin and Van had met 20 years earlier while Shooting Star was recording its first album. At that time, Kevin was a young engineer for Gus Dudgeon . Out of this chance meeting grew the plans to record and release Shooting Star's seventh album, Leap of Faith (July 2000). The recording took place at Sound Stage Studios in Nashville, Tennessee from December 1999 through February 2000. Shooting Star celebrated its 20th year as recording artists in 2000 with the release of Leap of Faith and a fall tour. Shane Michaels joined as the band's new violinist in May 2000, replacing Christian Howes (1999–2000), who had replaced Terry Brock. Original drummer Steve Thomas returned to the fold in late 2003 and singer Keith Mitchell left in the summer of 2005 after reported voice problems. In July 2006 the group released the album Circles with Kevin Chalfant (ex-member of 707 and The Storm ) handling the lead vocals, but since Chalfant was unable to commit to touring, he was replaced in 2007 by Ronnie Platt. Original keyboardist Bill Guffey (born William Guffey III on July 28, 1952) died on April 12, 2007, at age 54. Violinist Shane Michaels left the band in June 2008 to concentrate on another project, Flannigan's Right Hook, and was replaced by Janet Jameson. Bassist Ron Verlin, who had left the group twice before (in 1984 and 1991) and had taken temporary leaves of absence since his return in 1994, departed permanently in 2009; since then, Laffoon has covered the position of bassist. Shooting Star was inducted into the Kansas Music Hall Of Fame on March 7, 2009. The band performed at Liberty Hall in Lawrence, Kansas with the McLain, Thomas, Lafoon, Platt, Jameson lineup, with special guest Ron Verlin on bass, and for two songs, original vocalist Gary West. Other former members were on hand that evening but did not perform. Ronnie Platt left the band in 2011 to work with Chicago band Arra. His final performance with Shooting Star was in September 2010, leading to a period between 2011 and 2012 where, for the first and only time in the band's history, Van McLain was the band's sole lead vocalist (with occasional help from the band's violinist, Janet Jameson). McLain spent the first part of 2012 focusing on a solo project to be released by Alligator Records before returning to Shooting Star in the second half of 2012 (This album, New Blue , finally received an official release in 2022, four years after Van's passing). Keith Mitchell returned as lead vocalist in 2012 but left again in 2013 due to health problems. Janet Jameson also left the band at this time. Topeka, Kansas native Todd Pettygrove, from the band Vandelyn Kross, then joined in June 2013 as the new lead singer, making his live debut with the group the following month at Moondance Jam in Walker, Minnesota . Shooting Star returned to the UK in October 2013 to play "Firefest", the melodic rock festival that takes place each year at Nottingham Rock City . In July 2014, former Shooting Star vocalist Ronnie Platt joined Kansas as the replacement for departing lead vocalist Steve Walsh . Marking 35 years since their first album, Shooting Star released Into the Night in July 2015, which was initially available as a free download at the band's website. During this time period, Van McLain, Dennis Laffoon and Steve Thomas, in addition to their Shooting Star duties, had also performed in the Overland Park, Kansas area as a trio – The Star Blues Band. In September 2015 McLain experienced "flu-like" symptoms that became increasingly worse. After experiencing slurred speech, he was taken to the emergency room where he began to show severe symptoms of encephalitis . He was diagnosed with West Nile fever (only the second confirmed case of West Nile in Kansas in 2015). After several weeks of treatment for West Nile, Van began to move past the initial virus stage, but the virus had weakened him to such a point he had been hospitalized for over 8 months while dealing with a variety of respiratory and pulmonary issues that resulted from his condition. On September 24, 2017, a special Shooting Star Relief Fund concert was held in Kansas City to assist McLain with his continuing recovery from West Nile fever. The concert featured members of the KC music scene including The Elders , 2nd House, members of The Rainmakers , and a Shooting Star Past & Present performance with Steve Thomas, Dennis Laffoon, and Todd Pettygrove performing with guests Gary West, Ron Verlin, Norm Dahlor, Janet Jameson, and Pettygrove's former bandmate Chet Galloway, handpicked and standing in for Van, on guitar. Shooting Star had remained inactive since McLain's illness began in 2015. McLain died on March 2, 2018, from complications of his West Nile virus infection, at age 62. Shooting Star announced in late 2018 they would play a concert on January 19, 2019, in Kansas City with a revamped lineup to include former violin player Janet Jameson and new guitarist/vocalist Chet Galloway. According to the band's official website, McLain's family fully supported a reforming and continuation of Shooting Star, and the current lineup planned to announce additional shows. By 1974, Van began serious songwriting. The band decided to stop playing cover songs and perform their own music. Later that year, they recorded a four-song demo tape and planned a trip to London , England to shop their songs for a record deal. They left on January 6, 1975, and after three weeks of shopping their music to different record labels, they were offered a recording contract with Arista Records . Upon signing, The Shooting Stars were then given the opportunity to play a showcase performance at the legendary Marquee Club in London. The band then made their way to Morgan Studios to record their first single, Take the Money & Run . Shortly after this record was cut, Steve Miller released his song Take the Money & Run , which became a huge hit. Arista Records then released The Shooting Stars from their contract, and they returned to Kansas City. In 1977 Van persuaded fellow musician Gary West (born Gary Hodgden) to join them as a singer and songwriting partner. Gary, with his brother Ron West, had been a member of the premier Kansas City rock band of the 1960s, The Chesmann Square. After The Chesmann dissolved in 1974, Ron West formed the band Missouri and Gary West moved with the Chesmann's lead guitarist Jim McAllister to New York City. There they formed the group The Beckies with songwriter Michael Brown , formerly of the group The Left Banke , and former Kansas Citian Scott Trusty. The Beckies released one album on Sire Records . Upon Gary's return to Kansas City, he and Van began songwriting in earnest. Later on, in 1977, they added Ron Verlin on bass, Steve Thomas on drums, and Bill Guffey on keyboards for a new lineup of The Shooting Stars. With the addition of Charles Waltz on violin, keyboards, and vocals in early 1978, the name was shortened to Shooting Star and they started recording demos in Gary's garage, all the while playing gigs around the Midwest. After saving enough money and putting a press kit together they tried to secure another record deal in New York City. Through connections that Gary had made while a member of The Beckies, the band booked a showcase at the punk rock club CBGB . The representative for a New York management firm was in the crowd that night and offered them a contract. With a management deal secured, Shooting Star returned to Kansas City to continue writing new material.Six months later, the band's management arranged for them to play another showcase at the New York City club Tracks. Three record companies, Atlantic Records , Virgin Records , and A&M Records , made offers to sign the band. Virgin, then a small British record label, succeeded. The label was looking for a rock group to break into the US market, and Shooting Star became the first American band on their roster. In May 1979 Shooting Star returned to London to record their eponymous debut album with producer Gus Dudgeon of Elton John fame. The album Shooting Star was released in January 1980, and the band embarked on a national tour opening for Robin Trower and Triumph . With their debut, the band gained popularity with the songs "You Got What I Need," "Tonight," "Bring It On," and "Last Chance." "Wild In the Streets", a B-side release, was a staple of live show encores; the song was eventually released on CD as a bonus track. "You Got What I Need" ended up peaking at #76 on the Billboard Hot 100 . The debut album stalled out at #147 on the Billboard Top 200 and Van McLain explained his version as to why: "We had the number one most played AOR song in the country with 'Last Chance' and our record company, Virgin, had gotten into a fight with Atlantic Records , who was their distribution. We ended up not being able to get our album in the stores for six months. We should have sold a ton of albums from having that popular of a song on the radio, but when people went to the stores, they couldn't buy the album because it was not in the stores." With the radio success, and Virgin switching over to Epic Records for their distribution, Shooting Star returned to the studio in 1981 to record Hang On for Your Life (July 1981) with producer Dennis McKay. The album generated FM airplay with the songs "Flesh and Blood," "Breakout" and the title track. "Hollywood" was released as a single and climbed the Billboard Hot 100 , topping out at #70. In support of the album, the band toured with ZZ Top , Cheap Trick , Todd Rundgren , Jefferson Starship , and Journey . They appeared on the radio shows Rock Line, King Biscuit Flower Hour (KBFH), The Source , and Westwood One . [ citation needed ] Keyboardist Bill Guffey left the group after the recording of Hang On for Your Life . In 1982 Shooting Star began recording their third album, III Wishes (July 1982), at the legendary Caribou Ranch studio near Boulder, Colorado . At the helm was Journey producer Kevin Elson. Without missing a beat, they returned to touring with such acts as REO Speedwagon , John Mellencamp , Jefferson Starship , Kansas , and others. 1983 saw their continued collaboration with Kevin Elson on their fourth album, Burning (June 1983). This record produced the songs "Straight Ahead," "Winner" and "Train Rolls On." In 1984 the band experienced the departure of bassist Ron Verlin, who had become disenchanted with the music industry. Bassist Norm Dahlor was recruited to take over for Ron. That same year the band was asked to record two songs for the movie soundtrack Up the Creek . The songs were "Get Ready Boy" and "Take It." Virgin Records then picked up Geffen Records as their distributor and the group began to record their fifth album, Silent Scream , with producer Ron Nevison . It was released in April 1985 and produced the radio hit "Summer Sun." The band's accompanying music video was popular on MTV and other video channels. Van, Norm, and Steve were also the backing band on Ian Hunter 's single "Great Expectations." The band then toured with Heart , Bryan Adams , and ZZ Top .In 1986, after almost a decade of touring and five albums, Shooting Star decided to go on hiatus. A farewell show was played on December 27, 1986, at Memorial Hall in Kansas City, Kansas and after a few more concerts, Shooting Star went their separate ways in late spring of 1987. Gary West, with Van McLain's help, began work on demos that were more in a pop/rhythm and blues direction. CBS Records signed West but then lost interest. Guitarist McLain, in a 2013 interview with Goldmine Magazine , explained why the group disbanded: "We signed with Geffen, and we put out Silent Scream . Geffen got into a fight with all the radio promo guys, and they fired them the week our album came out. We had 200 ads on the radio, out of 300 reporting stations, in the first week. 'Summer Sun' was being added everywhere, and it looked like the album would be a smash. After the fight with the promo guys, it dropped to 40 stations. What do you do? We really worked hard on that record, and it was the one. It just crushed Gary when it all fell apart over something that ridiculous; It literally drove him out of the music business. You put your heart and soul into this stuff, and you expect these business guys to come through for you. We got hosed four or five times. Over the next several years fans from around the world were frustrated by not being able to find Shooting Star records, which all went out of print, while the band continued to receive radio airplay". Being dropped by CBS further discouraged Gary, and he left the music business. In July 1989 V&R Records, the band's own label, acquired the rights to release The Best of Shooting Star . This release marked the first time that any Shooting Star record appeared on CD and included two previously unreleased songs, "Christmas Together," a 1985 single which had been played on Kansas City radio, and "Touch Me Tonight," a new song by Van which peaked on the Billboard Hot 100 at #67. Enigma Records, a heavy metal label that was starting to acquire more mainstream artists, bought the rights to the album and retitled it Touch Me Tonight – The Best Of Shooting Star . In the November 4, 1989, issue of Billboard, the album was the first album to reach that magazine's pop albums chart without being available as a vinyl record. The band also released the first two albums on one CD called Shooting Star/Hang on for Your Life ; it omitted two songs from the albums ("Stranger" and "Sweet Elatia"). This CD became a collectible until the release of the band's entire catalog on CD.With the success of The Best Of and fans' desire for new material, Shooting Star was offered a new recording contract with Enigma Records . Returning to the group were original members Ron Verlin, Van McLain, and Steve Thomas. The other members were Dennis Laffoon on keyboards and vocalist Keith Mitchell. Charles Waltz was originally slated to rejoin but had moved to California and was busy with another band, Toledo Waltz, while Gary West had left the music business entirely. Thomas played drums on "Touch Me Tonight" but departed shortly afterward as he was unable to commit to music full-time during this period. He was subsequently replaced by Rod Lincoln. In Los Angeles, the band made a video for "Touch Me Tonight." It received extensive airplay on MTV , making their request chart and rose to #67 on the Billboard Hot 100 . This was the highest-charting single of the band's career. The song also appeared in the Dolph Lundgren movie I Come in Peace . In February 1991 the band released their sixth effort, It's Not Over . During the recording of this project, Enigma Records went bankrupt, and the group decided to finish it on their own. Released on their own V & R label, the album received critical acclaim throughout Europe and helped broaden the Shooting Star audience. After the album's release, Ron Verlin was replaced on bass by Eric Johnson (not the famous guitarist) and the band toured with Bad English , Bryan Adams , and 38 Special . After selling about 10,000 copies of It's Not Over , the group was contacted by JRS Records (whose parent company was SCS Music), which agreed to take over distribution of the album nationally. But the group became dissatisfied with JRS, claiming they did very little to promote the album, and filed a lawsuit against them on October 14, 1992, in Johnson County, Kansas District Court. By 1993, disappointed over the collapse of Enigma, the JRS fiasco and the general decline in popularity of classic rock music, the band went into semi-retirement but resurfaced each year to play occasional concerts with Verlin back on bass. In 1997 the violin became a part of their sound again with the addition of violinist Terry Brock (not the same guy who performed as a background vocalist with Kansas on their Drastic Measures tour). In 1998, after recovering from a battle with esophageal cancer, Van was asked to perform at a cancer benefit concert in Chicago. On stage were members of Night Ranger , Cheap Trick , Survivor and 38 Special. Van received a heartfelt response from the fans and his friends on stage, which rekindled interest in playing again. Upon returning home from the show, he began writing songs and contemplated recording them. In the summer of 1999, while vacationing in Nashville , Tennessee , Van was reunited with producer/engineer Kevin Beamish . Kevin and Van had met 20 years earlier while Shooting Star was recording its first album. At that time, Kevin was a young engineer for Gus Dudgeon . Out of this chance meeting grew the plans to record and release Shooting Star's seventh album, Leap of Faith (July 2000). The recording took place at Sound Stage Studios in Nashville, Tennessee from December 1999 through February 2000.Shooting Star celebrated its 20th year as recording artists in 2000 with the release of Leap of Faith and a fall tour. Shane Michaels joined as the band's new violinist in May 2000, replacing Christian Howes (1999–2000), who had replaced Terry Brock. Original drummer Steve Thomas returned to the fold in late 2003 and singer Keith Mitchell left in the summer of 2005 after reported voice problems. In July 2006 the group released the album Circles with Kevin Chalfant (ex-member of 707 and The Storm ) handling the lead vocals, but since Chalfant was unable to commit to touring, he was replaced in 2007 by Ronnie Platt. Original keyboardist Bill Guffey (born William Guffey III on July 28, 1952) died on April 12, 2007, at age 54. Violinist Shane Michaels left the band in June 2008 to concentrate on another project, Flannigan's Right Hook, and was replaced by Janet Jameson. Bassist Ron Verlin, who had left the group twice before (in 1984 and 1991) and had taken temporary leaves of absence since his return in 1994, departed permanently in 2009; since then, Laffoon has covered the position of bassist. Shooting Star was inducted into the Kansas Music Hall Of Fame on March 7, 2009. The band performed at Liberty Hall in Lawrence, Kansas with the McLain, Thomas, Lafoon, Platt, Jameson lineup, with special guest Ron Verlin on bass, and for two songs, original vocalist Gary West. Other former members were on hand that evening but did not perform. Ronnie Platt left the band in 2011 to work with Chicago band Arra. His final performance with Shooting Star was in September 2010, leading to a period between 2011 and 2012 where, for the first and only time in the band's history, Van McLain was the band's sole lead vocalist (with occasional help from the band's violinist, Janet Jameson). McLain spent the first part of 2012 focusing on a solo project to be released by Alligator Records before returning to Shooting Star in the second half of 2012 (This album, New Blue , finally received an official release in 2022, four years after Van's passing). Keith Mitchell returned as lead vocalist in 2012 but left again in 2013 due to health problems. Janet Jameson also left the band at this time. Topeka, Kansas native Todd Pettygrove, from the band Vandelyn Kross, then joined in June 2013 as the new lead singer, making his live debut with the group the following month at Moondance Jam in Walker, Minnesota . Shooting Star returned to the UK in October 2013 to play "Firefest", the melodic rock festival that takes place each year at Nottingham Rock City . In July 2014, former Shooting Star vocalist Ronnie Platt joined Kansas as the replacement for departing lead vocalist Steve Walsh . Marking 35 years since their first album, Shooting Star released Into the Night in July 2015, which was initially available as a free download at the band's website. During this time period, Van McLain, Dennis Laffoon and Steve Thomas, in addition to their Shooting Star duties, had also performed in the Overland Park, Kansas area as a trio – The Star Blues Band. In September 2015 McLain experienced "flu-like" symptoms that became increasingly worse. After experiencing slurred speech, he was taken to the emergency room where he began to show severe symptoms of encephalitis . He was diagnosed with West Nile fever (only the second confirmed case of West Nile in Kansas in 2015). After several weeks of treatment for West Nile, Van began to move past the initial virus stage, but the virus had weakened him to such a point he had been hospitalized for over 8 months while dealing with a variety of respiratory and pulmonary issues that resulted from his condition. On September 24, 2017, a special Shooting Star Relief Fund concert was held in Kansas City to assist McLain with his continuing recovery from West Nile fever. The concert featured members of the KC music scene including The Elders , 2nd House, members of The Rainmakers , and a Shooting Star Past & Present performance with Steve Thomas, Dennis Laffoon, and Todd Pettygrove performing with guests Gary West, Ron Verlin, Norm Dahlor, Janet Jameson, and Pettygrove's former bandmate Chet Galloway, handpicked and standing in for Van, on guitar. Shooting Star had remained inactive since McLain's illness began in 2015. McLain died on March 2, 2018, from complications of his West Nile virus infection, at age 62. Shooting Star announced in late 2018 they would play a concert on January 19, 2019, in Kansas City with a revamped lineup to include former violin player Janet Jameson and new guitarist/vocalist Chet Galloway. According to the band's official website, McLain's family fully supported a reforming and continuation of Shooting Star, and the current lineup planned to announce additional shows. Steve Thomas – drums (1977–1987, 1989, 2003–present) Dennis Laffoon – keyboards, bass, backing vocals (1989–present) Janet Jameson – violin, vocals (2008–2013, 2018–present) Todd Pettygrove – lead vocals (2013–present) Chet Galloway – lead vocals, guitars (2018–present) Bill Guffey – keyboards (1977–1981; died 2007) Van McLain – lead vocals, guitars (1977–1987, 1989–2018; his death) Ron Verlin – bass (1977–1983, 1989–1991, 1994–2009) Charles Waltz – violin, keyboards, backing vocals (1977–1987) Gary West – lead vocals, guitars, keyboards (1977–1987) Norm Dahlor – bass (1984–1987) Keith Mitchell – lead vocals (1989–2005, 2012–2013) Rod Lincoln – drums (1989–2003) Eric Johnson – bass (1991–1994) Terry Brock – violin (1997–1999) Christian Howes – violin (1999–2000) Shane Michaels – violin (2000–2008) Kevin Chalfant – lead vocals (2005–2007) Ronnie Platt – lead vocals (2007–2011) Bill Guffey – keyboards Van McLain – lead vocals, guitars Steve Thomas – drums Ron Verlin – bass Charles Waltz – violin, keyboards, backing vocals Gary West – lead vocals, guitars, keyboards Van McLain – lead vocals, guitars Steve Thomas – drums Ron Verlin – bass Charles Waltz – violin, keyboards, backing vocals Gary West – lead vocals, guitars, keyboards Van McLain – lead vocals, guitars Steve Thomas – drums Charles Waltz – violin, keyboards, backing vocals Gary West – lead vocals, guitars, keyboards Norm Dahlor – bass Disbanded Van McLain – lead vocals, guitars Steve Thomas – drums Dennis Laffoon – keyboards, backing vocals Keith Mitchell – lead vocals Ron Verlin – bass Van McLain – lead vocals, guitars Dennis Laffoon – keyboards, backing vocals Keith Mitchell – lead vocals Ron Verlin – bass Rod Lincoln – drums Van McLain – lead vocals, guitars Dennis Laffoon – keyboards, backing vocals Keith Mitchell – lead vocals Rod Lincoln – drums Eric Johnson – bass Van McLain – lead vocals, guitars Dennis Laffoon – keyboards, backing vocals Keith Mitchell – lead vocals Rod Lincoln – drums Ron Verlin – bass Van McLain – lead vocals, guitars Dennis Laffoon – keyboards, backing vocals Keith Mitchell – lead vocals Rod Lincoln – drums Ron Verlin – bass Terry Brock – violin Van McLain – lead vocals, guitars Dennis Laffoon – keyboards, backing vocals Keith Mitchell – lead vocals Rod Lincoln – drums Ron Verlin – bass Christian Howes – violin Van McLain – lead vocals, guitars Dennis Laffoon – keyboards, backing vocals Keith Mitchell – lead vocals Rod Lincoln – drums Ron Verlin – bass Shane Michaels – violin Van McLain – lead vocals, guitars Dennis Laffoon – keyboards, backing vocals Keith Mitchell – lead vocals Ron Verlin – bass Shane Michaels – violin Steve Thomas – drums Van McLain – lead vocals, guitars Dennis Laffoon – keyboards, backing vocals Ron Verlin – bass Shane Michaels – violin Steve Thomas – drums Kevin Chalfant – lead vocals Van McLain – lead vocals, guitars Dennis Laffoon – keyboards, backing vocals Ron Verlin – bass Shane Michaels – violin Steve Thomas – drums Ronnie Platt – lead vocals Van McLain – lead vocals, guitars Dennis Laffoon – keyboards, backing vocals Ron Verlin – bass Steve Thomas – drums Ronnie Platt – lead vocals Janet Jameson – violin, backing vocals Van McLain – lead vocals, guitars Dennis Laffoon – keyboards, bass, backing vocals Steve Thomas – drums Ronnie Platt – lead vocals Janet Jameson – violin, backing vocals Van McLain – lead vocals, guitars Dennis Laffoon – keyboards, bass, backing vocals Steve Thomas – drums Janet Jameson – violin, backing vocals Van McLain – lead vocals, guitars Dennis Laffoon – keyboards, bass, backing vocals Steve Thomas – drums Janet Jameson – violin, backing vocals Keith Mitchell – lead vocals Van McLain – lead vocals, guitars Dennis Laffoon – keyboards, bass, backing vocals Steve Thomas – drums Todd Pettygrove – lead vocals Dennis Laffoon – keyboards, bass, backing vocals Steve Thomas – drums Todd Pettygrove – lead vocals Chet Galloway – lead vocals, guitars Janet Jameson – violin, backing vocalsSteve Thomas – drums (1977–1987, 1989, 2003–present) Dennis Laffoon – keyboards, bass, backing vocals (1989–present) Janet Jameson – violin, vocals (2008–2013, 2018–present) Todd Pettygrove – lead vocals (2013–present) Chet Galloway – lead vocals, guitars (2018–present)Bill Guffey – keyboards (1977–1981; died 2007) Van McLain – lead vocals, guitars (1977–1987, 1989–2018; his death) Ron Verlin – bass (1977–1983, 1989–1991, 1994–2009) Charles Waltz – violin, keyboards, backing vocals (1977–1987) Gary West – lead vocals, guitars, keyboards (1977–1987) Norm Dahlor – bass (1984–1987) Keith Mitchell – lead vocals (1989–2005, 2012–2013) Rod Lincoln – drums (1989–2003) Eric Johnson – bass (1991–1994) Terry Brock – violin (1997–1999) Christian Howes – violin (1999–2000) Shane Michaels – violin (2000–2008) Kevin Chalfant – lead vocals (2005–2007) Ronnie Platt – lead vocals (2007–2011) Bill Guffey – keyboards Van McLain – lead vocals, guitars Steve Thomas – drums Ron Verlin – bass Charles Waltz – violin, keyboards, backing vocals Gary West – lead vocals, guitars, keyboards Van McLain – lead vocals, guitars Steve Thomas – drums Ron Verlin – bass Charles Waltz – violin, keyboards, backing vocals Gary West – lead vocals, guitars, keyboards Van McLain – lead vocals, guitars Steve Thomas – drums Charles Waltz – violin, keyboards, backing vocals Gary West – lead vocals, guitars, keyboards Norm Dahlor – bass Disbanded Van McLain – lead vocals, guitars Steve Thomas – drums Dennis Laffoon – keyboards, backing vocals Keith Mitchell – lead vocals Ron Verlin – bass Van McLain – lead vocals, guitars Dennis Laffoon – keyboards, backing vocals Keith Mitchell – lead vocals Ron Verlin – bass Rod Lincoln – drums Van McLain – lead vocals, guitars Dennis Laffoon – keyboards, backing vocals Keith Mitchell – lead vocals Rod Lincoln – drums Eric Johnson – bass Van McLain – lead vocals, guitars Dennis Laffoon – keyboards, backing vocals Keith Mitchell – lead vocals Rod Lincoln – drums Ron Verlin – bass Van McLain – lead vocals, guitars Dennis Laffoon – keyboards, backing vocals Keith Mitchell – lead vocals Rod Lincoln – drums Ron Verlin – bass Terry Brock – violin Van McLain – lead vocals, guitars Dennis Laffoon – keyboards, backing vocals Keith Mitchell – lead vocals Rod Lincoln – drums Ron Verlin – bass Christian Howes – violin Van McLain – lead vocals, guitars Dennis Laffoon – keyboards, backing vocals Keith Mitchell – lead vocals Rod Lincoln – drums Ron Verlin – bass Shane Michaels – violin Van McLain – lead vocals, guitars Dennis Laffoon – keyboards, backing vocals Keith Mitchell – lead vocals Ron Verlin – bass Shane Michaels – violin Steve Thomas – drums Van McLain – lead vocals, guitars Dennis Laffoon – keyboards, backing vocals Ron Verlin – bass Shane Michaels – violin Steve Thomas – drums Kevin Chalfant – lead vocals Van McLain – lead vocals, guitars Dennis Laffoon – keyboards, backing vocals Ron Verlin – bass Shane Michaels – violin Steve Thomas – drums Ronnie Platt – lead vocals Van McLain – lead vocals, guitars Dennis Laffoon – keyboards, backing vocals Ron Verlin – bass Steve Thomas – drums Ronnie Platt – lead vocals Janet Jameson – violin, backing vocals Van McLain – lead vocals, guitars Dennis Laffoon – keyboards, bass, backing vocals Steve Thomas – drums Ronnie Platt – lead vocals Janet Jameson – violin, backing vocals Van McLain – lead vocals, guitars Dennis Laffoon – keyboards, bass, backing vocals Steve Thomas – drums Janet Jameson – violin, backing vocals Van McLain – lead vocals, guitars Dennis Laffoon – keyboards, bass, backing vocals Steve Thomas – drums Janet Jameson – violin, backing vocals Keith Mitchell – lead vocals Van McLain – lead vocals, guitars Dennis Laffoon – keyboards, bass, backing vocals Steve Thomas – drums Todd Pettygrove – lead vocals Dennis Laffoon – keyboards, bass, backing vocals Steve Thomas – drums Todd Pettygrove – lead vocals Chet Galloway – lead vocals, guitars Janet Jameson – violin, backing vocalsThese songs received airplay on rock stations and were frequently performed live, but they were not released as singles:These songs received airplay on rock stations and were frequently performed live, but they were not released as singles:

Wiki

West Nile

https://api.wikimedia.org/core/v1/wikipedia/en/page/Dengue_fever/html

Dengue fever

Dengue fever is a mosquito-borne tropical disease caused by dengue virus . It is frequently asymptomatic ; if symptoms appear they typically begin 3 to 14 days after infection. These may include a high fever , headache , vomiting , muscle and joint pains , and a characteristic skin itching and skin rash . Recovery generally takes two to seven days. In a small proportion of cases, the disease develops into severe dengue (previously known as dengue hemorrhagic fever or dengue shock syndrome) with bleeding , low levels of blood platelets , blood plasma leakage, and dangerously low blood pressure . Dengue virus has four confirmed serotypes ; infection with one type usually gives lifelong immunity to that type, but only short-term immunity to the others. Subsequent infection with a different type increases the risk of severe complications. The symptoms of dengue resemble many other diseases including malaria , influenza , and Zika . Blood tests are available to confirm the diagnosis including detecting viral RNA , or antibodies to the virus. There is no specific treatment for dengue fever. In mild cases, treatment is focused on treating pain symptoms. Severe cases of dengue require hospitalisation; treatment of acute dengue is supportive and includes giving fluid either by mouth or intravenously . Dengue is spread by several species of female mosquitoes of the Aedes genus , principally Aedes aegypti . Infection can be prevented by mosquito elimination and the prevention of bites. Two types of dengue vaccine have been approved and are commercially available. Dengvaxia became available in 2016 but it is only recommended to prevent re-infection in individuals who have been previously infected. The second vaccine, Qdenga, became available in 2022 and is suitable for adults, adolescents and children from four years of age. The earliest descriptions of a dengue outbreak date from 1779; its viral cause and spread were understood by the early 20th century. Already endemic in more than one hundred countries, dengue is spreading from tropical and subtropical regions to the Iberian Peninsula and the southern states of the US, partly attributed to climate change. It is classified as a neglected tropical disease . During 2023, more than 5 million infections were reported, with more than 5,000 dengue-related deaths. As most cases are asymptomatic or mild, the actual numbers of dengue cases and deaths are under-reported. Typically, people infected with dengue virus are asymptomatic (80%) or have only mild symptoms such as an uncomplicated fever. Others have more severe illness (5%), and in a small proportion it is life-threatening. The incubation period (time between exposure and onset of symptoms) ranges from 3 to 14 days, but most often it is 4 to 7 days. The characteristic symptoms of mild dengue are sudden-onset fever, headache (typically located behind the eyes), muscle and joint pains, nausea, vomiting, swollen glands and a rash. If this progresses to severe dengue the symptoms are severe abdominal pain, persistent vomiting, rapid breathing, bleeding gums or nose, fatigue, restlessness, blood in vomit or stool, extreme thirst, pale and cold skin, and feelings of weakness. The course of infection is divided into three phases: febrile, critical, and recovery. The febrile phase involves high fever (40 °C/104 °F), and is associated with generalized pain and a headache; this usually lasts two to seven days. There may also be nausea, vomiting, a rash, and pains in the muscle and joints. Most people recover within a week or so. In about 5% of cases, symptoms worsen and can become life-threatening. This is called severe dengue , (formerly called dengue hemorrhagic fever or dengue shock syndrome ). Severe dengue can lead to shock, internal bleeding, organ failure and even death. Warning signs include severe stomach pain, vomiting, difficulty breathing, and blood in the nose, gums, vomit or stools. During this period, there is leakage of plasma from the blood vessels, together with a reduction in platelets . This may result in fluid accumulation in the chest and abdominal cavity as well as depletion of fluid from the circulation and decreased blood supply to vital organs . The recovery phase usually lasts two to three days. The improvement is often striking, and can be accompanied with severe itching and a slow heart rate . Complications following severe dengue include fatigue, somnolence, headache, concentration impairment and memory impairment. A pregnant woman who develops dengue is at higher risk of miscarriage , low birth weight birth, and premature birth . The course of infection is divided into three phases: febrile, critical, and recovery. The febrile phase involves high fever (40 °C/104 °F), and is associated with generalized pain and a headache; this usually lasts two to seven days. There may also be nausea, vomiting, a rash, and pains in the muscle and joints. Most people recover within a week or so. In about 5% of cases, symptoms worsen and can become life-threatening. This is called severe dengue , (formerly called dengue hemorrhagic fever or dengue shock syndrome ). Severe dengue can lead to shock, internal bleeding, organ failure and even death. Warning signs include severe stomach pain, vomiting, difficulty breathing, and blood in the nose, gums, vomit or stools. During this period, there is leakage of plasma from the blood vessels, together with a reduction in platelets . This may result in fluid accumulation in the chest and abdominal cavity as well as depletion of fluid from the circulation and decreased blood supply to vital organs . The recovery phase usually lasts two to three days. The improvement is often striking, and can be accompanied with severe itching and a slow heart rate . Complications following severe dengue include fatigue, somnolence, headache, concentration impairment and memory impairment. A pregnant woman who develops dengue is at higher risk of miscarriage , low birth weight birth, and premature birth . Complications following severe dengue include fatigue, somnolence, headache, concentration impairment and memory impairment. A pregnant woman who develops dengue is at higher risk of miscarriage , low birth weight birth, and premature birth . Dengue virus (DENV) is an RNA virus of the family Flaviviridae ; genus Flavivirus . Other members of the same genus include yellow fever virus , West Nile virus , and Zika virus . Dengue virus genome (genetic material) contains about 11,000 nucleotide bases , which code for the three structural protein molecules (C, prM and E) that form the virus particle and seven other protein molecules that are required for replication of the virus. There are four confirmed strains of the virus, called serotypes , referred to as DENV-1, DENV-2, DENV-3 and DENV-4. The distinctions between the serotypes are based on their antigenicity . Dengue virus is most frequently transmitted by the bite of mosquitos in the Aedes genus, particularly A. aegypti . They prefer to feed at dusk and dawn, but they may bite and thus spread infection at any time of day. Other Aedes species that may transmit the disease include A. albopictus , A. polynesiensis and A. scutellaris . Humans are the primary host of the virus, but it also circulates in nonhuman primates , and can infect other mammals. An infection can be acquired via a single bite. For 2 to 10 days after becoming newly infected, a person's bloodstream will contain a high level of virus particles (the viremic period). A female mosquito that takes a blood meal from the infected host then propagates the virus in the cells lining its gut. Over the next few days, the virus spreads to other tissues including the mosquito's salivary glands and is released into its saliva. Next time the mosquito feeds, the infectious saliva will be injected into the bloodstream of its victim, thus spreading the disease. The virus seems to have no detrimental effect on the mosquito, which remains infected for life. Dengue can also be transmitted via infected blood products and through organ donation . Vertical transmission (from mother to child) during pregnancy or at birth has been reported. The principal risk for infection with dengue is the bite of an infected mosquito. This is more probable in areas where the disease is endemic, especially where there is high population density, poor sanitation, and standing water where mosquitoes can breed. It can be mitigated by taking steps to avoid bites such as by wearing clothing that fully covers the skin, using mosquito netting while resting, and/or the application of insect repellent ( DEET being the most effective). Chronic diseases – such as asthma, sickle cell anemia, and diabetes mellitus – increase the risk of developing a severe form of the disease. Other risk factors for severe disease include female sex, and high body mass index , Infection with one serotype is thought to produce lifelong immunity to that type, but only short-term protection against the other three. Subsequent re-infection with a different serotype increases the risk of severe complications due to phenomenon known as antibody-dependent enhancement (ADE). The exact mechanism of ADE is not fully understood. It appears that ADE occurs when the antibodies generated during an immune response recognize and bind to a pathogen, but they fail to neutralize it. Instead, the antibody-virus complex has an enhanced ability to bind to the Fcγ receptors of the target immune cells, enabling the virus to infect the cell and reproduce itself. When a mosquito carrying dengue virus bites a person, the virus enters the skin together with the mosquito's saliva. The virus infects nearby skin cells called keratinocytes , as well as specialized immune cell located in the skin, called a Langerhans cells . The Langerhans cells migrate to the lymph nodes , where the infection spreads to white blood cells , and reproduces inside the cells while they move throughout the body. The white blood cells respond by producing several signaling proteins, such as cytokines and interferons , which are responsible for many of the symptoms, such as the fever, the flu-like symptoms, and the severe pains. In severe infection, the virus production inside the body is greatly increased, and many more organs (such as the liver and the bone marrow ) can be affected. Fluid from the bloodstream leaks through the wall of small blood vessels into body cavities due to increased capillary permeability . As a result, blood volume decreases, and the blood pressure becomes so low that it cannot supply sufficient blood to vital organs. The spread of the virus to the bone marrow leads to reduced numbers of platelets, which are necessary for effective blood clotting; this increases the risk of bleeding, the other major complication of dengue fever. The principal risk for infection with dengue is the bite of an infected mosquito. This is more probable in areas where the disease is endemic, especially where there is high population density, poor sanitation, and standing water where mosquitoes can breed. It can be mitigated by taking steps to avoid bites such as by wearing clothing that fully covers the skin, using mosquito netting while resting, and/or the application of insect repellent (DEET being the most effective); it's also advisable to treat clothing, nets and tents with 0.5% permethrin . Protection of the home can be achieved with door and window screens, by using air conditioning, and by regularly emptying and cleaning all receptacles both indoors and outdoors which may accumulate water (such as buckets, planters, pools or trashcans). The primary method of controlling A. aegypti is by eliminating its habitats . This is done by eliminating open sources of water, or if this is not possible, by adding insecticides or biological control agents to these areas. Generalized spraying with organophosphate or pyrethroid insecticides, while sometimes done, is not thought to be effective. Reducing open collections of water through environmental modification is the preferred method of control, given the concerns of negative health effects from insecticides and greater logistical difficulties with control agents. Ideally, mosquito control would be a community activity, e.g. when all members of a community clear blocked gutters and street drains and keep their yards free of containers with standing water. If residences have direct water connections this eliminates the need for wells or street pumps and water-carrying containers. As of March 2024, there are two vaccines to protect against dengue infection; Dengvaxia and Qdenga . Dengvaxia (formerly CYD-TDV) became available in 2015, and is approved for use in the US, EU and in some Asian and Latin American countries. It is an attenuated virus, is suitable for individuals aged 6–45 years and protects against all four serotypes of dengue. Due to safety concerns about antibody-dependent enhancement (ADE), it should only be given to individuals who have previously been infected with dengue, in order to protect them from reinfection. It is given subcutaneously as three doses at six month intervals. Qdenga (formerly TAK-003) completed clinical trials in 2022 and was approved for use in the European Union in December 2022; it has been approved by a number of other countries including Indonesia and Brazil, and has been recommended by the SAGE committee of the World Health Organization. It is indicated for the prevention of dengue disease in individuals four years of age and older, and can be administered to people who have not been previously infected with dengue. It is a live attenuated vaccine containing the four serotypes of dengue virus, administered subcutaneously as two doses three months apart. Dengue virus (DENV) is an RNA virus of the family Flaviviridae ; genus Flavivirus . Other members of the same genus include yellow fever virus , West Nile virus , and Zika virus . Dengue virus genome (genetic material) contains about 11,000 nucleotide bases , which code for the three structural protein molecules (C, prM and E) that form the virus particle and seven other protein molecules that are required for replication of the virus. There are four confirmed strains of the virus, called serotypes , referred to as DENV-1, DENV-2, DENV-3 and DENV-4. The distinctions between the serotypes are based on their antigenicity . Dengue virus is most frequently transmitted by the bite of mosquitos in the Aedes genus, particularly A. aegypti . They prefer to feed at dusk and dawn, but they may bite and thus spread infection at any time of day. Other Aedes species that may transmit the disease include A. albopictus , A. polynesiensis and A. scutellaris . Humans are the primary host of the virus, but it also circulates in nonhuman primates , and can infect other mammals. An infection can be acquired via a single bite. For 2 to 10 days after becoming newly infected, a person's bloodstream will contain a high level of virus particles (the viremic period). A female mosquito that takes a blood meal from the infected host then propagates the virus in the cells lining its gut. Over the next few days, the virus spreads to other tissues including the mosquito's salivary glands and is released into its saliva. Next time the mosquito feeds, the infectious saliva will be injected into the bloodstream of its victim, thus spreading the disease. The virus seems to have no detrimental effect on the mosquito, which remains infected for life. Dengue can also be transmitted via infected blood products and through organ donation . Vertical transmission (from mother to child) during pregnancy or at birth has been reported. The principal risk for infection with dengue is the bite of an infected mosquito. This is more probable in areas where the disease is endemic, especially where there is high population density, poor sanitation, and standing water where mosquitoes can breed. It can be mitigated by taking steps to avoid bites such as by wearing clothing that fully covers the skin, using mosquito netting while resting, and/or the application of insect repellent ( DEET being the most effective). Chronic diseases – such as asthma, sickle cell anemia, and diabetes mellitus – increase the risk of developing a severe form of the disease. Other risk factors for severe disease include female sex, and high body mass index , Infection with one serotype is thought to produce lifelong immunity to that type, but only short-term protection against the other three. Subsequent re-infection with a different serotype increases the risk of severe complications due to phenomenon known as antibody-dependent enhancement (ADE). The exact mechanism of ADE is not fully understood. It appears that ADE occurs when the antibodies generated during an immune response recognize and bind to a pathogen, but they fail to neutralize it. Instead, the antibody-virus complex has an enhanced ability to bind to the Fcγ receptors of the target immune cells, enabling the virus to infect the cell and reproduce itself. When a mosquito carrying dengue virus bites a person, the virus enters the skin together with the mosquito's saliva. The virus infects nearby skin cells called keratinocytes , as well as specialized immune cell located in the skin, called a Langerhans cells . The Langerhans cells migrate to the lymph nodes , where the infection spreads to white blood cells , and reproduces inside the cells while they move throughout the body. The white blood cells respond by producing several signaling proteins, such as cytokines and interferons , which are responsible for many of the symptoms, such as the fever, the flu-like symptoms, and the severe pains. In severe infection, the virus production inside the body is greatly increased, and many more organs (such as the liver and the bone marrow ) can be affected. Fluid from the bloodstream leaks through the wall of small blood vessels into body cavities due to increased capillary permeability . As a result, blood volume decreases, and the blood pressure becomes so low that it cannot supply sufficient blood to vital organs. The spread of the virus to the bone marrow leads to reduced numbers of platelets, which are necessary for effective blood clotting; this increases the risk of bleeding, the other major complication of dengue fever. The principal risk for infection with dengue is the bite of an infected mosquito. This is more probable in areas where the disease is endemic, especially where there is high population density, poor sanitation, and standing water where mosquitoes can breed. It can be mitigated by taking steps to avoid bites such as by wearing clothing that fully covers the skin, using mosquito netting while resting, and/or the application of insect repellent (DEET being the most effective); it's also advisable to treat clothing, nets and tents with 0.5% permethrin . Protection of the home can be achieved with door and window screens, by using air conditioning, and by regularly emptying and cleaning all receptacles both indoors and outdoors which may accumulate water (such as buckets, planters, pools or trashcans). The primary method of controlling A. aegypti is by eliminating its habitats . This is done by eliminating open sources of water, or if this is not possible, by adding insecticides or biological control agents to these areas. Generalized spraying with organophosphate or pyrethroid insecticides, while sometimes done, is not thought to be effective. Reducing open collections of water through environmental modification is the preferred method of control, given the concerns of negative health effects from insecticides and greater logistical difficulties with control agents. Ideally, mosquito control would be a community activity, e.g. when all members of a community clear blocked gutters and street drains and keep their yards free of containers with standing water. If residences have direct water connections this eliminates the need for wells or street pumps and water-carrying containers. As of March 2024, there are two vaccines to protect against dengue infection; Dengvaxia and Qdenga . Dengvaxia (formerly CYD-TDV) became available in 2015, and is approved for use in the US, EU and in some Asian and Latin American countries. It is an attenuated virus, is suitable for individuals aged 6–45 years and protects against all four serotypes of dengue. Due to safety concerns about antibody-dependent enhancement (ADE), it should only be given to individuals who have previously been infected with dengue, in order to protect them from reinfection. It is given subcutaneously as three doses at six month intervals. Qdenga (formerly TAK-003) completed clinical trials in 2022 and was approved for use in the European Union in December 2022; it has been approved by a number of other countries including Indonesia and Brazil, and has been recommended by the SAGE committee of the World Health Organization. It is indicated for the prevention of dengue disease in individuals four years of age and older, and can be administered to people who have not been previously infected with dengue. It is a live attenuated vaccine containing the four serotypes of dengue virus, administered subcutaneously as two doses three months apart. The World Health Organization 's International Classification of Diseases divides dengue fever into two classes: uncomplicated and severe. Severe dengue is defined as that associated with severe bleeding, severe organ dysfunction, or severe plasma leakage. Severe dengue can develop suddenly, sometimes after a few days as the fever subsides. Leakage of plasma from the capillaries results in extreme low blood pressure and hypovolemic shock ; Patients with severe plasma leakage may have fluid accumulation in the lungs or abdomen , insufficient protein in the blood , or thickening of the blood . Severe dengue is a medical emergency which can cause damage to organs, leading to multiple organ failure and death. Mild cases of dengue fever can easily be confused with several common diseases including Influenza , measles , chikungunya , and zika . Dengue, chikungunya and zika share the same mode of transmission ( Aedes mosquitoes) and are often endemic in the same regions, so that it is possible to be infected simultaneously by more than one disease. For travellers, dengue fever diagnosis should be considered in anyone who develops a fever within two weeks of being in the tropics or subtropics . Warning symptoms of severe dengue include abdominal pain, persistent vomiting, odema, bleeding, lethargy, and liver enlargement. Once again, these symptoms can be confused with other diseases such as malaria, gastroenteritis, leptospirosis, and typhus. Blood tests can be used to confirm a diagnosis of dengue. During the first few days of infection, enzyme-linked immunosorbent assay ( ELISA ) can be used to detect the NS1 antigen ; however this antigen is produced by all flaviviruses. Four or five days into the infection, it is possible to reliably detect anti-dengue IgM antibodies, but this does not determine the serotype. Nucleic acid amplification tests provide the most reliable method of diagnosis. As of March 2024, there is no specific antiviral treatment available for dengue fever. Most cases of dengue fever have mild symptoms, and recovery takes place in a few days. No treatment is required for these cases. Acetaminophen (Paracetamol, Tylenol ) may be used to relieve mild fever or pain. Other common pain relievers, including aspirin , ibuprofen (Advil, Motrin IB, others) and naproxen sodium (Aleve) should be avoided as they can increase the risk of bleeding complications. For moderate illness, those who can drink, are passing urine, have no warning signs and are otherwise reasonably healthy can be monitored carefully at home. Supportive care with analgesics, fluid replacement, and bed rest are recommended. Severe dengue is a life-threatening emergency, requiring hospitalization and potentially intensive care. Warning signs include dehydration , decreasing platelets and increasing hematocrit . Treatment modes include intravenous fluids, and transfusion with platelets or plasma. Most people with dengue recover without any ongoing problems. The risk of death among those with severe dengue is 0.8% to 2.5%, and with adequate treatment this is less than 1%. However, those who develop significantly low blood pressure may have a fatality rate of up to 26%. The risk of death among children less than five years old is four times greater than among those over the age of 10. Elderly people are also at higher risk of a poor outcome. As of March 2023, dengue is endemic in more than 100 countries with cases reported in every continent with the exception of Antarctica. The Americas, Southeast Asia and the Western Pacific regions are the most seriously affected. It is difficult to estimate the full extent of the disease, as many cases are mild and not correctly diagnosed. WHO currently estimates that 3.9 billion people are at risk of dengue infection. In 2013, it was estimated that 390 million dengue infections occur every year, with 500,000 of these developing severe symptoms and 25,000 deaths. Generally, areas where dengue is endemic have only one serotype of the virus in circulation. The disease is said to be hyperendemic in areas where more than one serotype is circulating; this increases the risk of severe disease on a second or subsequent infection. Infections are most commonly acquired in urban environments where the virus is primarily transmitted by the mosquito species Aedes aegypti . This species has adapted to the urban environment, is generally found close to human habitation, prefers humans as its host, and takes advantage of small bodies of standing water (such as tanks and buckets) in which to breed. In rural settings the virus is transmitted to humans by A. aegypti and other related mosquitoes such as Aedes albopictus . Both these species have expanding ranges. Dengue has increased in incidence in recent decades, with WHO recording a ten fold increase between 2010 and 2019 (from 500,000 to 5 million recorded cases). This increase is tied closely to the increasing range of Aedes mosquitoes, which is attributed to a combination of urbanization , population growth, and an increasingly warm climate . In endemic areas, dengue infections peak when rainfall is optimal for mosquito breeding. The disease infects all races, sexes, and ages equally. In endemic areas, the infection is most commonly seen in children who then acquire a lifelong partial immunity. The first historical record of a case of probable dengue fever is in a Chinese medical encyclopedia from the Jin Dynasty (266–420) which referred to a "water poison" associated with flying insects. The principal mosquito vector of dengue, Aedes aegypti , spread out of Africa in the 15th to 19th centuries due to the slave trade and consequent expansion of international trading. There have been descriptions of epidemics of dengue-like illness in the 17th century, and it is likely that epidemics in Jakarta , Cairo , and Philadelphia during the 18th century were caused by dengue. It is assumed that dengue was constantly present in many tropical urban centres throughout the 19th and early 20th centuries, even though significant outbreaks were infrequent. The marked spread of dengue during and after the Second World War has been attributed partly to disruption caused by the war, and partly to subsequent urbanisation in south-east Asia. As novel serotypes were introduced to regions already endemic with dengue, outbreaks of severe disease followed. The severe hemorrhagic form of the disease was first reported in the Philippines in 1953; by the 1970s, it had become recognised as a major cause of child mortality in Southeast Asia. In Central and South America, the Aedes mosquito had been eradicated in the 1950s; however the eradication program was discontinued in the 1970s and the diesase re-established itself in the region during the 1980s, becoming hyperendemic and causing significant epidemics. Dengue has continued to increase in prevalence during the 21st century, as the mosquito vector continues to expand its range. This is attributed partly to continuing urbanisation, and partly to the impact of a warmer climate. The name came into English in the early 19th century from West Indian Spanish, which borrowed it from the Kiswahili term dinga (in full kidingapopo , "disease caused by an evil spirit"). The borrowed term changed to dengue in Spanish due to this word existing in Spanish with the meaning "fastidiousness" and this folk etymology referring to the dislike of movement by affected patients. Slaves in the West Indies having contracted dengue were said to have the posture and gait of a dandy , and the disease was known as "dandy fever". The term break-bone fever was applied by physician and United States Founding Father Benjamin Rush , in a 1789 report of the 1780 epidemic in Philadelphia , due to the associated muscle and joint pains. In the report title he uses the more formal term "bilious remitting fever". The term dengue fever came into general use only after 1828. Other historical terms include "breakheart fever" and "la dengue". Terms for severe disease include "infectious thrombocytopenic purpura" and "Philippine", "Thai", or "Singapore hemorrhagic fever". The name came into English in the early 19th century from West Indian Spanish, which borrowed it from the Kiswahili term dinga (in full kidingapopo , "disease caused by an evil spirit"). The borrowed term changed to dengue in Spanish due to this word existing in Spanish with the meaning "fastidiousness" and this folk etymology referring to the dislike of movement by affected patients. Slaves in the West Indies having contracted dengue were said to have the posture and gait of a dandy , and the disease was known as "dandy fever". The term break-bone fever was applied by physician and United States Founding Father Benjamin Rush , in a 1789 report of the 1780 epidemic in Philadelphia , due to the associated muscle and joint pains. In the report title he uses the more formal term "bilious remitting fever". The term dengue fever came into general use only after 1828. Other historical terms include "breakheart fever" and "la dengue". Terms for severe disease include "infectious thrombocytopenic purpura" and "Philippine", "Thai", or "Singapore hemorrhagic fever". Research directions include dengue pathogenesis (the process by which the disease develops in humans), as well as the biology, ecology and behaviour of the mosquito vector. Improved diagnostics would enable faster and more appropriate treatment. Attempts are ongoing to develop an antiviral medicine targeting the NS3 or NS5 proteins. In addition to the two vaccines which are already available, several vaccine candidates are in development. Outbreaks of dengue fever increase the need for blood products while decreasing the number of potential blood donors due to potential infection with the virus. Someone who has a dengue infection is typically not allowed to donate blood for at least the next six months. International Anti-Dengue Day is observed every year on 15 June in a number of countries. The idea was first agreed upon in 2010 with the first event held in Jakarta , Indonesia, in 2011. Further events were held in 2012 in Yangon , Myanmar, and in 2013 in Vietnam . Goals are to increase public awareness about dengue, mobilize resources for its prevention and control and, to demonstrate the Southeast Asian region's commitment in tackling the disease. Efforts are ongoing as of 2019 to make it a global event. The Philippines has an awareness month in June since 1998. A National Dengue Day is held in India annually on 16 May. A study estimate that the global burden of dengue in 2013 amounted to US$8·9 billion. Outbreaks of dengue fever increase the need for blood products while decreasing the number of potential blood donors due to potential infection with the virus. Someone who has a dengue infection is typically not allowed to donate blood for at least the next six months. International Anti-Dengue Day is observed every year on 15 June in a number of countries. The idea was first agreed upon in 2010 with the first event held in Jakarta , Indonesia, in 2011. Further events were held in 2012 in Yangon , Myanmar, and in 2013 in Vietnam . Goals are to increase public awareness about dengue, mobilize resources for its prevention and control and, to demonstrate the Southeast Asian region's commitment in tackling the disease. Efforts are ongoing as of 2019 to make it a global event. The Philippines has an awareness month in June since 1998. A National Dengue Day is held in India annually on 16 May. A study estimate that the global burden of dengue in 2013 amounted to US$8·9 billion.

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West Nile

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List of infectious diseases

This is a list of infectious diseases arranged by name, along with the infectious agents that cause them, the vaccines that can prevent or cure them when they exist and their current status. Some on the list are vaccine-preventable diseases .Blood infection: Fever, chills, vomiting, confusion Urinary tract infection: bloody urine, cloudy urine Pneumonia: Fever, chills, coughing high fever that lasts 4–6 days pharyngitis (sore throat) conjunctivitis (inflamed eyes, usually without pus formation like pink eye) enlargement of the lymph nodes of the neck headache, malaise, and weakness Incubation period of 5–9 days Hemolymphatic phase: Fever, lymphadenopathy Neurological phase: Sleep disorders, neurological symptoms, psychiatric symptoms Suramin by injection is used for T. b. rhodesiense Symptoms of vaginal candidiasis are vaginal itching or soreness, pain during sexual intercourse In men, painful or burning sensation when urinating Isolation of C. diphtheriae culture Histopathologic diagnosis Toxin demonstration In vivo tests (guinea pig inoculation) In vitro test: Elek's gel precipitation test, PCR, ELISA, ICA Clinical criteria URT illness with sore throat Low-grade fever An adherent, dense, grey pseudomembrane covering the posterior aspect of the pharynx Pneumonia: fever, lung consolidation, pleural effusion, tachypnea, tachycardia, or hypotension Meningitis: fever, confusion, hypotension, headache, nuchal rigidity, or changing mental status Bacteremia: fever, murmur, evidence of an embolic event, hypotension, phlebitis, tachycardia, tachypnea, splenomegaly, or evidence of heart failure Skin and soft tissue infection, osteomyelitis, septic arthritis, or discitis: fever, cellulitis, arthritis, arthralgia, localized pain, decubitus ulcer, vascular insufficiency of the lower extremity, back pain, wound infection, or neurologic dysfunction Urinary tract infection or pelvic abscess: fever, flank pain, pelvic pain, or abdominal pain fever severe headache muscle aches ( myalgia ) chills and shaking, similar to the symptoms of influenza nausea vomiting loss of appetite unintentional weight loss abdominal pain cough Skin lesion consistent with leprosy and with definite sensory loss. Positive skin smears. Neurological infection Headache, lethargy, confusion, seizures, sudden onset of neurological deficit Cardiac conditions In recorded cases, it has caused damage to heart valves whether natural or prosthetic Lymphocutaneous disease Ocular disease Disseminated nocardiosis Fever, moderate or very high can be seen

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West Nile

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Viral meningitis

Viral meningitis , also known as aseptic meningitis , is a type of meningitis due to a viral infection . It results in inflammation of the meninges (the membranes covering the brain and spinal cord ). Symptoms commonly include headache , fever , sensitivity to light and neck stiffness . Viruses are the most common cause of aseptic meningitis . [ medical citation needed ] Most cases of viral meningitis are caused by enteroviruses (common stomach viruses). However, other viruses can also cause viral meningitis, such as West Nile virus , mumps , measles , herpes simplex types I and II, varicella and lymphocytic choriomeningitis (LCM) virus. Based on clinical symptoms, viral meningitis cannot be reliably differentiated from bacterial meningitis , although viral meningitis typically follows a more benign clinical course. Viral meningitis has no evidence of bacteria present in cerebral spinal fluid (CSF). Therefore, lumbar puncture with CSF analysis is often needed to identify the disease. In most cases, there is no specific treatment, with efforts generally aimed at relieving symptoms (headache, fever or nausea). A few viral causes, such as HSV , have specific treatments. In the United States, viral meningitis is the cause of more than half of all cases of meningitis . With the prevalence of bacterial meningitis in decline, the viral disease is garnering more and more attention. The estimated incidence has a considerable range, from 0.26 to 17 cases per 100,000 people. For enteroviral meningitis, the most common cause of viral meningitis, there are up to 75,000 cases annually in the United States alone. While the disease can occur in both children and adults, it is more common in children. Viral meningitis characteristically presents with fever , headache and neck stiffness . Fever is the result of cytokines released that affect the thermoregulatory (temperature control) neurons of the hypothalamus . Cytokines and increased intracranial pressure stimulate nociceptors in the brain that lead to headaches. Neck stiffness is the result of inflamed meninges stretching due to flexion of the spine. The various layers of meninges act form a separation between the brain and the skull. In contrast to bacterial meningitis , symptoms associated with viral meningitis are often less severe and do not progress as quickly. Nausea, vomiting and photophobia (light sensitivity) also commonly occur, as do general signs of a viral infection, such as muscle aches and malaise . Increased cranial pressure from viral meningitis stimulates the area postrema , which causes nausea and vomiting. Widened pulse pressure (systolic - diastolic blood pressure), bradycardia, and irregular respiration would be alarming for Cushing's reflex, a sign of acutely elevated intracranial pressure. Photophobia is due to meningeal irritation. In severe cases, people may experience concomitant encephalitis ( meningoencephalitis ), which is suggested by symptoms such as altered mental status, seizures or focal neurologic deficits . Babies with viral meningitis may only appear irritable, sleepy or have trouble eating. Infection in the neonatal period may be the result of infection during pregnancy. In severe cases, people may experience concomitant encephalitis ( meningoencephalitis ), which is suggested by symptoms such as altered mental status, seizures or focal neurologic deficits . The pediatric population may show some additional signs and symptoms that include jaundice and bulging fontanelles . A biphasic fever is more often seen in children compared to adults. The first fever arrives with the onset of general constitutional symptoms, and the second accompanying the onset of the neurological symptoms. Symptoms can vary depending on the virus responsible for infection. Enteroviral meningitis (the most common cause) typically presents with the classic headache, photophobia, fever, nausea, vomiting, and nuchal rigidity. With coxsackie and echo virus' specifically, a maculopapular rash may be present, or even the typical vesicles seen with Herpangina . Lymphocytic choriomeningitis virus (LCMV) can be differentiated from the common presenting meningeal symptoms by the appearance of a prodromal influenza-like sickness about 10 days before other symptoms begin. Mumps meningitis can present similarly to isolated mumps , with possible parotid and testicular swelling. Interestingly, research has shown that HSV-2 meningitis most often occurs in people with no history of genital herpes, and that a severe frontal headache is among the most common presenting symptoms. Patients with varicella zoster meningitis may present with herpes zoster ( Shingles ) in conjunction with classic meningeal signs. Meningitis can be an indication that an individual with HIV is undergoing seroconversion, the time when the human body is forming antibodies in response to the virus. The most common causes of viral meningitis in the United States are non-polio enteroviruses . The viruses that cause meningitis are typically acquired from sick contacts. However, in most cases, people infected with viruses that may cause meningitis do not actually develop meningitis. Viruses that can cause meningitis include: Viral Meningitis is mostly caused by an infectious agent that has colonized somewhere in its host . People who are already in an immunocompromised state are at the highest risk of pathogen entry. Some of the most common examples of immunocompromised individuals include those with HIV, cancer, diabetes, malnutrition, certain genetic disorders, and patients on chemotherapy. Potential sites for this include the skin, respiratory tract , gastrointestinal tract , nasopharynx , and genitourinary tract . The organism invades the submucosa at these sites by invading host defenses, such as local immunity, physical barriers, and phagocytes or macrophages . After pathogen invasion, the immune system is activated. An infectious agent can enter the central nervous system and cause meningeal disease via invading the bloodstream, a retrograde neuronal pathway, or by direct contiguous spread. Immune cells and damaged endothelial cells release matrix metalloproteinases (MMPs), cytokines , and nitric oxide . MMPs and NO induce vasodilation in the cerebral vasculature . Cytokines induce capillary wall changes in the blood brain barrier , which leads to expression of more leukocyte receptors, thus increasing white blood cell binding and extravasation . The barrier that the meninges create between the brain and the bloodstream are what normally protect the brain from the body's immune system . Damage to the meninges and endothelial cells increases cytotoxic reactive oxygen species production, which damages pathogens as well as nearby cells. In meningitis , the barrier is disrupted, so once viruses have entered the brain, they are isolated from the immune system and can spread. This leads to elevated intracranial pressure, cerebral edema , meningeal irritation, and neuronal death. The diagnosis of viral meningitis is made by clinical history, physical exam, and several diagnostic tests. Kernig and Brudzinski signs may be elucidated with specific physical exam maneuvers, and can help diagnose meningitis at the bedside. Most importantly however, cerebrospinal fluid (CSF) is collected via lumbar puncture (also known as spinal tap). This fluid, which normally surrounds the brain and spinal cord, is then analyzed for signs of infection. CSF findings that suggest a viral cause of meningitis include an elevated white blood cell count (usually 10-100 cells/µL) with a lymphocytic predominance in combination with a normal glucose level. Increasingly, cerebrospinal fluid PCR tests have become especially useful for diagnosing viral meningitis, with an estimated sensitivity of 95-100%. Additionally, samples from the stool, urine, blood and throat can also help to identify viral meningitis. CSF vs serum c-reactive protein and procalcitonin have not been shown to elucidate whether meningitis is bacterial or viral. In certain cases, a CT scan of the head should be done before a lumbar puncture such as in those with poor immune function or those with increased intracranial pressure . If the patient has focal neurological deficits, papilledema , a Glasgow Coma Score less than 12, or a recent history of seizures, lumbar puncture should be reconsidered. Differential diagnosis for viral meningitis includes meningitis caused by bacteria, mycoplasma, fungus, and drugs such as NSAIDS, TMP-SMX, IVIG. Further considerations include brain tumors, lupus, vasculitis, and Kawasaki disease in the pediatric population. Because there is no clinical differentiation between bacterial and viral meningitis, people with suspected disease should be sent to the hospital for further evaluation. Treatment for viral meningitis is generally supportive . Rest, hydration, antipyretics , and pain or anti-inflammatory medications may be given as needed. However, if there is initial uncertainty as to whether the meningitis is bacterial or viral in origin, empiric antibiotics are often given until bacterial infection is ruled out. Herpes simplex virus , varicella zoster virus and cytomegalovirus have a specific antiviral therapy. For herpes the treatment of choice is aciclovir . If encephalitis is suspected, empiric treatment with IV aciclovir is often warranted. Surgical management is indicated where there is extremely increased intracranial pressure, infection of an adjacent bony structure (e.g. mastoiditis ), skull fracture, or abscess formation. The majority of people that have viral meningitis get better within 7–10 days. From 1988 to 1999, about 36,000 cases occurred each year. As recently as 2017, the incidence in the U.S. alone increased to 75,000 cases per year for enteroviral meningitis. With the advent and implementation of vaccinations for organisms such as Streptococcus pneumoniae, Haemophilus influenza type B, and Neisseria meningitis , rates of bacterial meningitis have been in decline, making viral meningitis more common. Countries without high rates of immunization still carry higher rates of bacterial disease. While the disease can occur in both children and adults, it is more common in children. Rates of infection tend to reach a peak in the summer and fall. During an outbreak in Romania and in Spain viral meningitis was more common among adults. While, people aged younger than 15 made up 33.8% of cases. In contrast in Finland in 1966 and in Cyprus in 1996, Gaza 1997, China 1998 and Taiwan 1998, the incidence of viral meningitis was higher among children. It has been proposed that viral meningitis might lead to inflammatory injury of the vertebral artery wall . The Meningitis Research Foundation is conducting a study to see if new genomic techniques can improve the speed, accuracy and cost of diagnosing meningitis in children in the UK. The research team will develop a new method to be used for the diagnosis of meningitis, analysing the genetic material of microorganisms found in CSF (cerebrospinal fluid). The new method will first be developed using CSF samples where the microorganism is known, but then will be applied to CSF samples where the microorganism is unknown (estimated at around 40%) to try and identify a cause. There is also research investigating whether high-throughput sequencing , wherein the investigator does not need to compare DNA results with known genomic sequences, could be used in specifically diagnosing unknown causes of viral meningitis. While there is some emerging evidence that bacterial meningitis may have a negative impact on cognitive function, there is no such evidence for viral meningitis.

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West Nile

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Mosquito control

Mosquito control manages the population of mosquitoes to reduce their damage to human health, economies, and enjoyment. Mosquito control is a vital public-health practice throughout the world and especially in the tropics because mosquitoes spread many diseases, such as malaria and the Zika virus . Mosquito-control operations are targeted to multiple problems: Disease organisms transmitted by mosquitoes include West Nile virus , Saint Louis encephalitis virus , Eastern equine encephalomyelitis virus , Everglades virus , Highlands J virus , La Crosse Encephalitis virus in the United States; dengue fever , yellow fever , Ilheus virus, malaria , Zika virus and filariasis in the American tropics ; Rift Valley fever , Wuchereria bancrofti , Japanese encephalitis , chikungunya and filariasis in Africa and Asia; and Murray Valley encephalitis in Australia. Vertical transmission from adult mosquitos to larvae is possible. Depending on the situation, source reduction, biocontrol, larviciding (killing of larvae ), or adulticiding (killing of adults) may be used to manage mosquito populations. These techniques are accomplished using habitat modification, pesticide , biological-control agents, and trapping. The advantage of non-toxic methods of control is they can be used in Conservation Areas . Integrated pest management (IPM) is the use of the most environmentally appropriate method or combination of methods to control pest populations. Typical mosquito-control programs using IPM first conduct surveys, in order to determine the species composition , relative abundance and seasonal distribution of adult and larval mosquitoes, and only then is a control strategy defined.Adult mosquito populations may be monitored by landing rate counts, mechanical traps or by, lidar technology For landing rate counts, an inspector visits a set number of sites every day, counting the number of adult female mosquitoes that land on a part of the body, such as an arm or both legs, within a given time interval. Mechanical traps use a fan to blow adult mosquitoes into a collection bag that is taken back to the laboratory for analysis of catch. The mechanical traps use visual cues (light, black/white contrasts) or chemical attractants that are normally given off by mosquito hosts (e.g., carbon dioxide , ammonia , lactic acid , octenol ) to attract adult female mosquitoes. These cues are often used in combination. Entomology lidar detection has the possibility of showing the difference between male and female mosquitoes. Monitoring larval mosquito populations involves collecting larvae from standing water with a dipper or a turkey baster . The habitat, approximate total number of larvae and pupae , and species are noted for each collection. An alternative method works by providing artificial breeding spots ( ovitraps ) and collecting and counting the developing larvae at fixed intervals. Monitoring these mosquito populations is crucial to see what species are present, if mosquito numbers are rising or falling, and detecting any diseases they carry. Mosquito Alert is a cooperative citizen science project, currently run as a non-profit and coordinated by four public research centers in Spain. The aim of the project is to study, monitor, and fight the spread of invasive mosquitos. The project provided the first detection of the Asian bush mosquito Aedes japonicus in Spain in 2018, providing the first report of a population of mosquitos that were located 1,300 km from their previously nearest known location in Europe. Mechanical control is the management and control using physical means. Since many mosquitoes breed in standing water , source reduction can be as simple as emptying water from containers around the home. This is something that homeowners can accomplish. Mosquito breeding grounds can be eliminated at home by removing unused plastic pools , old tires , or buckets ; by clearing clogged gutters and repairing leaks around faucets ; by regularly (at most every 4 days) changing water in bird baths ; and by filling or draining puddles, swampy areas, and tree stumps. Eliminating such mosquito breeding areas can be an extremely effective and permanent way to reduce mosquito populations without resorting to insecticides. However, this may not be possible in parts of the developing world where water cannot be readily replaced due to irregular water supply. Many individuals also believe mosquito control is the government's responsibility, so if these methods are not done regularly by homeowners then the effectiveness is reduced. Open water marsh management (OWMM) involves the use of shallow ditches, to create a network of water flow within marshes and to connect the marsh to a pond or canal. The network of ditches drains the mosquito habitat and lets in fish which will feed on mosquito larvae. This reduces the need for other control methods such as pesticides . Simply giving the predators access to the mosquito larvae can result in long-term mosquito control. Open-water marsh management is used on both the eastern and western coasts of the United States. [ citation needed ] Rotational impoundment management (RIM) involves the use of large pumps and culverts with gates to control the water level within an impounded marsh. RIM allows mosquito control to occur while still permitting the marsh to function in a state as close to its natural condition as possible. Water is pumped into the marsh in the late spring and summer to prevent the female mosquito from laying her eggs on the soil. The marsh is allowed to drain in the fall, winter, and early spring. Gates in the culverts are used to permit fish, crustaceans, and other marsh organisms to enter and exit the marsh. RIM allows the mosquito-control goals to be met while at the same time reducing the need for pesticide use within the marsh. Rotational impoundment management is used to a great extent on the east coast of Florida. A 2019 study also explored the idea of using unmanned aerial vehicles as a valid strategy to identify and prioritize water bodies where disease vectors such as Ny . darlingi are most likely to breed. An oil drip can or oil drip barrel was a common and nontoxic anti-mosquito measure. The thin layer of oil on top of the water prevents mosquito breeding in two ways: mosquito larvae in the water cannot penetrate the oil film with their breathing tube, and so drown and die; also adult mosquitoes do not lay eggs on the oiled water. A traditional approach to controlling mosquito populations is the use of ovitraps or lethal ovitraps , which provide artificial breeding spots for mosquitoes to lay their eggs. While ovitraps only trap eggs, lethal ovitraps usually contain a chemical inside the trap that is used to kill the adult mosquito and/or the larvae in the trap. Studies have shown that with enough of these lethal ovitraps, Aedes mosquito populations can be controlled. A recent approach is the automatic lethal ovitrap, which works like a traditional ovitrap but automates all steps needed to provide the breeding spots and to destroy the developing larvae. In 2016 researchers from Laurentian University released a design for a low cost trap called an Ovillanta which consists of attractant-laced water in a section of discarded rubber tire. At regular intervals the water is run through a filter to remove any deposited eggs and larva. The water, which then contains an 'oviposition' pheromone deposited during egg-laying, is reused to attract more mosquitoes. Two studies have shown that this type of trap can attract about seven times as many mosquito eggs as a conventional ovitrap. Some newer mosquito traps or known mosquito attractants emit a plume of carbon dioxide together with other mosquito attractants such as sugary scents, lactic acid , octenol , warmth, water vapor and sounds. By mimicking a mammal's scent and outputs, the trap draws female mosquitoes toward it, where they are typically sucked into a net or holder by an electric fan where they are collected. According to the American Mosquito Control Association, the trap will kill some mosquitoes, but their effectiveness in any particular case will depend on a number of factors such as the size and species of the mosquito population and the type and location of the breeding habitat. They are useful in specimen collection studies to determine the types of mosquitoes prevalent in an area but are typically far too inefficient to be useful in reducing mosquito populations. This is a process of achieving sustainable mosquito control in an eco friendly manner by providing artificial breeding grounds with an ovitrap or an ovillanta utilizing common household utensils and destroying larvae by non-hazardous natural means such as throwing them in dry places or feeding them to larvae eating fishes like Gambusia affinis , or suffocating them by spreading a thin plastic sheet over the entire water surface to block atmospheric air. Shifting the water with larvae to another vessel and pouring a few drops of kerosene oil or insecticide/larvicide in it is another option for killing wrigglers, but not preferred due to its environmental impact . Most of the ornamental fishes eat mosquito larvae. [ citation needed ]Since many mosquitoes breed in standing water , source reduction can be as simple as emptying water from containers around the home. This is something that homeowners can accomplish. Mosquito breeding grounds can be eliminated at home by removing unused plastic pools , old tires , or buckets ; by clearing clogged gutters and repairing leaks around faucets ; by regularly (at most every 4 days) changing water in bird baths ; and by filling or draining puddles, swampy areas, and tree stumps. Eliminating such mosquito breeding areas can be an extremely effective and permanent way to reduce mosquito populations without resorting to insecticides. However, this may not be possible in parts of the developing world where water cannot be readily replaced due to irregular water supply. Many individuals also believe mosquito control is the government's responsibility, so if these methods are not done regularly by homeowners then the effectiveness is reduced. Open water marsh management (OWMM) involves the use of shallow ditches, to create a network of water flow within marshes and to connect the marsh to a pond or canal. The network of ditches drains the mosquito habitat and lets in fish which will feed on mosquito larvae. This reduces the need for other control methods such as pesticides . Simply giving the predators access to the mosquito larvae can result in long-term mosquito control. Open-water marsh management is used on both the eastern and western coasts of the United States. [ citation needed ] Rotational impoundment management (RIM) involves the use of large pumps and culverts with gates to control the water level within an impounded marsh. RIM allows mosquito control to occur while still permitting the marsh to function in a state as close to its natural condition as possible. Water is pumped into the marsh in the late spring and summer to prevent the female mosquito from laying her eggs on the soil. The marsh is allowed to drain in the fall, winter, and early spring. Gates in the culverts are used to permit fish, crustaceans, and other marsh organisms to enter and exit the marsh. RIM allows the mosquito-control goals to be met while at the same time reducing the need for pesticide use within the marsh. Rotational impoundment management is used to a great extent on the east coast of Florida. A 2019 study also explored the idea of using unmanned aerial vehicles as a valid strategy to identify and prioritize water bodies where disease vectors such as Ny . darlingi are most likely to breed. An oil drip can or oil drip barrel was a common and nontoxic anti-mosquito measure. The thin layer of oil on top of the water prevents mosquito breeding in two ways: mosquito larvae in the water cannot penetrate the oil film with their breathing tube, and so drown and die; also adult mosquitoes do not lay eggs on the oiled water. A traditional approach to controlling mosquito populations is the use of ovitraps or lethal ovitraps , which provide artificial breeding spots for mosquitoes to lay their eggs. While ovitraps only trap eggs, lethal ovitraps usually contain a chemical inside the trap that is used to kill the adult mosquito and/or the larvae in the trap. Studies have shown that with enough of these lethal ovitraps, Aedes mosquito populations can be controlled. A recent approach is the automatic lethal ovitrap, which works like a traditional ovitrap but automates all steps needed to provide the breeding spots and to destroy the developing larvae. In 2016 researchers from Laurentian University released a design for a low cost trap called an Ovillanta which consists of attractant-laced water in a section of discarded rubber tire. At regular intervals the water is run through a filter to remove any deposited eggs and larva. The water, which then contains an 'oviposition' pheromone deposited during egg-laying, is reused to attract more mosquitoes. Two studies have shown that this type of trap can attract about seven times as many mosquito eggs as a conventional ovitrap. Some newer mosquito traps or known mosquito attractants emit a plume of carbon dioxide together with other mosquito attractants such as sugary scents, lactic acid , octenol , warmth, water vapor and sounds. By mimicking a mammal's scent and outputs, the trap draws female mosquitoes toward it, where they are typically sucked into a net or holder by an electric fan where they are collected. According to the American Mosquito Control Association, the trap will kill some mosquitoes, but their effectiveness in any particular case will depend on a number of factors such as the size and species of the mosquito population and the type and location of the breeding habitat. They are useful in specimen collection studies to determine the types of mosquitoes prevalent in an area but are typically far too inefficient to be useful in reducing mosquito populations.This is a process of achieving sustainable mosquito control in an eco friendly manner by providing artificial breeding grounds with an ovitrap or an ovillanta utilizing common household utensils and destroying larvae by non-hazardous natural means such as throwing them in dry places or feeding them to larvae eating fishes like Gambusia affinis , or suffocating them by spreading a thin plastic sheet over the entire water surface to block atmospheric air. Shifting the water with larvae to another vessel and pouring a few drops of kerosene oil or insecticide/larvicide in it is another option for killing wrigglers, but not preferred due to its environmental impact . Most of the ornamental fishes eat mosquito larvae. [ citation needed ]Chemical control is the management and control using chemical means. Control of larvae can be accomplished through use of contact poisons, growth regulators, surface films, stomach poisons (including bacterial agents), and biological agents such as fungi, nematodes, copepods, and fish. A chemical commonly used in the United States is methoprene , considered slightly toxic to larger animals, which mimics and interferes with natural growth hormones in mosquito larvae, preventing development. Methoprene is frequently distributed in time-release briquette form in breeding areas. Another chemical is Temefos or temephos , a sand granular insecticide is used to treat water infected with disease carrying insects. It is believed by some researchers that the larvae of Anopheles gambiae (important vectors of malaria) can survive for several days on moist mud, and that treatments should therefore include mud and soil several meters from puddles. Control of adult mosquitoes is the most familiar aspect of mosquito control to most of the public. It is accomplished by ground-based applications or via aerial application of residual chemical insecticides such as Duet . Generally modern mosquito-control programs in developed countries use low-volume applications of insecticides, although some programs may still use thermal fogging. Beside fogging there are some other insect repellents for indoors and outdoors. An example of a synthetic insect repellent is DEET . A naturally occurring repellent is citronella . Indoor Residual Spraying ( IRS ) is another method of adulticide. Walls of properties are sprayed with an insecticide, the mosquitoes die when they land on the surface covered in insecticide. To control adult mosquitoes in India, van mounted fogging machines and hand fogging machines are used. DDT was formerly used throughout the world for large area mosquito control, but it is now banned in most developed countries. Controversially, DDT remains in common use in many developing countries (14 countries were reported to be using it in 2009 ), which claim that the public-health cost of switching to other control methods would exceed the harm caused by using DDT. It is sometimes approved for use only in specific, limited circumstances where it is most effective, such as application to walls. [ citation needed ] The role of DDT in combating mosquitoes has been the subject of considerable controversy. Although DDT has been proven to affect biodiversity and cause eggshell thinning in birds such as the bald eagle, some say that DDT is the most effective weapon in combating mosquitoes, and hence malaria. While some of this disagreement is based on differences in the extent to which disease control is valued as opposed to the value of biodiversity, [ citation needed ] there is also genuine disagreement amongst experts about the costs and benefits of using DDT. [ dubious – discuss ] Notwithstanding, DDT-resistant mosquitoes have started to increase in numbers, especially in tropics due to mutations, reducing the effectiveness of this chemical; these mutations can rapidly spread over vast areas if pesticides are applied indiscriminately (Chevillon et al. 1999). In areas where DDT resistance is encountered, malathion , propoxur or lindane is used.Control of larvae can be accomplished through use of contact poisons, growth regulators, surface films, stomach poisons (including bacterial agents), and biological agents such as fungi, nematodes, copepods, and fish. A chemical commonly used in the United States is methoprene , considered slightly toxic to larger animals, which mimics and interferes with natural growth hormones in mosquito larvae, preventing development. Methoprene is frequently distributed in time-release briquette form in breeding areas. Another chemical is Temefos or temephos , a sand granular insecticide is used to treat water infected with disease carrying insects. It is believed by some researchers that the larvae of Anopheles gambiae (important vectors of malaria) can survive for several days on moist mud, and that treatments should therefore include mud and soil several meters from puddles. Control of adult mosquitoes is the most familiar aspect of mosquito control to most of the public. It is accomplished by ground-based applications or via aerial application of residual chemical insecticides such as Duet . Generally modern mosquito-control programs in developed countries use low-volume applications of insecticides, although some programs may still use thermal fogging. Beside fogging there are some other insect repellents for indoors and outdoors. An example of a synthetic insect repellent is DEET . A naturally occurring repellent is citronella . Indoor Residual Spraying ( IRS ) is another method of adulticide. Walls of properties are sprayed with an insecticide, the mosquitoes die when they land on the surface covered in insecticide. To control adult mosquitoes in India, van mounted fogging machines and hand fogging machines are used. DDT was formerly used throughout the world for large area mosquito control, but it is now banned in most developed countries. Controversially, DDT remains in common use in many developing countries (14 countries were reported to be using it in 2009 ), which claim that the public-health cost of switching to other control methods would exceed the harm caused by using DDT. It is sometimes approved for use only in specific, limited circumstances where it is most effective, such as application to walls. [ citation needed ] The role of DDT in combating mosquitoes has been the subject of considerable controversy. Although DDT has been proven to affect biodiversity and cause eggshell thinning in birds such as the bald eagle, some say that DDT is the most effective weapon in combating mosquitoes, and hence malaria. While some of this disagreement is based on differences in the extent to which disease control is valued as opposed to the value of biodiversity, [ citation needed ] there is also genuine disagreement amongst experts about the costs and benefits of using DDT. [ dubious – discuss ] Notwithstanding, DDT-resistant mosquitoes have started to increase in numbers, especially in tropics due to mutations, reducing the effectiveness of this chemical; these mutations can rapidly spread over vast areas if pesticides are applied indiscriminately (Chevillon et al. 1999). In areas where DDT resistance is encountered, malathion , propoxur or lindane is used.Biological control is the management and control using biological means. Biological pest control , or "biocontrol", is the use of the natural enemies of pests like mosquitoes to manage the pest's populations. There are several types of biocontrol, including the direct introduction of parasites, pathogens, and predators to target mosquitoes. Effective biocontrol agents include predatory fish that feed on mosquito larvae such as mosquitofish ( Gambusia affinis ) and some cyprinids (carps and minnows) and killifish . Tilapia also consume mosquito larvae. Direct introduction of tilapia and mosquitofish into ecosystems around the world have had disastrous consequences. However, utilizing a controlled system via aquaponics provides the mosquito control without the adverse effects to the ecosystem. Other predators include dragonfly (fly) naiads , which consume mosquito larvae in the breeding waters, adult dragonflies , which eat adult mosquitoes, and some species of lizard and gecko . Biocontrol agents that have had lesser degrees of success include the predator mosquito Toxorhynchites and predator crustaceans — Mesocyclops copepods , nematodes and fungi . Predators such as birds, bats, lizards, and frogs have been used, but their effectiveness is only anecdotal. Instead of chemical insecticides, some researchers are studying biocides. Like all animals, mosquitoes are subject to disease. Invertebrate pathologists study these diseases in the hope that some of them can be utilized for mosquito management. Microbial pathogens of mosquitoes include viruses, bacteria, fungi, protozoa, nematodes and microsporidia. [ page needed ] Most notably, scientists in Burkina Faso were studying the Metarhizium fungal species. This fungus in a high concentration can slowly kill mosquitoes. To increase the lethality of the fungus, a gene from a spider was inserted into the fungus causing it to produce a neurotoxin . But it is only activated when in mosquito hemolymph. Research was done to show the fungi would not affect other insects or humans. Two other species of fungi that can kill adult mosquitoes are Metarhizium anisopliae and Beauveria bassiana . Dead spores of the soil bacterium Bacillus thuringiensis , especially Bt israelensis (BTI) interfere with dipteran larval digestive systems. It can be dispersed by hand or dropped by helicopter in large areas. BTI loses effectiveness after the larvae turn into pupae, because they stop eating. [ citation needed ] BTI was reported to be widely applied in West Africa with limited adverse effects, and may pose lesser risk than chemical pesticides. In the Wolbachia method, both male and female mosquitos that carry the Wolbachia bacterium are released into natural populations. Wolbachia boosts the natural immune response of the mosquito so that it does not easily get infected and become a host vector for mosquito-borne diseases. Therefore it is unable to easily transmit those viruses to people. This is known as replacement strategy as it aims to replace the natural population with Wolbachia -carrying ones. Since 2011, the World Mosquito Program has conducted several trials and projects, in 14 countries across Asia, Latin America and Oceania. This approach also uses Wolbachia but involves the release of only male mosquitos that carry the Wolbachia bacterium. When these male mosquitos mate with wild female mosquitos, her eggs do not hatch due to lack of biocompatibility. Wolbachia is not endemic to wild mosquito populations although it is endemic in 50% of all insect species. This is known as suppression strategy as it aims to suppress the natural reproduction cycle. Wolbachia-Aedes suppression has been piloted in various countries such as Myanmar (1967), French Polynesia (2009, 2012), USA (2014-2016, 2018), Thailand (2016), Australia (2017), Singapore (since 2016) and Puerto Rico (2020). Maui and Kuai, Hawaii - A series of IIT projects were planned to protect endangered bird species from avian malaria . The projects involve the release of large numbers of male mosquitos infected with a strain of Wolbachia that is incompatible with the strain carried by resident females. These mosquitos would not be irradiated or subject to genetic modification. Introducing large numbers of sterile males is another approach to reducing mosquito numbers. This is called Sterile Insect Technique (SIT). Radiation is used to disrupt DNA in the mosquitoes and randomly create mutations. Males with mutations that disrupt their fertility are selected and released in mass into the wild population. These sterile males mate with wild type females and no offspring is produced, reducing the population size. Guangzhou, China - A combination of SIT with IIT, were used in a mosquito control program in Guangzhou, China. The pilot trial was carried out with the support of the IAEA in cooperation with the Food and Agriculture Organization of the United Nations (FAO). The pilot demonstrated the successful near-elimination of field populations of the world's most invasive mosquito species, Aedes albopictus (Asian tiger mosquito). The two-year trial (2016–2017) covered a 32.5-hectare area on two relatively isolated islands in the Pearl River in Guangzhou. It involved the release of about 200 million irradiated mass-reared adult male mosquitoes exposed to Wolbachia bacteria. Biological pest control , or "biocontrol", is the use of the natural enemies of pests like mosquitoes to manage the pest's populations. There are several types of biocontrol, including the direct introduction of parasites, pathogens, and predators to target mosquitoes. Effective biocontrol agents include predatory fish that feed on mosquito larvae such as mosquitofish ( Gambusia affinis ) and some cyprinids (carps and minnows) and killifish . Tilapia also consume mosquito larvae. Direct introduction of tilapia and mosquitofish into ecosystems around the world have had disastrous consequences. However, utilizing a controlled system via aquaponics provides the mosquito control without the adverse effects to the ecosystem. Other predators include dragonfly (fly) naiads , which consume mosquito larvae in the breeding waters, adult dragonflies , which eat adult mosquitoes, and some species of lizard and gecko . Biocontrol agents that have had lesser degrees of success include the predator mosquito Toxorhynchites and predator crustaceans — Mesocyclops copepods , nematodes and fungi . Predators such as birds, bats, lizards, and frogs have been used, but their effectiveness is only anecdotal.Instead of chemical insecticides, some researchers are studying biocides. Like all animals, mosquitoes are subject to disease. Invertebrate pathologists study these diseases in the hope that some of them can be utilized for mosquito management. Microbial pathogens of mosquitoes include viruses, bacteria, fungi, protozoa, nematodes and microsporidia. [ page needed ] Most notably, scientists in Burkina Faso were studying the Metarhizium fungal species. This fungus in a high concentration can slowly kill mosquitoes. To increase the lethality of the fungus, a gene from a spider was inserted into the fungus causing it to produce a neurotoxin . But it is only activated when in mosquito hemolymph. Research was done to show the fungi would not affect other insects or humans. Two other species of fungi that can kill adult mosquitoes are Metarhizium anisopliae and Beauveria bassiana . Dead spores of the soil bacterium Bacillus thuringiensis , especially Bt israelensis (BTI) interfere with dipteran larval digestive systems. It can be dispersed by hand or dropped by helicopter in large areas. BTI loses effectiveness after the larvae turn into pupae, because they stop eating. [ citation needed ] BTI was reported to be widely applied in West Africa with limited adverse effects, and may pose lesser risk than chemical pesticides. In the Wolbachia method, both male and female mosquitos that carry the Wolbachia bacterium are released into natural populations. Wolbachia boosts the natural immune response of the mosquito so that it does not easily get infected and become a host vector for mosquito-borne diseases. Therefore it is unable to easily transmit those viruses to people. This is known as replacement strategy as it aims to replace the natural population with Wolbachia -carrying ones. Since 2011, the World Mosquito Program has conducted several trials and projects, in 14 countries across Asia, Latin America and Oceania.This approach also uses Wolbachia but involves the release of only male mosquitos that carry the Wolbachia bacterium. When these male mosquitos mate with wild female mosquitos, her eggs do not hatch due to lack of biocompatibility. Wolbachia is not endemic to wild mosquito populations although it is endemic in 50% of all insect species. This is known as suppression strategy as it aims to suppress the natural reproduction cycle. Wolbachia-Aedes suppression has been piloted in various countries such as Myanmar (1967), French Polynesia (2009, 2012), USA (2014-2016, 2018), Thailand (2016), Australia (2017), Singapore (since 2016) and Puerto Rico (2020). Maui and Kuai, Hawaii - A series of IIT projects were planned to protect endangered bird species from avian malaria . The projects involve the release of large numbers of male mosquitos infected with a strain of Wolbachia that is incompatible with the strain carried by resident females. These mosquitos would not be irradiated or subject to genetic modification. Maui and Kuai, Hawaii - A series of IIT projects were planned to protect endangered bird species from avian malaria . The projects involve the release of large numbers of male mosquitos infected with a strain of Wolbachia that is incompatible with the strain carried by resident females. These mosquitos would not be irradiated or subject to genetic modification. Introducing large numbers of sterile males is another approach to reducing mosquito numbers. This is called Sterile Insect Technique (SIT). Radiation is used to disrupt DNA in the mosquitoes and randomly create mutations. Males with mutations that disrupt their fertility are selected and released in mass into the wild population. These sterile males mate with wild type females and no offspring is produced, reducing the population size. Guangzhou, China - A combination of SIT with IIT, were used in a mosquito control program in Guangzhou, China. The pilot trial was carried out with the support of the IAEA in cooperation with the Food and Agriculture Organization of the United Nations (FAO). The pilot demonstrated the successful near-elimination of field populations of the world's most invasive mosquito species, Aedes albopictus (Asian tiger mosquito). The two-year trial (2016–2017) covered a 32.5-hectare area on two relatively isolated islands in the Pearl River in Guangzhou. It involved the release of about 200 million irradiated mass-reared adult male mosquitoes exposed to Wolbachia bacteria. Guangzhou, China - A combination of SIT with IIT, were used in a mosquito control program in Guangzhou, China. The pilot trial was carried out with the support of the IAEA in cooperation with the Food and Agriculture Organization of the United Nations (FAO). The pilot demonstrated the successful near-elimination of field populations of the world's most invasive mosquito species, Aedes albopictus (Asian tiger mosquito). The two-year trial (2016–2017) covered a 32.5-hectare area on two relatively isolated islands in the Pearl River in Guangzhou. It involved the release of about 200 million irradiated mass-reared adult male mosquitoes exposed to Wolbachia bacteria. These techniques share the characteristic of introducing lethal genes and reducing the size of the mosquito population over time. Another control approach under investigation for Aedes aegypti uses a strain that is genetically modified to require the antibiotic tetracycline to develop beyond the larval stage. Modified males develop normally in a nursery while they are supplied with this chemical and can be released into the wild. However, their subsequent offspring will lack tetracycline in the wild and never mature. Field trials were conducted in the Cayman Islands, Malaysia and Brazil to control the mosquitoes that cause dengue fever. In April 2014, Brazil's National Technical Commission for Biosecurity approved the commercial release of the modified mosquito. The FDA is the lead agency for regulating genetically-engineered mosquitoes in the United States. In 2014 and 2018 research was reported into other genetic methods including cytoplasmic incompatibility, chromosomal translocations, sex distortion and gene replacement. Although several years away from the field trial stage, if successful these other methods have the potential to be cheaper and to eradicate the Aedes aegypti mosquito more efficiently. A pioneering experimental demonstration of the gene drive method eradicated small populations of Anopheles gambiae . In 2020, Oxitec 's non-biting Friendly Aedes aegypti mosquito was approved for release by the US EPA and Florida state authorities. Malaysia - In several experiments, researchers released batches of male adult Aedes mosquitos with genetic modifications to study the effects of dispersal and reproduction in natural populations. Mosquito traps were ultilized for the purpose of these studies. The process allowed for the opportunity to determine which mosquitoes were affected, and provided a group to be re-released with genetic modifications resulting in the OX513A variant to reduce reproduction. Adult mosquitoes are attracted inside the traps where they died of dehydration. Research is being conducted that indicates that dismantling a protein associated with eggshell organization, factor EOF1 (factor 1), which may be unique to mosquitoes, may be a means to hamper their reproduction effectively in the wild without creating a resistant population or affecting other animals. Another control approach under investigation for Aedes aegypti uses a strain that is genetically modified to require the antibiotic tetracycline to develop beyond the larval stage. Modified males develop normally in a nursery while they are supplied with this chemical and can be released into the wild. However, their subsequent offspring will lack tetracycline in the wild and never mature. Field trials were conducted in the Cayman Islands, Malaysia and Brazil to control the mosquitoes that cause dengue fever. In April 2014, Brazil's National Technical Commission for Biosecurity approved the commercial release of the modified mosquito. The FDA is the lead agency for regulating genetically-engineered mosquitoes in the United States. In 2014 and 2018 research was reported into other genetic methods including cytoplasmic incompatibility, chromosomal translocations, sex distortion and gene replacement. Although several years away from the field trial stage, if successful these other methods have the potential to be cheaper and to eradicate the Aedes aegypti mosquito more efficiently. A pioneering experimental demonstration of the gene drive method eradicated small populations of Anopheles gambiae . In 2020, Oxitec 's non-biting Friendly Aedes aegypti mosquito was approved for release by the US EPA and Florida state authorities. Malaysia - In several experiments, researchers released batches of male adult Aedes mosquitos with genetic modifications to study the effects of dispersal and reproduction in natural populations. Mosquito traps were ultilized for the purpose of these studies. The process allowed for the opportunity to determine which mosquitoes were affected, and provided a group to be re-released with genetic modifications resulting in the OX513A variant to reduce reproduction. Adult mosquitoes are attracted inside the traps where they died of dehydration.Malaysia - In several experiments, researchers released batches of male adult Aedes mosquitos with genetic modifications to study the effects of dispersal and reproduction in natural populations. Mosquito traps were ultilized for the purpose of these studies. The process allowed for the opportunity to determine which mosquitoes were affected, and provided a group to be re-released with genetic modifications resulting in the OX513A variant to reduce reproduction. Adult mosquitoes are attracted inside the traps where they died of dehydration.Research is being conducted that indicates that dismantling a protein associated with eggshell organization, factor EOF1 (factor 1), which may be unique to mosquitoes, may be a means to hamper their reproduction effectively in the wild without creating a resistant population or affecting other animals. In Singapore , under the Control of Vectors and Pesticides Act there a legal duty on occupiers to prevent Aedes mosquitos from breeding in their homes. If breeding mosquitos are found by inspectors, occupiers are subject to a fine of 5,000 Singapore dollars or imprisonment for a term not exceeding 3 months or both. Some biologists have proposed the deliberate extinction of certain mosquito species. Biologist Olivia Judson has advocated " specicide " of thirty mosquito species by introducing a genetic element which can insert itself into another crucial gene, to create recessive " knockout genes ". She says that the Anopheles mosquitoes (which spread malaria ) and Aedes mosquitoes (which spread dengue fever , yellow fever , elephantiasis , zika , and other diseases) represent only 30 out of some 3,500 mosquito species; eradicating these would save at least one million human lives per year, at a cost of reducing the genetic diversity of the family Culicidae by 1%. She further argues that since species become extinct "all the time" the disappearance of a few more will not destroy the ecosystem : "We're not left with a wasteland every time a species vanishes. Removing one species sometimes causes shifts in the populations of other species — but different need not mean worse." In addition, anti-malarial and mosquito control programs offer little realistic hope to the 300 million people in developing nations who will be infected with acute illnesses each year. Although trials are ongoing, she writes that if they fail: "We should consider the ultimate swatting." Biologist E. O. Wilson has advocated the extinction of several species of mosquito, including malaria vector Anopheles gambiae . Wilson stated, "I'm talking about a very small number of species that have co-evolved with us and are preying on humans, so it would certainly be acceptable to remove them. I believe it's just common sense." Insect ecologist Steven Juliano has argued that "it's difficult to see what the downside would be to removal, except for collateral damage". Entomologist Joe Conlon stated that "If we eradicated them tomorrow, the ecosystems where they are active will hiccup and then get on with life. Something better or worse would take over." However, David Quammen has pointed out that mosquitoes protect forests from human exploitation and may act as competitors for other insects. In terms of malaria control, if populations of mosquitoes were temporarily reduced to zero in a region, then this would exterminate malaria, and the mosquito population could then be allowed to rebound.

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RNA virus

An RNA virus is a virus — other than a retrovirus — that has ribonucleic acid ( RNA ) as its genetic material . The nucleic acid is usually single-stranded RNA ( ssRNA ) but it may be double-stranded (dsRNA). Notable human diseases caused by RNA viruses include the common cold , influenza , SARS , MERS , COVID-19 , Dengue virus , hepatitis C , hepatitis E , West Nile fever , Ebola virus disease , rabies , polio , mumps , and measles . The International Committee on Taxonomy of Viruses (ICTV) classifies RNA viruses as those that belong to Group III , Group IV or Group V of the Baltimore classification system. This category excludes Group VI , viruses with RNA genetic material but which use DNA intermediates in their life cycle : these are called retroviruses , including HIV-1 and HIV-2 which cause AIDS . As of May 2020, all known RNA viruses encoding an RNA-directed RNA polymerase are believed to form a monophyletic group, known as the realm Riboviria . The majority of such RNA viruses fall into the kingdom Orthornavirae and the rest have a positioning not yet defined . The realm does not contain all RNA viruses: Deltavirus , Asunviroidae , and Pospiviroidae are taxa of RNA viruses that were mistakenly included in 2019, [lower-alpha 1] but corrected in 2020. RNA viruses can be further classified according to the sense or polarity of their RNA into negative-sense and positive-sense , or ambisense RNA viruses. Positive-sense viral RNA is similar to mRNA and thus can be immediately translated by the host cell. Negative-sense viral RNA is complementary to mRNA and thus must be converted to positive-sense RNA by an RNA-dependent RNA polymerase before translation. Purified RNA of a positive-sense virus can directly cause infection though it may be less infectious than the whole virus particle. In contrast, purified RNA of a negative-sense virus is not infectious by itself as it needs to be transcribed into positive-sense RNA; each virion can be transcribed to several positive-sense RNAs. Ambisense RNA viruses resemble negative-sense RNA viruses, except they translate genes from their negative and positive strands. The double-stranded (ds)RNA viruses represent a diverse group of viruses that vary widely in host range (humans, animals, plants, fungi , [lower-alpha 2] and bacteria ), genome segment number (one to twelve), and virion organization ( Triangulation number , capsid layers, spikes, turrets, etc.). Members of this group include the rotaviruses , which are the most common cause of gastroenteritis in young children, and picobirnaviruses , which are the most common virus in fecal samples of both humans and animals with or without signs of diarrhea. Bluetongue virus is an economically important pathogen that infects cattle and sheep. In recent years, progress has been made in determining atomic and subnanometer resolution structures of a number of key viral proteins and virion capsids of several dsRNA viruses, highlighting the significant parallels in the structure and replicative processes of many of these viruses. [ page needed ] RNA viruses generally have very high mutation rates compared to DNA viruses , because viral RNA polymerases lack the proofreading ability of DNA polymerases . The genetic diversity of RNA viruses is one reason why it is difficult to make effective vaccines against them. Retroviruses also have a high mutation rate even though their DNA intermediate integrates into the host genome (and is thus subject to host DNA proofreading once integrated), because errors during reverse transcription are embedded into both strands of DNA before integration. Some genes of RNA virus are important to the viral replication cycles and mutations are not tolerated. For example, the region of the hepatitis C virus genome that encodes the core protein is highly conserved , because it contains an RNA structure involved in an internal ribosome entry site . On average, dsRNA viruses show a lower sequence redundancy relative to ssRNA viruses. Contrarily, dsDNA viruses contain the most redundant genome sequences while ssDNA viruses have the least. The sequence complexity of viruses has been shown to be a key characteristic for accurate reference-free viral classification. RNA viruses can be further classified according to the sense or polarity of their RNA into negative-sense and positive-sense , or ambisense RNA viruses. Positive-sense viral RNA is similar to mRNA and thus can be immediately translated by the host cell. Negative-sense viral RNA is complementary to mRNA and thus must be converted to positive-sense RNA by an RNA-dependent RNA polymerase before translation. Purified RNA of a positive-sense virus can directly cause infection though it may be less infectious than the whole virus particle. In contrast, purified RNA of a negative-sense virus is not infectious by itself as it needs to be transcribed into positive-sense RNA; each virion can be transcribed to several positive-sense RNAs. Ambisense RNA viruses resemble negative-sense RNA viruses, except they translate genes from their negative and positive strands. The double-stranded (ds)RNA viruses represent a diverse group of viruses that vary widely in host range (humans, animals, plants, fungi , [lower-alpha 2] and bacteria ), genome segment number (one to twelve), and virion organization ( Triangulation number , capsid layers, spikes, turrets, etc.). Members of this group include the rotaviruses , which are the most common cause of gastroenteritis in young children, and picobirnaviruses , which are the most common virus in fecal samples of both humans and animals with or without signs of diarrhea. Bluetongue virus is an economically important pathogen that infects cattle and sheep. In recent years, progress has been made in determining atomic and subnanometer resolution structures of a number of key viral proteins and virion capsids of several dsRNA viruses, highlighting the significant parallels in the structure and replicative processes of many of these viruses. [ page needed ]RNA viruses generally have very high mutation rates compared to DNA viruses , because viral RNA polymerases lack the proofreading ability of DNA polymerases . The genetic diversity of RNA viruses is one reason why it is difficult to make effective vaccines against them. Retroviruses also have a high mutation rate even though their DNA intermediate integrates into the host genome (and is thus subject to host DNA proofreading once integrated), because errors during reverse transcription are embedded into both strands of DNA before integration. Some genes of RNA virus are important to the viral replication cycles and mutations are not tolerated. For example, the region of the hepatitis C virus genome that encodes the core protein is highly conserved , because it contains an RNA structure involved in an internal ribosome entry site . On average, dsRNA viruses show a lower sequence redundancy relative to ssRNA viruses. Contrarily, dsDNA viruses contain the most redundant genome sequences while ssDNA viruses have the least. The sequence complexity of viruses has been shown to be a key characteristic for accurate reference-free viral classification. Animal RNA viruses are classified by the ICTV. There are three distinct groups of RNA viruses depending on their genome and mode of replication: Retroviruses (Group VI) have a single-stranded RNA genome but, in general, are not considered RNA viruses because they use DNA intermediates to replicate. Reverse transcriptase , a viral enzyme that comes from the virus itself after it is uncoated, converts the viral RNA into a complementary strand of DNA, which is copied to produce a double-stranded molecule of viral DNA. After this DNA is integrated into the host genome using the viral enzyme integrase , expression of the encoded genes may lead to the formation of new virions.Numerous RNA viruses are capable of genetic recombination when at least two viral genomes are present in the same host cell. Very rarely viral RNA can recombine with host RNA. RNA recombination appears to be a major driving force in determining genome architecture and the course of viral evolution among Picornaviridae ( (+)ssRNA ), e.g. poliovirus . In the Retroviridae ((+)ssRNA), e.g. HIV , damage in the RNA genome appears to be avoided during reverse transcription by strand switching, a form of recombination. Recombination also occurs in the Reoviridae (dsRNA), e.g. reovirus; Orthomyxoviridae ((-)ssRNA), e.g. influenza virus ; and Coronaviridae ((+)ssRNA), e.g. SARS . Recombination in RNA viruses appears to be an adaptation for coping with genome damage. Recombination can occur infrequently between animal viruses of the same species but of divergent lineages. The resulting recombinant viruses may sometimes cause an outbreak of infection in humans. Classification is based principally on the type of genome (double-stranded, negative- or positive-single-strand) and gene number and organization. Currently, there are 5 orders and 47 families of RNA viruses recognized. There are also many unassigned species and genera. Related to but distinct from the RNA viruses are the viroids and the RNA satellite viruses . These are not currently classified as RNA viruses and are described on their own pages. A study of several thousand RNA viruses has shown the presence of at least five main taxa: a levivirus and relatives group; a picornavirus supergroup; an alphavirus supergroup plus a flavivirus supergroup; the dsRNA viruses; and the -ve strand viruses. The lentivirus group appears to be basal to all the remaining RNA viruses. The next major division lies between the picornasupragroup and the remaining viruses. The dsRNA viruses appear to have evolved from a +ve RNA ancestor and the -ve RNA viruses from within the dsRNA viruses. The closest relation to the -ve stranded RNA viruses is the Reoviridae . This is the single largest group of RNA viruses and has been organized by the ICTV into the phyla Kitrinoviricota , Lenarviricota , and Pisuviricota in the kingdom Orthornavirae and realm Riboviria . Positive-strand RNA viruses can also be classified based on the RNA-dependent RNA polymerase. Three groups have been recognised: Bymoviruses, comoviruses, nepoviruses, nodaviruses, picornaviruses, potyviruses, sobemoviruses and a subset of luteoviruses (beet western yellows virus and potato leafroll virus)—the picorna like group (Picornavirata). Carmoviruses, dianthoviruses, flaviviruses, pestiviruses, statoviruses, tombusviruses, single-stranded RNA bacteriophages, hepatitis C virus and a subset of luteoviruses (barley yellow dwarf virus)—the flavi like group (Flavivirata). Alphaviruses, carlaviruses, furoviruses, hordeiviruses, potexviruses, rubiviruses, tobraviruses, tricornaviruses, tymoviruses, apple chlorotic leaf spot virus, beet yellows virus and hepatitis E virus—the alpha like group (Rubivirata). A division of the alpha-like (Sindbis-like) supergroup on the basis of a novel domain located near the N termini of the proteins involved in viral replication has been proposed. The two groups proposed are: the 'altovirus' group (alphaviruses, furoviruses, hepatitis E virus, hordeiviruses, tobamoviruses, tobraviruses, tricornaviruses and probably rubiviruses); and the 'typovirus' group (apple chlorotic leaf spot virus, carlaviruses, potexviruses and tymoviruses). The alpha like supergroup can be further divided into three clades : the rubi-like, tobamo-like, and tymo-like viruses. Additional work has identified five groups of positive-stranded RNA viruses containing four, three, three, three, and one order(s), respectively. These fourteen orders contain 31 virus families (including 17 families of plant viruses) and 48 genera (including 30 genera of plant viruses). This analysis suggests that alphaviruses and flaviviruses can be separated into two families—the Togaviridae and Flaviridae, respectively—but suggests that other taxonomic assignments, such as the pestiviruses, hepatitis C virus, rubiviruses, hepatitis E virus, and arteriviruses, may be incorrect. The coronaviruses and toroviruses appear to be distinct families in distinct orders and not distinct genera of the same family as currently classified. The luteoviruses appear to be two families rather than one, and apple chlorotic leaf spot virus appears not to be a closterovirus but a new genus of the Potexviridae. The evolution of the picornaviruses based on an analysis of their RNA polymerases and helicases appears to date to the divergence of eukaryotes . Their putative ancestors include the bacterial group II retroelements , the family of HtrA proteases and DNA bacteriophages . Partitiviruses are related to and may have evolved from a totivirus ancestor. Hypoviruses and barnaviruses appear to share an ancestry with the potyvirus and sobemovirus lineages respectively. This analysis also suggests that the dsRNA viruses are not closely related to each other but instead belong to four additional classes—Birnaviridae, Cystoviridae, Partitiviridae, and Reoviridae—and one additional order (Totiviridae) of one of the classes of positive ssRNA viruses in the same subphylum as the positive-strand RNA viruses. One study has suggested that there are two large clades: One includes the families Caliciviridae , Flaviviridae , and Picornaviridae and a second that includes the families Alphatetraviridae , Birnaviridae , Cystoviridae , Nodaviridae , and Permutotretraviridae . These viruses have multiple types of genome ranging from a single RNA molecule up to eight segments. Despite their diversity it appears that they may have originated in arthropods and to have diversified from there. A number of satellite viruses—viruses that require the assistance of another virus to complete their life cycle—are also known. Their taxonomy has yet to be settled. The following four genera have been proposed for positive sense single stranded RNA satellite viruses that infect plants— Albetovirus , Aumaivirus , Papanivirus and Virtovirus . A family— Sarthroviridae which includes the genus Macronovirus —has been proposed for the positive sense single stranded RNA satellite viruses that infect arthropods .This is the single largest group of RNA viruses and has been organized by the ICTV into the phyla Kitrinoviricota , Lenarviricota , and Pisuviricota in the kingdom Orthornavirae and realm Riboviria . Positive-strand RNA viruses can also be classified based on the RNA-dependent RNA polymerase. Three groups have been recognised: Bymoviruses, comoviruses, nepoviruses, nodaviruses, picornaviruses, potyviruses, sobemoviruses and a subset of luteoviruses (beet western yellows virus and potato leafroll virus)—the picorna like group (Picornavirata). Carmoviruses, dianthoviruses, flaviviruses, pestiviruses, statoviruses, tombusviruses, single-stranded RNA bacteriophages, hepatitis C virus and a subset of luteoviruses (barley yellow dwarf virus)—the flavi like group (Flavivirata). Alphaviruses, carlaviruses, furoviruses, hordeiviruses, potexviruses, rubiviruses, tobraviruses, tricornaviruses, tymoviruses, apple chlorotic leaf spot virus, beet yellows virus and hepatitis E virus—the alpha like group (Rubivirata). A division of the alpha-like (Sindbis-like) supergroup on the basis of a novel domain located near the N termini of the proteins involved in viral replication has been proposed. The two groups proposed are: the 'altovirus' group (alphaviruses, furoviruses, hepatitis E virus, hordeiviruses, tobamoviruses, tobraviruses, tricornaviruses and probably rubiviruses); and the 'typovirus' group (apple chlorotic leaf spot virus, carlaviruses, potexviruses and tymoviruses). The alpha like supergroup can be further divided into three clades : the rubi-like, tobamo-like, and tymo-like viruses. Additional work has identified five groups of positive-stranded RNA viruses containing four, three, three, three, and one order(s), respectively. These fourteen orders contain 31 virus families (including 17 families of plant viruses) and 48 genera (including 30 genera of plant viruses). This analysis suggests that alphaviruses and flaviviruses can be separated into two families—the Togaviridae and Flaviridae, respectively—but suggests that other taxonomic assignments, such as the pestiviruses, hepatitis C virus, rubiviruses, hepatitis E virus, and arteriviruses, may be incorrect. The coronaviruses and toroviruses appear to be distinct families in distinct orders and not distinct genera of the same family as currently classified. The luteoviruses appear to be two families rather than one, and apple chlorotic leaf spot virus appears not to be a closterovirus but a new genus of the Potexviridae. The evolution of the picornaviruses based on an analysis of their RNA polymerases and helicases appears to date to the divergence of eukaryotes . Their putative ancestors include the bacterial group II retroelements , the family of HtrA proteases and DNA bacteriophages . Partitiviruses are related to and may have evolved from a totivirus ancestor. Hypoviruses and barnaviruses appear to share an ancestry with the potyvirus and sobemovirus lineages respectively. The evolution of the picornaviruses based on an analysis of their RNA polymerases and helicases appears to date to the divergence of eukaryotes . Their putative ancestors include the bacterial group II retroelements , the family of HtrA proteases and DNA bacteriophages . Partitiviruses are related to and may have evolved from a totivirus ancestor. Hypoviruses and barnaviruses appear to share an ancestry with the potyvirus and sobemovirus lineages respectively. This analysis also suggests that the dsRNA viruses are not closely related to each other but instead belong to four additional classes—Birnaviridae, Cystoviridae, Partitiviridae, and Reoviridae—and one additional order (Totiviridae) of one of the classes of positive ssRNA viruses in the same subphylum as the positive-strand RNA viruses. One study has suggested that there are two large clades: One includes the families Caliciviridae , Flaviviridae , and Picornaviridae and a second that includes the families Alphatetraviridae , Birnaviridae , Cystoviridae , Nodaviridae , and Permutotretraviridae . These viruses have multiple types of genome ranging from a single RNA molecule up to eight segments. Despite their diversity it appears that they may have originated in arthropods and to have diversified from there. A number of satellite viruses—viruses that require the assistance of another virus to complete their life cycle—are also known. Their taxonomy has yet to be settled. The following four genera have been proposed for positive sense single stranded RNA satellite viruses that infect plants— Albetovirus , Aumaivirus , Papanivirus and Virtovirus . A family— Sarthroviridae which includes the genus Macronovirus —has been proposed for the positive sense single stranded RNA satellite viruses that infect arthropods .There are twelve families and a number of unassigned genera and species recognised in this group. There are three orders and 34 families recognised in this group. In addition, there are a number of unclassified species and genera. Satellite viruses An unclassified astrovirus/hepevirus-like virus has also been described. With the exception of the Hepatitis D virus , this group of viruses has been placed into a single phylum— Negarnaviricota . This phylum has been divided into two subphyla— Haploviricotina and Polyploviricotina . Within the subphylum Haploviricotina four classes are currently recognised: Chunqiuviricetes , Milneviricetes , Monjiviricetes and Yunchangviricetes . In the subphylum Polyploviricotina two classes are recognised: Ellioviricetes and Insthoviricetes . Six classes, seven orders and twenty four families are currently recognized in this group. A number of unassigned species and genera are yet to be classified.

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West Nile

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Insect repellent

An insect repellent (also commonly called " bug spray ") is a substance applied to the skin, clothing, or other surfaces to discourage insects (and arthropods in general) from landing or climbing on that surface. Insect repellents help prevent and control the outbreak of insect-borne (and other arthropod -bourne) diseases such as malaria , Lyme disease , dengue fever , bubonic plague , river blindness , and West Nile fever . Pest animals commonly serving as vectors for disease include insects such as flea , fly , and mosquito ; and ticks (arachnids). [ citation needed ] Some insect repellents are insecticides (bug killers), but most simply discourage insects and send them flying or crawling away. Nearly any would be fatal upon reaching the median lethal dose , but classification as an insecticide implies death even at lower doses.Synthetic repellents tend to be more effective and/or longer lasting than "natural" repellents. For protection against mosquito bites, the U.S. Centers for Disease Control (CDC) recommends DEET , icaridin (picaridin, KBR 3023), oil of lemon eucalyptus ( para-menthane-diol or PMD), IR3535 and 2-undecanone with the caveat that higher percentages of the active ingredient provide longer protection. In 2015, Researchers at New Mexico State University tested 10 commercially available products for their effectiveness at repelling mosquitoes. On the mosquito Aedes aegypti , the vector of Zika virus, only one repellent that did not contain DEET had a strong effect for the duration of the 240 minutes test: a lemon eucalyptus oil repellent. All DEET-containing mosquito repellents were active. In one comparative study from 2004, IR3535 was as effective or better than DEET in protection against Aedes aegypti and Culex quinquefasciatus mosquitoes. Other sources (official publications of the associations of German physicians as well as of German druggists ) suggest the contrary and state DEET is still the most efficient substance available and the substance of choice for stays in malaria regions, while IR3535 has little effect. However, some plant-based repellents may provide effective relief as well. Essential oil repellents can be short-lived in their effectiveness. A test of various insect repellents by an independent consumer organization found that repellents containing DEET or icaridin are more effective than repellents with "natural" active ingredients. All the synthetics gave almost 100% repellency for the first 2 hours, where the natural repellent products were most effective for the first 30 to 60 minutes, and required reapplication to be effective over several hours. Although highly toxic to cats, permethrin is recommended as protection against mosquitoes for clothing, gear, or bed nets. In an earlier report, the CDC found oil of lemon eucalyptus to be more effective than other plant-based treatments, with a similar effectiveness to low concentrations of DEET. However, a 2006 published study found in both cage and field studies that a product containing 40% oil of lemon eucalyptus was just as effective as products containing high concentrations of DEET. Research has also found that neem oil is mosquito repellent for up to 12 hours. Citronella oil 's mosquito repellency has also been verified by research, including effectiveness in repelling Aedes aegypti , but requires reapplication after 30 to 60 minutes. There are also products available based on sound production, particularly ultrasound (inaudibly high-frequency sounds) which purport to be insect repellents. However, these electronic devices have been shown to be ineffective based on studies done by the United States Environmental Protection Agency and many universities. Children may be at greater risk for adverse reactions to repellents, in part, because their exposure may be greater. Children can be at greater risk of accidental eye contact or ingestion. As with chemical exposures in general, pregnant women should take care to avoid exposures to repellents when practical, as the fetus may be vulnerable. Some experts also recommend against applying chemicals such as DEET and sunscreen simultaneously since that would increase DEET penetration. Canadian researcher, Xiaochen Gu, a professor at the University of Manitoba's faculty of Pharmacy who led a study about mosquitos, advises that DEET should be applied 30 or more minutes later. Gu also recommends insect repellent sprays instead of lotions which are rubbed into the skin "forcing molecules into the skin". Regardless of which repellent product used, it is recommended to read the label before use and carefully follow directions. Usage instructions for repellents vary from country to country. Some insect repellents are not recommended for use on younger children. In the DEET Reregistration Eligibility Decision (RED) the United States Environmental Protection Agency (EPA) reported 14 to 46 cases of potential DEET associated seizures , including 4 deaths. The EPA states: "... it does appear that some cases are likely related to DEET toxicity ," but observed that with 30% of the US population using DEET, the likely seizure rate is only about one per 100 million users. The Pesticide Information Project of Cooperative Extension Offices of Cornell University states that, " Everglades National Park employees having extensive DEET exposure were more likely to have insomnia, mood disturbances and impaired cognitive function than were lesser exposed co-workers". The EPA states that citronella oil shows little or no toxicity and has been used as a topical insect repellent for 60 years. However, the EPA also states that citronella may irritate skin and cause dermatitis in certain individuals. Canadian regulatory authorities concern with citronella based repellents is primarily based on data-gaps in toxicology , not on incidents. Within countries of the European Union, implementation of Regulation 98/8/EC, commonly referred to as the Biocidal Products Directive, has severely limited the number and type of insect repellents available to European consumers. Only a small number of active ingredients have been supported by manufacturers in submitting dossiers to the EU Authorities. In general, only formulations containing DEET, icaridin (sold under the trade name Saltidin and formerly known as Bayrepel or KBR3023), IR3535 and citriodiol ( p-menthane-3,8-diol ) are available. Most "natural" insect repellents such as citronella, neem oil, and herbal extracts are no longer permitted for sale as insect repellents in the EU due to their lack of effectiveness; this does not preclude them from being sold for other purposes, as long as the label does not indicate they are a biocide (insect repellent). [ citation needed ] A 2018 study found that Icaridin , is highly toxic to salamander larvae , in what the authors described as conservative exposure doses. The LC50 standard was additionally found to be completely inadequate in the context of finding this result. Permethrin is highly toxic to cats but not to dogs or humans. Children may be at greater risk for adverse reactions to repellents, in part, because their exposure may be greater. Children can be at greater risk of accidental eye contact or ingestion. As with chemical exposures in general, pregnant women should take care to avoid exposures to repellents when practical, as the fetus may be vulnerable. Some experts also recommend against applying chemicals such as DEET and sunscreen simultaneously since that would increase DEET penetration. Canadian researcher, Xiaochen Gu, a professor at the University of Manitoba's faculty of Pharmacy who led a study about mosquitos, advises that DEET should be applied 30 or more minutes later. Gu also recommends insect repellent sprays instead of lotions which are rubbed into the skin "forcing molecules into the skin". Regardless of which repellent product used, it is recommended to read the label before use and carefully follow directions. Usage instructions for repellents vary from country to country. Some insect repellents are not recommended for use on younger children. In the DEET Reregistration Eligibility Decision (RED) the United States Environmental Protection Agency (EPA) reported 14 to 46 cases of potential DEET associated seizures , including 4 deaths. The EPA states: "... it does appear that some cases are likely related to DEET toxicity ," but observed that with 30% of the US population using DEET, the likely seizure rate is only about one per 100 million users. The Pesticide Information Project of Cooperative Extension Offices of Cornell University states that, " Everglades National Park employees having extensive DEET exposure were more likely to have insomnia, mood disturbances and impaired cognitive function than were lesser exposed co-workers". The EPA states that citronella oil shows little or no toxicity and has been used as a topical insect repellent for 60 years. However, the EPA also states that citronella may irritate skin and cause dermatitis in certain individuals. Canadian regulatory authorities concern with citronella based repellents is primarily based on data-gaps in toxicology , not on incidents. Within countries of the European Union, implementation of Regulation 98/8/EC, commonly referred to as the Biocidal Products Directive, has severely limited the number and type of insect repellents available to European consumers. Only a small number of active ingredients have been supported by manufacturers in submitting dossiers to the EU Authorities. In general, only formulations containing DEET, icaridin (sold under the trade name Saltidin and formerly known as Bayrepel or KBR3023), IR3535 and citriodiol ( p-menthane-3,8-diol ) are available. Most "natural" insect repellents such as citronella, neem oil, and herbal extracts are no longer permitted for sale as insect repellents in the EU due to their lack of effectiveness; this does not preclude them from being sold for other purposes, as long as the label does not indicate they are a biocide (insect repellent). [ citation needed ]A 2018 study found that Icaridin , is highly toxic to salamander larvae , in what the authors described as conservative exposure doses. The LC50 standard was additionally found to be completely inadequate in the context of finding this result. Permethrin is highly toxic to cats but not to dogs or humans. Several natural ingredients are certified by the United States Environmental Protection Agency as insect repellents, namely catnip oil, oil of lemon eucalyptus (OLE) (and its active ingredient p-Menthane-3,8-diol ), oil of citronella , and 2-Undecanone , which is usually produced synthetically but has also been isolated from many plant sources. Many other studies have also investigated the potential of natural compounds from plants as insect repellents. Moreover, there are many preparations from naturally occurring sources that have been used as a repellent to certain insects. Some of these act as insecticides while others are only repellent. Below is a list of some natural products with repellent activity: Some old studies suggested that the ingestion of large doses of thiamine (vitamin B 1 ) could be effective as an oral insect repellent against mosquito bites. However, there is now conclusive evidence that thiamin has no efficacy against mosquito bites. Some claim that plants such as wormwood or sagewort, lemon balm , lemon grass , lemon thyme , and the mosquito plant (Pelargonium) will act against mosquitoes. However, scientists have determined that these plants are "effective" for a limited time only when the leaves are crushed and applied directly to the skin. There are several, widespread, unproven theories about mosquito control , such as the assertion that vitamin B , in particular B 1 (thiamine), garlic , ultrasonic devices or incense can be used to repel or control mosquitoes. Moreover, manufacturers of "mosquito repelling" ultrasonic devices have been found to be fraudulent, and their devices were deemed "useless" according to a review of scientific studies. Several natural ingredients are certified by the United States Environmental Protection Agency as insect repellents, namely catnip oil, oil of lemon eucalyptus (OLE) (and its active ingredient p-Menthane-3,8-diol ), oil of citronella , and 2-Undecanone , which is usually produced synthetically but has also been isolated from many plant sources. Many other studies have also investigated the potential of natural compounds from plants as insect repellents. Moreover, there are many preparations from naturally occurring sources that have been used as a repellent to certain insects. Some of these act as insecticides while others are only repellent. Below is a list of some natural products with repellent activity:Some old studies suggested that the ingestion of large doses of thiamine (vitamin B 1 ) could be effective as an oral insect repellent against mosquito bites. However, there is now conclusive evidence that thiamin has no efficacy against mosquito bites. Some claim that plants such as wormwood or sagewort, lemon balm , lemon grass , lemon thyme , and the mosquito plant (Pelargonium) will act against mosquitoes. However, scientists have determined that these plants are "effective" for a limited time only when the leaves are crushed and applied directly to the skin. There are several, widespread, unproven theories about mosquito control , such as the assertion that vitamin B , in particular B 1 (thiamine), garlic , ultrasonic devices or incense can be used to repel or control mosquitoes. Moreover, manufacturers of "mosquito repelling" ultrasonic devices have been found to be fraudulent, and their devices were deemed "useless" according to a review of scientific studies. People can reduce the number of mosquito bites they receive (to a greater or lesser degree) by:Testing and scientific certainty were desired at the end of the 1940s. To that end products meant to be used by humans were tested with model animals to speed trials. Eddy & McGregor 1949 and Wiesmann & Lotmar 1949 used mice , Wasicky et al. 1949 canaries and guinea pigs , Kasman et al. 1953 also guinea pigs, Starnes & Granett 1953 rabbits , and many used cattle .

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West Nile

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Cooper's hawk

Cooper's hawk ( Accipiter cooperii ) is a medium-sized hawk native to the North American continent and found from southern Canada to Mexico. This species is a member of the genus Accipiter , sometimes referred to as true hawks, which are famously agile, relatively small hawks common to wooded habitats around the world and also the most diverse of all diurnal raptor genera. As in many birds of prey , the male is smaller than the female. The birds found east of the Mississippi River tend to be larger on average than the birds found to the west. It is easily confused with the smaller but similar sharp-shinned hawk . ( A. striatus ) The species was named in 1828 by Charles Lucien Bonaparte in honor of his friend and fellow ornithologist, William Cooper . Other common names for Cooper's hawk include: big blue darter , chicken hawk , flying cross , hen hawk , quail hawk , striker , and swift hawk . Many of the names applied to Cooper's hawks refer to their ability to hunt large and evasive prey using extremely well-developed agility. This species primarily hunts small-to-medium-sized birds, but will also commonly take small mammals and sometimes reptiles. Like most related hawks, Cooper's hawks prefer to nest in tall trees with extensive canopy cover and can commonly produce up to two to four fledglings depending on conditions. Breeding attempts may be compromised by poor weather, predators and anthropogenic causes , in particular the use of industrial pesticides and other chemical pollution in the 20th century. Despite declines due to manmade causes, the bird remains a stable species. Cooper's hawk was formally described by the French naturalist Charles Lucien Bonaparte in 1828 from a specimen collected near Bordentown , New Jersey. He coined the binomial name Falco cooperii . The specific epithet and the common name were chosen to honour the naturalist William Cooper , one of the founders of the New York Lyceum of Natural History (later the New York Academy of Sciences ) in New York City. Other common names have been known to include the big blue darter, chicken hawk , hen hawk, Mexican hawk, quail hawk, striker and swift hawk. Cooper's hawk is a member of the genus Accipiter , sometimes referred to as true hawks (and the members of which are at times commonly referred to as goshawks or sparrowhawks). This genus is the most diverse of all in the species-rich family Accipitridae , with nearly 50 recognized species, and is also the most diverse of all diurnal raptor genera. The genus Accipiter appeared to diversify in the last few million years due to an increase in accessible avian prey. They appear to be a sister genus to Circus or harriers , albeit a distantly related one. Other smaller genera including Harpagus and Erythrotriorchis also appear to bear some relation. Genetic studies of three Asian Accipiter species showed that they may not be a monophyletic group , with various clades divisions outside traditional subfamily lines, with even the sharp-shinned hawk-like and aptly named tiny hawk ( Accipiter supercilious ) appearing to cluster outside of the genus nearer very dissimilar genera like Buteo and Milvus . It appears that Cooper's hawk was the earliest Accipiter to colonize North America with a well-defined fossil record dating back perhaps 0.5-1 million years. Fossil evidence shows then that the goshawk came second and, despite the considerably wider range of the sharp-shinned hawk compared to the other two species, the ancestors of the sharp-shinned hawk came over the Bering Land Bridge last. Genetic testing has indicated that Cooper's hawk is quite closely related to the northern goshawk, with the similar superficial characteristics of Cooper's to the sharp-shinned hawk, a close relative of the Old World sparrowhawk , apparently obtained through convergent evolution . A natural hybrid of a Cooper's hawk and a northern goshawk with intermediate physical characteristics was verified via genetic testing of a migrant juvenile in Cape May and was thought to indicate a northward expansion of Cooper's range into historic goshawk haunts. No subspecies are recognized of Cooper's hawk. A previously described subspecies, A. c. mexicanus , was discounted due to being weakly differentiated. However, evidence based on genetic markers shows that westerly birds such those in British Columbia populations are genetically differentiated from those in the Upper Midwest , indicating that Cooper's hawk were restricted to at least two Pleistocene glacial refugia with the Rocky mountains acting as a natural barrier to gene flow between hawks on either side while breeding. Several of the other similar largish Accipiter species in the Americas appear to be closely related, possibly within a species complex , to Cooper's hawk, namely the bicolored hawk , widespread through Central and South America, and the Chilean hawk ( Accipiter chilensis ). While there is some degree of obvious differentiation from these species in appearance, distribution and behavior, more nebulous is the relationship of Cooper's hawk to the very similar Gundlach's hawk of Cuba . In general the relationship of Cooper's and Gundlach's hawk is muddled and genetic testing indicated that it is possible (but not certain) that Gundlach's may be insufficiently distinct to qualify as a separate species. It is almost certain that Cooper's hawk would at least qualify as the paraspecies for the Gundlach's and data has indicated fairly recent colonization and hybridization between the two hawks. Cooper's hawk is a medium-sized hawk and relatively large for an Accipiter . Compared to related species, they tend to have moderate-length wings, a long, often graduated or even wedge-shaped tail and long though moderately thick legs and toes. Their eyes tend to be set well forward in the sides of the relatively large and squarish-looking head (though the head can look somewhat rounded if the feathers on the nape are held flush) and a relatively short but robust bill. They have hooked bills that are well-adapted for tearing the flesh of prey, as is typical of raptorial birds. Generally, Cooper's hawks can be considered secretive, often perching within the canopy , but can use more open perches, especially in the western part of the range or in winter when they may use leafless or isolated trees, utility poles or exposed stumps . On perched hawks, the wing-tips tend to appear to cover less than one third of the tail, sometimes seeming to barely cover the covert feathers. As adults, they may be a solid blue-gray or brown-gray color above. Adults usually have a well-defined crown of blackish-brown feathers above a paler nape and hindneck offset against their streaked rufous cheeks. Their tail is blue-gray on top and pale underneath, barred with three black bands in a rather even pattern and ending in a rather conspicuous white tip. The adult's underside shows a bit of whitish base color overlaid heavily with coarse, irregular rufous to cinnamon bands, though these narrow into marginal shaft streaks around the throat. Against the rich color on the rest of the underside, the pure white crissum on adults is conspicuous. Adult females may average slightly more brownish or grayish above, while some adult males can range rarely into almost a powder blue color. Although little regional variation is known in the plumage, adult coloring in the Pacific Northwest averages slightly darker overall. Aberrant pale plumage was recorded in at least four total birds of both sexes, all of which were almost completely white and lacked any underside streaking. These birds had faded back color and lacking strong barring on the tail. An aberrant dark female was also recorded. As a juvenile, she had a blackish-brown (rather than mid-brown) back and dark inky feathers below with grayish ground color barely showing. Later she produced an aberrant male with similar characteristics that successfully fledged. The latter two were possible cases of melanism and such dark variations are virtually unprecedented in any Accipiter species. Juveniles of the species are generally dark brown above, though the feathers are not infrequently edged with rufous to cinnamon and have a variable whitish mottling about the back, wing coverts and, mainly, the scapulars. Juvenile Cooper's tend to have streaking or washing of tawny on the cheeks, ending in a light nuchal strip, giving them a hooded appearance unlike the capped appearance of adults (some juveniles, unlike adults, may manifest a slim supercilium as well). The crown is brown on juveniles rather than blackish as in adults. The tail is similar to that of the adult but more brownish and sometimes shows an additional fourth band. The juvenile has more pale white to cream base color showing than older birds, with variable dusky throat striping and mid-brown streaks, which appear as sharply defined from about the lower throat to the lower breast. The juvenile may have brown to black spots or bars on the thighs with thin black streaks mostly ending at the belly and conspicuous white crissum and undertail coverts. Juveniles can tend to appear more "disheveled" and less compact than adults in feather composition. In flight, though usually considered medium-sized, Cooper's hawks can appear fairly small. This effect is emphasized by the short wings relative to the elongated tail (unlike unrelated hawks, the wingspan is usually less than twice as broad as the total length). The species tends to have rounded wings, a long rounded tail and long legs, much like other Accipiters . Cooper's hawks have a strong flight with stiff beats and short glides, tending to do so on quite level wings with wrist thrust forward yet the head consistently projects. The 5 outer functional primaries are notched on their inner webs, the outermost is the longest, the next outermost nearly as long. When soaring, these hawks do so on flattish or, more commonly, slightly raised wings, with fairly straight leading edges. Against the barred underbody on adults, the wings are more or less flecked in similar color, with pale greyish flight feathers and a broadly white-tipped tail correspondingly barred with dark gray. Meanwhile, the upperside of adults is essentially all blue-grey. Juvenile are mostly dark above though manifest a hooded effect on the head and a rufous-buff edges and especially whitish mottling, the latter can be fairly apparent. Juveniles are mainly whitish below with neatly dark streaks about the wing linings, breast, flanks and thighs, with bars on the axillaries and flight feathers. The tail of the juvenile has a broadly white tip and bars like adults but the ground color is a paler shade of gray. Adults have eyes ranging from light orange to red, with males averaging darker in eye color, while those of juveniles are yellow. Among 370 breeding hawks from different parts of the range, 1-year-old males usually had light orange eyes and 1-year-old females usually yellow eyes. Meanwhile, males of 2 or more years old always had consistently darker eyes than the eyes of females of the same relative age, with most males of the age having largely either orange (40.4%) or dark orange (32.3%) eyes, while female eyes at this stage were light orange or lighter. From the second year, the eyes of Cooper's hawks may grow darker still but stop darkening shortly thereafter. 3-year or older males were found to have predominantly dark orange (37.3% vs 21.6% of similar age females), red (34.6% vs 3.3% of similar age females) or mid-orange (26.6% vs 55% of similar age females). For unclear reasons, far more adults in British Columbia and North Dakota (83% of males, 63% of females) had dark orange or red eyes (which also manifested at an earlier age in British Columbia) than mature hawks in Wisconsin (49% of males, 14% of females). Most females over 2 years old in Wisconsin were found to have light orange eyes. The purpose of bright eye color in the hawks may be correlated to feeding stimulation of nestling hawks (i.e. darker orange or red objects may be more perceptible and tend to be pecked at more so than duller colors). The eyes of this hawk, as in most predatory birds, face forward, enabling good depth perception for hunting and catching prey while flying at top speeds. Adults have greenish yellow ceres and have legs of orangish to yellow while these parts on juveniles are a paler hue, yellow-green to yellow. The prebasic molt begins in late April–May and takes about 4 months. The female usually begins to molt about 7–10 days sooner than the male. Molts occur inward towards the body on the wing feathers. Tail molt may generally start with the middle tail feathers, proceeding posteriorly to the upper tail coverts, also starting with the median feathers on the scapulars. Up to 36% of juvenile feathers may be retained in the second pre-basic molt. Arrested molt has been recorded in the late nesting period, often pausing after the third primary is molted. Molts tend to be halted especially when food supplies are down during the brooding stage, and may be resumed after the stress of feeding the brooding diminishes. Cooper's hawks are fairly variable in size. There is usually minimal to no overlap in dimensions between the sexes, with females being considerably larger than males. On average, she may be about 20% larger linearly and around 40% heavier (though can be up to 125% more massive). More westerly Cooper's hawks (roughly west of the Rocky mountains ) show slightly less pronounced sexual dimorphism than hawks of the species elsewhere. Sexual dimorphism in Cooper's hawks is most reliably measured by wing size, talon size, then body mass. Although there is some margin of error, within a given region dimensions of the two sexes never overlap in these regards (but may overlap marginally in tarsal and tail lengths). In general terms, Accipiter species are among the most sexually dimorphic in size of all raptorial birds. Sexual dimorphism in Accipiters may be due to greater male efficiency through smaller size and resulting agility in food gathering for the family group. Meanwhile, the female may be better suited to the rigors of brooding (including perhaps most nest defense) due to her larger size, also allowing the sexes to compete less on the same food sources. Geographic variation in body size has also been found, with more easterly hawks tending to be rather larger on average than those found in western North America. On the contrary, in the American southwest , the species may reportedly reach its largest sizes but there is little evidence that these birds average distinctly larger than the large bodied individuals measured in the more northeasterly parts of the species' range in North America, from eastern North Dakota to New Jersey . The size variation evidenced in Cooper's hawks is apparently the most pronounced of any of the three North American species of Accipiter . However, Cooper's hawks are one of an estimated 25% of studied bird species that do not appear to correspond to Bergmann's rule (i.e. being larger where living farther north) instead varying in size much more so by longitude . Furthermore, juveniles can differ somewhat in size, tending to be slightly lighter and smaller than older birds, but not infrequently averaging longer in tail and especially wing length. Total length of full-grown birds can vary from 35 to 46 cm (14 to 18 in) in males and 42 to 50 cm (17 to 20 in) in females. Wingspan may range from 62 to 99 cm (24 to 39 in) , with an average of around 84 cm (33 in) . Body mass, along with standard measurements, is much more frequently measured than total length or wingspan in different populations. Museum specimens from the western United States averaged 280 g (9.9 oz) in 48 males and 473 g (1.043 lb) in 20 females, while those sourced from the eastern United States averaged 338 g (11.9 oz) in 16 males and 566 g (1.248 lb) in 31 females. Average weight of 104 male migrating hawks in Cedar Grove, Wisconsin was 342 g (12.1 oz) (with adults averaging 4% heavier than juveniles), whilst the average of 115 females migrants was 518 g (1.142 lb) (with adult averaging about 5.5% heavier than juveniles). A different sample of Wisconsin Cooper's hawks reportedly averaged 327 g (11.5 oz) in males (sample size 60) and 580.3 g (1.279 lb) in females (sample size 57). At Cape May Point , New Jersey , weights were similar as in Wisconsin (although only hatching-year juveniles were apparently weighed), with averages of 339.2 and 347 g (11.96 and 12.24 oz) in two samples of males and 518 and 530.3 g (1.142 and 1.169 lb) in the two samples for females. Migrant hawks in the Goshute Mountains of Nevada were significantly lighter than the eastern ones at 269 g (9.5 oz) in 183 first year males and 281 g (9.9 oz) in 177 older males and 399 g (14.1 oz) in 310 first year females and 439 g (15.5 oz) in 416 older females. Weights were similar to the Goshutes in the Marin Headlands , California where 50 males (all first-years) averaged 288 g (10.2 oz) and 117 first-year females averaged 417 g (14.7 oz) . Averaged between early and late summer, the average mass of males in Oregon was 280.7 g (9.90 oz) and that of females was reported at 488.4 g (1.077 lb) . The average weights of Cooper's hawks from Oregon was about 19.4% lower in males and 14.5% lower in females than those from Wisconsin but the Oregon hawks evidenced less seasonal variation in weight. In British Columbia , males averaged 295.8 g (10.43 oz) and females averaged 525.5 g (1.159 lb) while in western and eastern North Dakota, males averaged 301.5 and 318.7 g (10.64 and 11.24 oz) and females averaged 514.3 and 563.3 g (1.134 and 1.242 lb) . In northern Florida, males averaged 288 g (10.2 oz) and females averaged 523 g (1.153 lb) . In general, males may weigh anywhere from 215 to 390 g (7.6 to 13.8 oz) and females anywhere from 305.8 to 701 g (0.674 to 1.545 lb) , the lightest hawks generally being juveniles recorded from the Goshutes of Nevada, the heaviest known being adults from Wisconsin. Among standard measurements, the wing chord may vary from 214 to 252 mm (8.4 to 9.9 in) in males and from 247 to 278 mm (9.7 to 10.9 in) in females. Wing chord is generally commensurate with body mass, averaging largest in the heavier hawks of eastern North Dakota, where males averaged 232.6 mm (9.16 in) and females 264.3 mm (10.41 in) , and in Wisconsin, where males averaged 236.9 mm (9.33 in) and females 267.1 mm (10.52 in) (those from Cape May also being similar to those two samples). However, smaller, more westerly hawks such as those in the Goshute mountains, where males measured at a mean of 224.1 mm (8.82 in) and females at a mean of 254.8 mm (10.03 in) , and in British Columbia, with a male mean of 227 mm (8.9 in) and female mean of 256.8 mm (10.11 in) , were proportionately longer winged relative to their other body proportions. The tail of males may vary from 166 to 211 mm (6.5 to 8.3 in) and that of females at 203 to 242 mm (8.0 to 9.5 in) , consistently over 200 mm (7.9 in) in females and averaging under 190 mm (7.5 in) in males. In tarsus length, males may vary from 55.2 to 73 mm (2.17 to 2.87 in) , with an average of 64.1 mm (2.52 in) in museum specimens, and females from 62 to 76 mm (2.4 to 3.0 in) , with an average of 71.1 mm (2.80 in) in museum specimens. The culmen may measure from 11.7 to 17.5 mm (0.46 to 0.69 in) in males, averaging about 16 mm (0.63 in) , and from 17.5 to 23 mm (0.69 to 0.91 in) in females, averaging about 19 mm (0.75 in) . The hallux claw , the enlarged rear talon featured on nearly all accipitrids, may measure from 17 to 21.7 mm (0.67 to 0.85 in) in males, averaging about 19.2 mm (0.76 in) , and from 19.8 to 26.7 mm (0.78 to 1.05 in) in females, averaging about 23.3 mm (0.92 in) . The footpad of Cooper's hawks may measure in males 61 to 70.2 mm (2.40 to 2.76 in) , averaging 66 mm (2.6 in) in 42, and in females 74.1 to 83.5 mm (2.92 to 3.29 in) , averaging 76.8 mm (3.02 in) in 23. For unclear reasons, the smaller-bodied hawks found in British Columbia were found to be proportionately larger footed, median toe length between sexes of 37.3 mm (1.47 in) , than the larger bodied ones in Wisconsin. Some authors have claimed that during breeding Cooper's hawks may utter well over 40 call variations, which would rank them as having among the most varied collection of calls recorded for any raptor. However, many such variations are probably quite subtle (marginal differences in harshness, clarity, tempo and volume) and other authors have diagnosed only four overall call types. The typical call of a Cooper's hawk is a harsh, cackling yelp. This call may be translated as keh-keh-keh ..., males tending to have a higher pitched, less raspy and faster-paced voice than females. However, some variants uttered by males were surprisingly actually deeper than the female's version of said calls. A still more modulated and raucous version is given during the dawn chorus. Some studies have indicated that pairs nesting in more deeply wooded areas may vocalize more frequently due to inferior sight lines. However, hawks nesting in urban areas of Arizona do not seem to vocalize less than their rural nesting counterparts. There is perhaps some evidence that individual hawk's voices may become lower pitched with age. When coming with food to the nest or while displaying during courtship, the male may let out a nighthawk -like kik , apparently this call is more prevalent in pairs using thicker woods. Infrequently, females may utter the kik call as well, apparently when looking for her mate or gathering nesting materials. Many soft calls have been recorded in intimate or "conversational" interactions, exclusively between breeding pairs and between mothers and their broods. The initial call of the young is a cheep or chirrp , which by the time they are fledgling young alters to a penetrating hunger call, eeeeeeee-oo or tseeeee-ar (among different transliterations). The higher pitched calls of the young may even extend to females nesting within their first year while still in immature plumage. Females have what is often thought of as their own hunger cry, whaaaa , heard especially in poorer food areas, when the male appears. Nonetheless, the females whaaaa call has also been uttered in different contexts, such as during nest building and during a "postural bowing" display, and some authors inferred that it may be a means of communicating to the male that it is not dangerous for him to approach her (as female Accipiters can be dangerous to the much smaller males). Generally, Cooper's hawks are silent outside the breeding season. Rarely, though, some males that appear to be isolated from any other hawks of their species have been known to call during winter. Accipiter species in North America are arguably the most vexing raptor to identify in the continent. The other two species in North America are the smaller sharp-shinned hawk ( Accipiter striatus ) and the larger northern goshawk ( Accipiter gentilis ). Compared to the other two Accipiters , Cooper's have an intermediate amount of feathering at top of the tarsus, as well as intermediate relative middle toe length and eye proportions, but have relatively the longest tail and the shortest wings of the three. Cooper's and sharp-shinned hawk are very similar (sometimes considered almost identical) in plumage characteristics at all stages of development. Most Cooper's hawks are considerably larger than most sharp-shinned hawks. Generally, Cooper's species is crow -sized, with the males about the size of a small crow and the females the size of a large crow , while most sharp-shinned hawks are about the size of a large jay . Also in the hand, Cooper's hawks and sharp-shinned hawks may be fairly reliably distinguished by their sizes, with the smallest male Cooper's always being heavier and larger clawed than the largest female sharp-shinned hawk (with a 97–98% difference in dimensions of the wing and tail). However, in the field, especially when hawks must be identified in at a distance or at unfavorable angles (such as when migrating) or at a brief glance (such as when hunting), even experienced birdwatchers may not always be able to certainly distinguish the two species, especially female sharp-shins against the nearly similarly sized male Cooper's. The sharp-shinned hawk usually evidences a slimmer, slighter look, with more dainty features, and has relatively longer wings and a shorter and more squared tail with a much thinner white tip. Other slight difference may be noted in plumage via the sharp-shins lacking the capped appearance of adult Cooper's (being more hooded) and being generally slightly darker above. Juvenile sharp-shins, upon relatively leisurely study, can be seen to differ from juvenile Cooper's by having clearer supercilia, browner cheeks and less extensive whitish mottling above and also coarser streaking below extending more to belly. Bare parts, mostly distinguishable as well at close range, differ by the more centered and clearly relatively larger eyes and notably stick-like legs of the sharp-shins. However, often these features can often be difficult to impossible to discern when the hawks are seen in the wild. More distinctive in the field is the larger, more protruding head of the flying Cooper's hawks rather than the compact, rounded head of the sharp-shins which barely appear to exceed the leading edge of the wings in flight. Sometimes Cooper's is considered to look like a "flying cross" in comparison to the sharp-shins. Accipiter hawks of all species are seen mostly flying with quick, consecutive wing beats and a short glide (sometimes abbreviated as "flap-flap-glide"), though the species may also soar as well. However, the sharp-shinned hawk has a more buoyant flight with faster wing beats than Cooper's and soars with flatter wings (although again variations in the field make these characteristics far from foolproof). As for the northern goshawk, the smallest male is still usually "clearly" larger than most large female Cooper's hawks. In the Goshutes mountains, migrant male goshawks overlapped with female Cooper's hawks only in the length of the tail and the tarsus, with the body mass especially being quite distinct. In Oregon, male goshawks averaged no less than 34% more massive than female Cooper's hawks, however the footpad of Cooper's females was almost the same size (7% larger on average in the latter) as the male goshawks (these may be features adapted to procuring birds as prey more so as bird-hunting raptors tend to have more elongated foot morphology). Proportionately, goshawks have longer, broader wings, shorter tail and a generally more Buteo -like form overall. Adult goshawks also have broad supercilia, pale gray color on the underside and a much darker coloring on the back. Given reasonable views, adult goshawks are very different looking and hard to mistake for any Cooper's hawk. Meanwhile, the juvenile goshawk is much paler edged above than the smaller Cooper's, including a panel formed along larger wing coverts. Below, juvenile goshawks have heavier streaks of a darker brown color than juvenile Cooper's. Also, the banding on the tail is off-set on goshawks, creating a zigzag effect on the tail, unlike the even barring on the juvenile Cooper's. Again, though, female Cooper's and male goshawks can come close to the same size and the not dissimilar juvenile plumage of the two species can lead to regular misidentification, especially to those with less prior experience viewing the more scarce goshawk. The most reliable way to distinguish a large juvenile Accipiter in the field are the differing proportions of the two species, followed by the heavier streaking below and irregular tail banding of the goshawk. For Cooper's hawk, there may be a possible and marginal overlap with the bicolored hawk ( Accipiter bicolor ) in southern Mexico and Central America. The latter species of similar form and size but at all ages is generally unmarked with bars or streaks below, also with a more or less uniform mantle. Vagrating migrant Cooper's hawks to Cuba may very rarely occur alongside another close relative, Gundlach's hawk ( Accipiter gundlachi ), which is quite similar in most aspects to Cooper's but is slightly larger with a darker hue about the back and the cap, a gray cheek, more dense and rich rufous color on the underside and wing panel in adults and darker and more heavy streaking in juvenile form. More unlikely to be mistaken for a Cooper's hawk are some buteonine hawks such as gray hawks ( Buteo plagiatus ), roadside hawks ( Rupornis magnirostris ) (in Mexico and points south) and broad-winged hawks ( Buteo platypterus ) which are all similar in size to Cooper's as well as the slightly larger red-shouldered hawk ( Buteo lineatus ). Even the most similar buteonine hawks have notably different proportions than a Cooper's hawk, possessing relatively much longer wings and a much shorter tail. Given reasonable views, all such species are fairly to extremely different in plumage even in juvenile form. Cooper's hawks are fairly variable in size. There is usually minimal to no overlap in dimensions between the sexes, with females being considerably larger than males. On average, she may be about 20% larger linearly and around 40% heavier (though can be up to 125% more massive). More westerly Cooper's hawks (roughly west of the Rocky mountains ) show slightly less pronounced sexual dimorphism than hawks of the species elsewhere. Sexual dimorphism in Cooper's hawks is most reliably measured by wing size, talon size, then body mass. Although there is some margin of error, within a given region dimensions of the two sexes never overlap in these regards (but may overlap marginally in tarsal and tail lengths). In general terms, Accipiter species are among the most sexually dimorphic in size of all raptorial birds. Sexual dimorphism in Accipiters may be due to greater male efficiency through smaller size and resulting agility in food gathering for the family group. Meanwhile, the female may be better suited to the rigors of brooding (including perhaps most nest defense) due to her larger size, also allowing the sexes to compete less on the same food sources. Geographic variation in body size has also been found, with more easterly hawks tending to be rather larger on average than those found in western North America. On the contrary, in the American southwest , the species may reportedly reach its largest sizes but there is little evidence that these birds average distinctly larger than the large bodied individuals measured in the more northeasterly parts of the species' range in North America, from eastern North Dakota to New Jersey . The size variation evidenced in Cooper's hawks is apparently the most pronounced of any of the three North American species of Accipiter . However, Cooper's hawks are one of an estimated 25% of studied bird species that do not appear to correspond to Bergmann's rule (i.e. being larger where living farther north) instead varying in size much more so by longitude . Furthermore, juveniles can differ somewhat in size, tending to be slightly lighter and smaller than older birds, but not infrequently averaging longer in tail and especially wing length. Total length of full-grown birds can vary from 35 to 46 cm (14 to 18 in) in males and 42 to 50 cm (17 to 20 in) in females. Wingspan may range from 62 to 99 cm (24 to 39 in) , with an average of around 84 cm (33 in) . Body mass, along with standard measurements, is much more frequently measured than total length or wingspan in different populations. Museum specimens from the western United States averaged 280 g (9.9 oz) in 48 males and 473 g (1.043 lb) in 20 females, while those sourced from the eastern United States averaged 338 g (11.9 oz) in 16 males and 566 g (1.248 lb) in 31 females. Average weight of 104 male migrating hawks in Cedar Grove, Wisconsin was 342 g (12.1 oz) (with adults averaging 4% heavier than juveniles), whilst the average of 115 females migrants was 518 g (1.142 lb) (with adult averaging about 5.5% heavier than juveniles). A different sample of Wisconsin Cooper's hawks reportedly averaged 327 g (11.5 oz) in males (sample size 60) and 580.3 g (1.279 lb) in females (sample size 57). At Cape May Point , New Jersey , weights were similar as in Wisconsin (although only hatching-year juveniles were apparently weighed), with averages of 339.2 and 347 g (11.96 and 12.24 oz) in two samples of males and 518 and 530.3 g (1.142 and 1.169 lb) in the two samples for females. Migrant hawks in the Goshute Mountains of Nevada were significantly lighter than the eastern ones at 269 g (9.5 oz) in 183 first year males and 281 g (9.9 oz) in 177 older males and 399 g (14.1 oz) in 310 first year females and 439 g (15.5 oz) in 416 older females. Weights were similar to the Goshutes in the Marin Headlands , California where 50 males (all first-years) averaged 288 g (10.2 oz) and 117 first-year females averaged 417 g (14.7 oz) . Averaged between early and late summer, the average mass of males in Oregon was 280.7 g (9.90 oz) and that of females was reported at 488.4 g (1.077 lb) . The average weights of Cooper's hawks from Oregon was about 19.4% lower in males and 14.5% lower in females than those from Wisconsin but the Oregon hawks evidenced less seasonal variation in weight. In British Columbia , males averaged 295.8 g (10.43 oz) and females averaged 525.5 g (1.159 lb) while in western and eastern North Dakota, males averaged 301.5 and 318.7 g (10.64 and 11.24 oz) and females averaged 514.3 and 563.3 g (1.134 and 1.242 lb) . In northern Florida, males averaged 288 g (10.2 oz) and females averaged 523 g (1.153 lb) . In general, males may weigh anywhere from 215 to 390 g (7.6 to 13.8 oz) and females anywhere from 305.8 to 701 g (0.674 to 1.545 lb) , the lightest hawks generally being juveniles recorded from the Goshutes of Nevada, the heaviest known being adults from Wisconsin. Among standard measurements, the wing chord may vary from 214 to 252 mm (8.4 to 9.9 in) in males and from 247 to 278 mm (9.7 to 10.9 in) in females. Wing chord is generally commensurate with body mass, averaging largest in the heavier hawks of eastern North Dakota, where males averaged 232.6 mm (9.16 in) and females 264.3 mm (10.41 in) , and in Wisconsin, where males averaged 236.9 mm (9.33 in) and females 267.1 mm (10.52 in) (those from Cape May also being similar to those two samples). However, smaller, more westerly hawks such as those in the Goshute mountains, where males measured at a mean of 224.1 mm (8.82 in) and females at a mean of 254.8 mm (10.03 in) , and in British Columbia, with a male mean of 227 mm (8.9 in) and female mean of 256.8 mm (10.11 in) , were proportionately longer winged relative to their other body proportions. The tail of males may vary from 166 to 211 mm (6.5 to 8.3 in) and that of females at 203 to 242 mm (8.0 to 9.5 in) , consistently over 200 mm (7.9 in) in females and averaging under 190 mm (7.5 in) in males. In tarsus length, males may vary from 55.2 to 73 mm (2.17 to 2.87 in) , with an average of 64.1 mm (2.52 in) in museum specimens, and females from 62 to 76 mm (2.4 to 3.0 in) , with an average of 71.1 mm (2.80 in) in museum specimens. The culmen may measure from 11.7 to 17.5 mm (0.46 to 0.69 in) in males, averaging about 16 mm (0.63 in) , and from 17.5 to 23 mm (0.69 to 0.91 in) in females, averaging about 19 mm (0.75 in) . The hallux claw , the enlarged rear talon featured on nearly all accipitrids, may measure from 17 to 21.7 mm (0.67 to 0.85 in) in males, averaging about 19.2 mm (0.76 in) , and from 19.8 to 26.7 mm (0.78 to 1.05 in) in females, averaging about 23.3 mm (0.92 in) . The footpad of Cooper's hawks may measure in males 61 to 70.2 mm (2.40 to 2.76 in) , averaging 66 mm (2.6 in) in 42, and in females 74.1 to 83.5 mm (2.92 to 3.29 in) , averaging 76.8 mm (3.02 in) in 23. For unclear reasons, the smaller-bodied hawks found in British Columbia were found to be proportionately larger footed, median toe length between sexes of 37.3 mm (1.47 in) , than the larger bodied ones in Wisconsin. Some authors have claimed that during breeding Cooper's hawks may utter well over 40 call variations, which would rank them as having among the most varied collection of calls recorded for any raptor. However, many such variations are probably quite subtle (marginal differences in harshness, clarity, tempo and volume) and other authors have diagnosed only four overall call types. The typical call of a Cooper's hawk is a harsh, cackling yelp. This call may be translated as keh-keh-keh ..., males tending to have a higher pitched, less raspy and faster-paced voice than females. However, some variants uttered by males were surprisingly actually deeper than the female's version of said calls. A still more modulated and raucous version is given during the dawn chorus. Some studies have indicated that pairs nesting in more deeply wooded areas may vocalize more frequently due to inferior sight lines. However, hawks nesting in urban areas of Arizona do not seem to vocalize less than their rural nesting counterparts. There is perhaps some evidence that individual hawk's voices may become lower pitched with age. When coming with food to the nest or while displaying during courtship, the male may let out a nighthawk -like kik , apparently this call is more prevalent in pairs using thicker woods. Infrequently, females may utter the kik call as well, apparently when looking for her mate or gathering nesting materials. Many soft calls have been recorded in intimate or "conversational" interactions, exclusively between breeding pairs and between mothers and their broods. The initial call of the young is a cheep or chirrp , which by the time they are fledgling young alters to a penetrating hunger call, eeeeeeee-oo or tseeeee-ar (among different transliterations). The higher pitched calls of the young may even extend to females nesting within their first year while still in immature plumage. Females have what is often thought of as their own hunger cry, whaaaa , heard especially in poorer food areas, when the male appears. Nonetheless, the females whaaaa call has also been uttered in different contexts, such as during nest building and during a "postural bowing" display, and some authors inferred that it may be a means of communicating to the male that it is not dangerous for him to approach her (as female Accipiters can be dangerous to the much smaller males). Generally, Cooper's hawks are silent outside the breeding season. Rarely, though, some males that appear to be isolated from any other hawks of their species have been known to call during winter. Accipiter species in North America are arguably the most vexing raptor to identify in the continent. The other two species in North America are the smaller sharp-shinned hawk ( Accipiter striatus ) and the larger northern goshawk ( Accipiter gentilis ). Compared to the other two Accipiters , Cooper's have an intermediate amount of feathering at top of the tarsus, as well as intermediate relative middle toe length and eye proportions, but have relatively the longest tail and the shortest wings of the three. Cooper's and sharp-shinned hawk are very similar (sometimes considered almost identical) in plumage characteristics at all stages of development. Most Cooper's hawks are considerably larger than most sharp-shinned hawks. Generally, Cooper's species is crow -sized, with the males about the size of a small crow and the females the size of a large crow , while most sharp-shinned hawks are about the size of a large jay . Also in the hand, Cooper's hawks and sharp-shinned hawks may be fairly reliably distinguished by their sizes, with the smallest male Cooper's always being heavier and larger clawed than the largest female sharp-shinned hawk (with a 97–98% difference in dimensions of the wing and tail). However, in the field, especially when hawks must be identified in at a distance or at unfavorable angles (such as when migrating) or at a brief glance (such as when hunting), even experienced birdwatchers may not always be able to certainly distinguish the two species, especially female sharp-shins against the nearly similarly sized male Cooper's. The sharp-shinned hawk usually evidences a slimmer, slighter look, with more dainty features, and has relatively longer wings and a shorter and more squared tail with a much thinner white tip. Other slight difference may be noted in plumage via the sharp-shins lacking the capped appearance of adult Cooper's (being more hooded) and being generally slightly darker above. Juvenile sharp-shins, upon relatively leisurely study, can be seen to differ from juvenile Cooper's by having clearer supercilia, browner cheeks and less extensive whitish mottling above and also coarser streaking below extending more to belly. Bare parts, mostly distinguishable as well at close range, differ by the more centered and clearly relatively larger eyes and notably stick-like legs of the sharp-shins. However, often these features can often be difficult to impossible to discern when the hawks are seen in the wild. More distinctive in the field is the larger, more protruding head of the flying Cooper's hawks rather than the compact, rounded head of the sharp-shins which barely appear to exceed the leading edge of the wings in flight. Sometimes Cooper's is considered to look like a "flying cross" in comparison to the sharp-shins. Accipiter hawks of all species are seen mostly flying with quick, consecutive wing beats and a short glide (sometimes abbreviated as "flap-flap-glide"), though the species may also soar as well. However, the sharp-shinned hawk has a more buoyant flight with faster wing beats than Cooper's and soars with flatter wings (although again variations in the field make these characteristics far from foolproof). As for the northern goshawk, the smallest male is still usually "clearly" larger than most large female Cooper's hawks. In the Goshutes mountains, migrant male goshawks overlapped with female Cooper's hawks only in the length of the tail and the tarsus, with the body mass especially being quite distinct. In Oregon, male goshawks averaged no less than 34% more massive than female Cooper's hawks, however the footpad of Cooper's females was almost the same size (7% larger on average in the latter) as the male goshawks (these may be features adapted to procuring birds as prey more so as bird-hunting raptors tend to have more elongated foot morphology). Proportionately, goshawks have longer, broader wings, shorter tail and a generally more Buteo -like form overall. Adult goshawks also have broad supercilia, pale gray color on the underside and a much darker coloring on the back. Given reasonable views, adult goshawks are very different looking and hard to mistake for any Cooper's hawk. Meanwhile, the juvenile goshawk is much paler edged above than the smaller Cooper's, including a panel formed along larger wing coverts. Below, juvenile goshawks have heavier streaks of a darker brown color than juvenile Cooper's. Also, the banding on the tail is off-set on goshawks, creating a zigzag effect on the tail, unlike the even barring on the juvenile Cooper's. Again, though, female Cooper's and male goshawks can come close to the same size and the not dissimilar juvenile plumage of the two species can lead to regular misidentification, especially to those with less prior experience viewing the more scarce goshawk. The most reliable way to distinguish a large juvenile Accipiter in the field are the differing proportions of the two species, followed by the heavier streaking below and irregular tail banding of the goshawk. For Cooper's hawk, there may be a possible and marginal overlap with the bicolored hawk ( Accipiter bicolor ) in southern Mexico and Central America. The latter species of similar form and size but at all ages is generally unmarked with bars or streaks below, also with a more or less uniform mantle. Vagrating migrant Cooper's hawks to Cuba may very rarely occur alongside another close relative, Gundlach's hawk ( Accipiter gundlachi ), which is quite similar in most aspects to Cooper's but is slightly larger with a darker hue about the back and the cap, a gray cheek, more dense and rich rufous color on the underside and wing panel in adults and darker and more heavy streaking in juvenile form. More unlikely to be mistaken for a Cooper's hawk are some buteonine hawks such as gray hawks ( Buteo plagiatus ), roadside hawks ( Rupornis magnirostris ) (in Mexico and points south) and broad-winged hawks ( Buteo platypterus ) which are all similar in size to Cooper's as well as the slightly larger red-shouldered hawk ( Buteo lineatus ). Even the most similar buteonine hawks have notably different proportions than a Cooper's hawk, possessing relatively much longer wings and a much shorter tail. Given reasonable views, all such species are fairly to extremely different in plumage even in juvenile form. Cooper's hawk's breeding range extends from southern Canada to northern Mexico. In southern Canada, they breed (but do not normally winter) in the southerly parts of the provinces of British Columbia , Alberta, Saskatchewan , Manitoba, Ontario , Quebec to extreme southwestern Nova Scotia . They reach their northerly limits as a breeder roughly in Jasper National Park and Cedar Lake, Manitoba . Cooper's hawks live almost throughout the contiguous United States , excepting some parts of the southern Great Plains , as well as perhaps a bit of northwestern Maine and northernmost Montana . Their breeding range terminates just before the southern part of Gulf Coast states, south Florida , the southern tip of Texas and all but inland northwestern Mexico. Their Mexican breeding range consists of northern Baja California , the mountains from eastern Sonora and Chihuahua to Durango , also recently in northern Coahuila , formerly east into Nuevo Leon and south to Michoacán and possibly still in Guerrero . In Oaxaca , records show that the species has been recorded year-around with the first confirmed breeding reported in 2001. In winter, they are found up to the southern half of Washington , the southern two-thirds of Idaho and Wyoming , southern South Dakota , the southern parts of Minnesota , Wisconsin and Michigan , extreme southwestern Ontario, southwestern and southeastern New York and New England up through all but northwestern Massachusetts and to the southeastern part of New Hampshire . In winter they range regularly throughout the parts of the southern United States where they do not breed, such as all Gulf Coast areas and in south Florida . Wintering Cooper's hawks are common through essentially all parts of Mexico, becoming less regular around Guatemala and isolated spots of the border of Honduras and Nicaragua , where the species is considered "infrequent but regular" as well as in central and southern Costa Rica and perhaps northern Panama . Vagrants have been recorded in Colombia . There are several cumulative records of Cooper's hawks also appearing in Cuba at times of migration but generally the species is still considered a vagrant rather than a regularly occurring species there. Cooper's hawks tend to occur in various types of temperate deciduous forest and mixed forest . They are also adaptable in all seasons to forested mountainous regions , especially foothills . The species may further make itself at home in some pure conifer forest, including the extreme southern part of the taiga but also in many parts of the west. The species can habituate favorably while breeding to various kinds of open woodlands , including small woodlots , riparian woodlands in dry country , pinyon woodlands, farmlands and floodplains . In fact, some authors felt the species increased locally in wooded parts of the Rocky mountains after human habitat fragmentation of once continuous woodland areas. Adaptability to forest fragmentation has also been reported in other parts of the range. In denser forest areas, these hawks tend to prefer easy access to edges , clearings , roads and waterways . For example, average distance between waterways and nests in Wisconsin and Utah was 66.1 and 224 m (217 and 735 ft) , respectively. However, in the Appalachians , there seemed to no detectable preference for access to water. Forest edges, in particular, tend to be key as these are peak hunting grounds for these hawks. Cooper's hawks usually occur at elevations from sea-level to 2,500 m (8,200 ft) , more infrequently up to 3,000 m (9,800 ft) . In the American southwest and northwestern Mexico, they are commonly considered a bird of wooded foothills, often dwelling above 1,000 m (3,300 ft) . Although they often live in areas where deciduous trees are predominant, almost throughout the range they are often attracted to stands of conifers, which, due to their density, provide more extensive shelter and perhaps a more sturdy nesting site. Therefore, in areas such as Massachusetts and Wisconsin, they most often used stands of white pines ( Pinus strobus ). Additional Wisconsin studies showed that exotic conifer stands now support many Cooper's hawks even where native woodland is available. Tall, native deciduous tree stands may still be used extensively elsewhere, i.e. American beeches ( Fagus grandifolia ) in New York (nearly 40% of nest trees used) and oaks in Maryland (60% of trees used as nests). This species often prefers fairly mature forest, i.e. in two different areas of Oregon , Cooper's hawks preferred areas with trees of 30–60 years old (and 656 trees per ha) and 50–70 years old (and 1159 trees per ha), respectively. On average, the number of trees per hectare in Arkansas were found to be 935.7. Canopy coverage is key to nesting Cooper's hawks, needing to be at minimum about 55–70%, averaging 55% in Wisconsin and 69.8% in Arizona. More so than breeding habitat, wintering habitat seems to be highly opportunistic. They may be found in any environment with some trees, including open woods , parkland and scrub areas . In Central America, wintering Cooper's hawks have been recorded in unusual habitats such as stunted cloud forest and treeless montane grassland . In most parts of the range, Cooper's hawks have shown to be somewhat adaptive to all gradients of human development , including urbanized areas and can even nest in many cities. They were once thought to be averse to cities and towns, but are now fairly common urban and suburban birds even when nesting. The species may even making use of isolated trees in suburbs, industrial parks and strip and shopping malls though large urban parks and other available wooded habitat is usually preferred in such areas when nesting. The cities provide plenty of prey species such as pigeons and doves and invasive species of bird for Cooper's hawk to prey on. Evidence from a well-studied population in the city of Tucson , Arizona shows that Cooper's hawks are now considerably more common within the city than elsewhere in the surrounding regions. Despite the success of Cooper's hawks in Tucson, attempts to find breeding activity in Phoenix and Casa Grande were unsuccessful, it is thought that the ambient temperature was too high or beyond thermal tolerance levels. Although more adaptable in habitat than the sharp-shinned hawk, studies from Pennsylvania have indicated that the species still more often than not prefers sizeable tracts of woodland for breeding and migrating to fragmented, developed areas. Similarly, in Tennessee , it was found for wintering Cooper's hawks that forested areas were 73% of the habitats used, which is far more prevalent than woodland available in the environs (with only 46% remaining wooded). Cooper's hawks tend to occur in various types of temperate deciduous forest and mixed forest . They are also adaptable in all seasons to forested mountainous regions , especially foothills . The species may further make itself at home in some pure conifer forest, including the extreme southern part of the taiga but also in many parts of the west. The species can habituate favorably while breeding to various kinds of open woodlands , including small woodlots , riparian woodlands in dry country , pinyon woodlands, farmlands and floodplains . In fact, some authors felt the species increased locally in wooded parts of the Rocky mountains after human habitat fragmentation of once continuous woodland areas. Adaptability to forest fragmentation has also been reported in other parts of the range. In denser forest areas, these hawks tend to prefer easy access to edges , clearings , roads and waterways . For example, average distance between waterways and nests in Wisconsin and Utah was 66.1 and 224 m (217 and 735 ft) , respectively. However, in the Appalachians , there seemed to no detectable preference for access to water. Forest edges, in particular, tend to be key as these are peak hunting grounds for these hawks. Cooper's hawks usually occur at elevations from sea-level to 2,500 m (8,200 ft) , more infrequently up to 3,000 m (9,800 ft) . In the American southwest and northwestern Mexico, they are commonly considered a bird of wooded foothills, often dwelling above 1,000 m (3,300 ft) . Although they often live in areas where deciduous trees are predominant, almost throughout the range they are often attracted to stands of conifers, which, due to their density, provide more extensive shelter and perhaps a more sturdy nesting site. Therefore, in areas such as Massachusetts and Wisconsin, they most often used stands of white pines ( Pinus strobus ). Additional Wisconsin studies showed that exotic conifer stands now support many Cooper's hawks even where native woodland is available. Tall, native deciduous tree stands may still be used extensively elsewhere, i.e. American beeches ( Fagus grandifolia ) in New York (nearly 40% of nest trees used) and oaks in Maryland (60% of trees used as nests). This species often prefers fairly mature forest, i.e. in two different areas of Oregon , Cooper's hawks preferred areas with trees of 30–60 years old (and 656 trees per ha) and 50–70 years old (and 1159 trees per ha), respectively. On average, the number of trees per hectare in Arkansas were found to be 935.7. Canopy coverage is key to nesting Cooper's hawks, needing to be at minimum about 55–70%, averaging 55% in Wisconsin and 69.8% in Arizona. More so than breeding habitat, wintering habitat seems to be highly opportunistic. They may be found in any environment with some trees, including open woods , parkland and scrub areas . In Central America, wintering Cooper's hawks have been recorded in unusual habitats such as stunted cloud forest and treeless montane grassland . In most parts of the range, Cooper's hawks have shown to be somewhat adaptive to all gradients of human development , including urbanized areas and can even nest in many cities. They were once thought to be averse to cities and towns, but are now fairly common urban and suburban birds even when nesting. The species may even making use of isolated trees in suburbs, industrial parks and strip and shopping malls though large urban parks and other available wooded habitat is usually preferred in such areas when nesting. The cities provide plenty of prey species such as pigeons and doves and invasive species of bird for Cooper's hawk to prey on. Evidence from a well-studied population in the city of Tucson , Arizona shows that Cooper's hawks are now considerably more common within the city than elsewhere in the surrounding regions. Despite the success of Cooper's hawks in Tucson, attempts to find breeding activity in Phoenix and Casa Grande were unsuccessful, it is thought that the ambient temperature was too high or beyond thermal tolerance levels. Although more adaptable in habitat than the sharp-shinned hawk, studies from Pennsylvania have indicated that the species still more often than not prefers sizeable tracts of woodland for breeding and migrating to fragmented, developed areas. Similarly, in Tennessee , it was found for wintering Cooper's hawks that forested areas were 73% of the habitats used, which is far more prevalent than woodland available in the environs (with only 46% remaining wooded). Cooper's hawk is a typical Accipiter in all respects. This species tends to be active earlier in the morning than sharp-shinned hawks and Eurasian sparrowhawks ( Accipiter nisus ) and is generally much more likely to be active in the morning than in the afternoon. These hawks may readily take to conifers to roost , generally sleeping with their heads tucked in. During daylight hours, they tend to preen while sitting on a perch about 11 times a day, and may take about 1–20 minutes to do so. When attaining water to drink, Cooper's hawks appear to prefer to come to relatively secluded waterways. In more arid regions, Cooper's hawks may seek out artificial bodies of water to drink from (especially in passage). Although a rare behavior, there are now several records of juvenile hawks of the species proning wherein they lie on their backs along a branch (or rarely the ground), apparently as a form of sunning . Cooper's hawks may come to walk on ground to gather nesting materials as well as to hunt. Cooper's hawks have a well-developed muscle mass that powers their flight, especially helping with acceleration during hunts and when carrying heavy prey. However, some other non-raptorial birds may have similar muscularity relative to their mass, such as the Canada goose ( Branta canadensis ) and even pied-billed grebes ( Podilymbus podiceps ), and these ample muscle masses may be correlated with migratory (rather than hunting) behavior. Cooper's hawks have been recorded as engaging in an exaggerated, nighthawk -like flight in non-courtship circumstances, such as during migration or by recent fledglings. During the late nesting stage, parent Cooper's hawks were recorded during daylight in Utah to engage in soaring flight 8.4% for males and 8.1% of the time for females with a further 6.4% and 2.8% of the time in different kinds of flights, perching the remainder of the time (about 2–6 minutes at each perch interspersed with brief flights). Another study found 13.7% and 10.7% of daylight at this later breeding stage to be in flight, the rest of time perching, with occasional inactive perching spells of around 15–40 minutes. However, that inactivity could last up to 5 hours during heavy rainfall. Breeding adults generally engage in agonistic behavior when an interloper of their sex is present; 11 responses showed that males responses consisted 64% of the provocations, 9% of the time by females and both members 27% of the time. Frequent aggressive interactions were recorded between females, often yearling and second year vs older females. Cooper's hawk's threat display appears to consist of them lowering their heads, raising their "crest" (capital tract), stretching out their wings, spreading the tail and engaging in vocalizations. Stress levels, as indicated by a study of corticosterone levels, were considered quite high when hawks are being handled by researchers, particularly in males (indicating that they experience higher levels of stress than females). Cooper's hawk is subject to frequent mobbing by various birds and some mammals, with good cause, but evidence shows that even main prey types like jays will sometimes shy away from engaging in full-fledged mobbing of a Cooper's, perhaps due to the risk in closely approaching this very agile predator, which can in an instant suddenly turn and kill a member of the mob. Therefore, less dangerous hawks such as Buteos are mobbed more vigorously than the more dangerous Cooper's. Many potential prey will confine their response to a hawk of this species to vocal scolding and/or attempt escape before an attack occurs. Like a majority of diurnal birds of prey in the Northern Hemisphere , Cooper's hawk is a partial migrant . They tend to be most migratory in the north and largely to partially sedentary elsewhere. With individual exceptions, hawks of the species largely migrate out of nearly all of their range in southern Canada as well as cooler parts of the Pacific Northwest , essentially all of Montana and northern parts of surrounding states, the Dakotas (but for southern South Dakota ), the northern parts of the Great Lake states, northern New York and much of New England . Despite being classed as sedentary, banding studies have revealed that many Cooper's hawks south of the typical migratory populations engage in some variety of seasonal winter movements. Migrants in the Florida Keys were determined via stable isotopes to have originated from mid-Atlantic states and the southeastern United States both (largely) south of the typical migratory range. While females in the urban areas of Tucson were sedentary (99%), about 6% of the females outside of the urban areas did not remain on their breeding grounds during winter. In British Columbia , many adults are non-migratory but juveniles do tend to migrate. From the Great Lakes region in particular, migrants appear to disperse in multiple directions to the south. Multi-directional movements, even to the north as well as potentially any other direction, are more common than previously thought in this and other migratory raptors, which has been previously described as "inefficient and indirect method of 'homing'". However, reaching regions where appropriate habitat and prey is available is probably far more significant in seasonal movements to birds of prey than climatic concerns. Fairly strong evidence has been found of habitual northbound migration by Cooper's hawks from Central and Southern California , usually over fairly short distances, often less than 320 km (200 mi) . However, the three longest distance movements from southern California were all northbound, i.e. 616 to 993 km (383 to 617 mi) . Cooper's hawks originating from Northern California do generally migrate south, mostly wintering in Mexico though sometimes covering up to 1,637 km (1,017 mi) to Central America. In Lansing, Michigan , evidence has been found of individual Cooper's hawks being annually devoted to the same wintering grounds, presumably due to their high quality. Migratory movements in the autumn are generally between late August to mid-October, peaking at the end of September and beginning of October in the east , but sometimes migration extend into November. Meanwhile, spring northward migration may be any time from the end of February to May, with the last ones leaving Mexico in April and very late individuals were passing over south Texas in late May. Generally, spring migration is more dispersed and less consistent than fall migration. There is evidence from the Great Lakes region that spring migration is occurring sooner due to warming temperatures in recent years. Passage appears to be timed to coincide with that of their main prey, medium-sized birds. In migration, first-year juveniles precede two-year-old hawks which themselves precede adults when moving south in fall. Furthermore, females of all ages tend to migrate sooner and spend longer in winter quarters than like-age males, the latter staying relatively north and traveling back again earlier. Interestingly, the sharp-shinned hawk (despite the even more dimorphic migration times between sexes) showed no strong difference in distance on migration between the sexes, unlike female Cooper's which sometimes can move considerably further than males. At regular western migration sites, the average difference of passage timing for Cooper's hawks of the earlier females and later males of like-age was five days. In the Marin Headlands , migration of the sexes differed by 6 days in juvenile, first-year females and males and by 11 days in older females and males. Like other Accipiters (but unlike falcons ), Cooper's appear to not start moving until day is warmer and thermals can be used. During migration they favor mountain ridges and coastlines , which coincide with migratory raptors routes in general. This species can seem to cross some bodies of water unlike most sharp-shinned hawks but seldom do so over wide bodies of water. However, they have been seen to turn up in such oceanic vicinities as the Florida Keys and Cuba , and so are capable of crossing larger than usual bodies of water. It is thought that Cooper's hawks also avoid the Great Plains while migrating as well. Like many other raptors, Cooper's hawks favor strong northwesterly winds during autumn passage. At coastal migration sites like Cape May , first year Cooper's hawks are far more regularly encountered than older individuals, with the juvenile Cooper's accounting for 92.7% of recorded individuals of the species (juveniles of various other raptor species also generally seem to favor coastal over montane migration when it is available). In Cape May, Cooper's hawks are the third most commonly recorded raptor species in passage behind the sharp-shinned hawk and the American kestrel ( Falco sparverius ) but are far less than numerous in migration or in winter in the nearby Delaware Bayshore locations of New Jersey than various other raptor species. Interestingly, in the Manzano Mountains and Goshute Mountains , juvenile sharp-shinned hawks were roughly twice as numerous as juvenile Cooper's hawks but the number of adults seen passing through of the two species was roughly the same. At the hawkwatch in Cedar Grove, Wisconsin , Cooper's hawk was not among the most regular species, being the 6th most frequently most recorded species. In central and southwestern Idaho , Cooper's hawk accounted for relatively few of the recorded raptors, i.e. 3.45% of 748 migrating raptors. A similarly low volume was observed relative to other bird of prey species in Yellowstone National Park , where Cooper's was only the 9th most frequently observed out of 17 species and averaged only 50 hawks in passage over the course of autumn. Nonetheless, Cooper's hawk was second only to sharp-shinned hawk as the most frequently recorded species seen migrating at nine major hawkwatchs throughout the western United States (and 1 in Canada) and, unlike the sharp-shinned, has shown a trend of increase in numbers overall in recent decades, despite some declines in numbers at Lipan Point and Bridger Range . Cooper's hawk was the 7th most often recorded raptor at four migration sites along the Gulf Coast , being much more frequently identified in the site at Veracruz , Mexico than the ones in the United States, but showed an annual stability of numbers that many of the more numerous raptors (including sharp-shinned hawks) in passage did not. Along the Kittatinny Ridge in Pennsylvania, studied Cooper's hawks that were migrating from further north spent only 12% of the day actually migrating, devoting the remainder of their time to perching and hunting along their passage. Fat stores were measured to consist of 4–12% of the body mass of migrants, being higher in autumn than in spring, and higher on average in adults over younger hawks and in females over males. Migration speeds appear to be largely similar to those of other raptors, with average speeds of 33.6 to 88 km/h (20.9 to 54.7 mph) , but one migrating from Colorado was recorded to cover about 26 km (16 mi) per day. Typically Cooper's hawk migrate singly but sometimes can be seen in groups of two to five. Flocking is not typically engaged in by raptors who migrate using powered flight, such as Accipiters , falcons and harriers , but many Buteo hawks do form loose flocks. 96.3% of 806 observed Cooper's hawk seen migrating in Johnson County, Iowa were solitary, although 30 migrating pairs were seen together. Like a majority of diurnal birds of prey in the Northern Hemisphere , Cooper's hawk is a partial migrant . They tend to be most migratory in the north and largely to partially sedentary elsewhere. With individual exceptions, hawks of the species largely migrate out of nearly all of their range in southern Canada as well as cooler parts of the Pacific Northwest , essentially all of Montana and northern parts of surrounding states, the Dakotas (but for southern South Dakota ), the northern parts of the Great Lake states, northern New York and much of New England . Despite being classed as sedentary, banding studies have revealed that many Cooper's hawks south of the typical migratory populations engage in some variety of seasonal winter movements. Migrants in the Florida Keys were determined via stable isotopes to have originated from mid-Atlantic states and the southeastern United States both (largely) south of the typical migratory range. While females in the urban areas of Tucson were sedentary (99%), about 6% of the females outside of the urban areas did not remain on their breeding grounds during winter. In British Columbia , many adults are non-migratory but juveniles do tend to migrate. From the Great Lakes region in particular, migrants appear to disperse in multiple directions to the south. Multi-directional movements, even to the north as well as potentially any other direction, are more common than previously thought in this and other migratory raptors, which has been previously described as "inefficient and indirect method of 'homing'". However, reaching regions where appropriate habitat and prey is available is probably far more significant in seasonal movements to birds of prey than climatic concerns. Fairly strong evidence has been found of habitual northbound migration by Cooper's hawks from Central and Southern California , usually over fairly short distances, often less than 320 km (200 mi) . However, the three longest distance movements from southern California were all northbound, i.e. 616 to 993 km (383 to 617 mi) . Cooper's hawks originating from Northern California do generally migrate south, mostly wintering in Mexico though sometimes covering up to 1,637 km (1,017 mi) to Central America. In Lansing, Michigan , evidence has been found of individual Cooper's hawks being annually devoted to the same wintering grounds, presumably due to their high quality. Migratory movements in the autumn are generally between late August to mid-October, peaking at the end of September and beginning of October in the east , but sometimes migration extend into November. Meanwhile, spring northward migration may be any time from the end of February to May, with the last ones leaving Mexico in April and very late individuals were passing over south Texas in late May. Generally, spring migration is more dispersed and less consistent than fall migration. There is evidence from the Great Lakes region that spring migration is occurring sooner due to warming temperatures in recent years. Passage appears to be timed to coincide with that of their main prey, medium-sized birds. In migration, first-year juveniles precede two-year-old hawks which themselves precede adults when moving south in fall. Furthermore, females of all ages tend to migrate sooner and spend longer in winter quarters than like-age males, the latter staying relatively north and traveling back again earlier. Interestingly, the sharp-shinned hawk (despite the even more dimorphic migration times between sexes) showed no strong difference in distance on migration between the sexes, unlike female Cooper's which sometimes can move considerably further than males. At regular western migration sites, the average difference of passage timing for Cooper's hawks of the earlier females and later males of like-age was five days. In the Marin Headlands , migration of the sexes differed by 6 days in juvenile, first-year females and males and by 11 days in older females and males. Like other Accipiters (but unlike falcons ), Cooper's appear to not start moving until day is warmer and thermals can be used. During migration they favor mountain ridges and coastlines , which coincide with migratory raptors routes in general. This species can seem to cross some bodies of water unlike most sharp-shinned hawks but seldom do so over wide bodies of water. However, they have been seen to turn up in such oceanic vicinities as the Florida Keys and Cuba , and so are capable of crossing larger than usual bodies of water. It is thought that Cooper's hawks also avoid the Great Plains while migrating as well. Like many other raptors, Cooper's hawks favor strong northwesterly winds during autumn passage. At coastal migration sites like Cape May , first year Cooper's hawks are far more regularly encountered than older individuals, with the juvenile Cooper's accounting for 92.7% of recorded individuals of the species (juveniles of various other raptor species also generally seem to favor coastal over montane migration when it is available). In Cape May, Cooper's hawks are the third most commonly recorded raptor species in passage behind the sharp-shinned hawk and the American kestrel ( Falco sparverius ) but are far less than numerous in migration or in winter in the nearby Delaware Bayshore locations of New Jersey than various other raptor species. Interestingly, in the Manzano Mountains and Goshute Mountains , juvenile sharp-shinned hawks were roughly twice as numerous as juvenile Cooper's hawks but the number of adults seen passing through of the two species was roughly the same. At the hawkwatch in Cedar Grove, Wisconsin , Cooper's hawk was not among the most regular species, being the 6th most frequently most recorded species. In central and southwestern Idaho , Cooper's hawk accounted for relatively few of the recorded raptors, i.e. 3.45% of 748 migrating raptors. A similarly low volume was observed relative to other bird of prey species in Yellowstone National Park , where Cooper's was only the 9th most frequently observed out of 17 species and averaged only 50 hawks in passage over the course of autumn. Nonetheless, Cooper's hawk was second only to sharp-shinned hawk as the most frequently recorded species seen migrating at nine major hawkwatchs throughout the western United States (and 1 in Canada) and, unlike the sharp-shinned, has shown a trend of increase in numbers overall in recent decades, despite some declines in numbers at Lipan Point and Bridger Range . Cooper's hawk was the 7th most often recorded raptor at four migration sites along the Gulf Coast , being much more frequently identified in the site at Veracruz , Mexico than the ones in the United States, but showed an annual stability of numbers that many of the more numerous raptors (including sharp-shinned hawks) in passage did not. Along the Kittatinny Ridge in Pennsylvania, studied Cooper's hawks that were migrating from further north spent only 12% of the day actually migrating, devoting the remainder of their time to perching and hunting along their passage. Fat stores were measured to consist of 4–12% of the body mass of migrants, being higher in autumn than in spring, and higher on average in adults over younger hawks and in females over males. Migration speeds appear to be largely similar to those of other raptors, with average speeds of 33.6 to 88 km/h (20.9 to 54.7 mph) , but one migrating from Colorado was recorded to cover about 26 km (16 mi) per day. Typically Cooper's hawk migrate singly but sometimes can be seen in groups of two to five. Flocking is not typically engaged in by raptors who migrate using powered flight, such as Accipiters , falcons and harriers , but many Buteo hawks do form loose flocks. 96.3% of 806 observed Cooper's hawk seen migrating in Johnson County, Iowa were solitary, although 30 migrating pairs were seen together. Cooper's hawks are known as bold and aggressive predators. Given their dietary habits, these hawks bore a poor reputation well into the 20th century, with one account describing the species as "noxious", an "avian outlaw" and "a relentless tyrant and murderer of small birds". Another describes the species as "bloodthirsty" and a "villain". Early accounts underestimated the opportunistic nature of Cooper's hawks' hunting behavior and provided little insight into the actual effect the hawks have on their prey. The maximum hunting range was estimated at 5.3 km 2 (2.0 sq mi) in Michigan and 2 km 2 (0.77 sq mi) in Wyoming . In another Michigan study, most Cooper's hawks were found to be flying 0.8 to 1.2 km (0.50 to 0.75 mi) from their wooded nests to hunt on agricultural ground. Males in New York usually covered more than 0.8 km (0.50 mi) , sometimes up to 3 km (1.9 mi) , during hunting efforts when flying away from the nest area. Due to scattered prey availability in North Florida , females were nearly nomadic, wandering anywhere where food could be accessed (i.e. chicken farms , feedlots , bird feeders , etc.), while males were more typically devoted to hunting on their regular home range. During hunts, Cooper's hawks rely on agile, twisting flights between bouts of perching and scanning, their flight suddenly picking up speed upon approach to the prey. Hunting hawks typically use forest edge , open woodland and fencelines and such while hunting. In southwestern Tennessee , the preferred hunting habitats in the non-breeding season were forest, then woodland edge , then lastly open country . Near Stevens Point in Wisconsin, males prefer to hunt in quiet woods while females preferred to stay within 100 m (330 ft) of the nest making males a more common sight. This differed strongly in Tucson where hawks while hunting mostly in manmade environments such as residential areas, regional parks , and golf courses more so than they were prevalent in the environment, though usually where there were large (albeit usually non-native) trees. Cooper's hawk does attack birds attracted to bird feeders with a fair amount of frequency. However, data from Indiana showed that birds using bird feeders were at no greater risk of attack than those in random transects, and the effect Cooper's can have on feeder birds may be at times exaggerated. If it sees birds when flying, a hunting hawk does not fly directly to them but instead circles around to available trees and bushes often perching for a few moments before launching its attack. If birds become aware of it, the hawk will tend to quickly gain height in hopes of intercepting some prey. It was found compared to some other North American raptors who are more likely to watch for prey on the ground and/or in the open, that Cooper's hawk had a rather enlarged binocular field . During hunts, these hawks may suddenly alight when detecting an available mammal. Sometimes, Cooper's hawks will engage in tandem hunts with one dashing around after the prey while another waits on the other side of a tree trunk or wooded thicket. Many birds are caught when they inadvertently fly around a tree where a hawk is inconspicuously perched. Young Cooper's are impetuous about crashing into bushes after prey, sometimes even into thorny cover such as barberries, whereas adults are said to be more "prudent". They may chase prey into cover or from bush to bush. The first instance of non-piratical scavenging on carrion was recorded when a Cooper's hawk was seen eating at a white-tailed deer ( Odocoileus virginianus ) carcass. When hunting bats, they can follow all twists and turns, and may succeed in capture in up to 90% of hunts. Much like goshawk, sometimes Cooper's hawks will capture rabbits by pursuing on the ground, half-running, half-flying. Other on-foot hunting efforts, especially when chasing quail , have been detected as well. When hunting sparrows , Cooper's hawks may make multiple passes on a bush before success and the efforts can take up to 45 minutes. During hunts of rock doves ( Columba livia) in urban areas, Cooper's hawks have been seen to engage in open air stoops to capture the prey. An unusual harrier -like flight was seen in be engaged in by a Cooper's hawk before an attack on aquatic prey in a marsh . Most prey is killed by repeatedly kneading the talons, with the kneading sometimes going on even after death, although in some cases birds are plucked while still alive. Despite its gracile appearance, Cooper's hawk, like the northern goshawk, is extremely powerful for its size and presumably able to capture larger prey relative to its size than other raptors such as falcons and Buteos (including red-tailed hawks ( Buteo jamaicensis )) due to its unusually high-speed foot velocity and resulting impact during prey captures. At times, after capture, Cooper's hawk have been seen to hold still living prey underwater, presumably trying to drown it. Subsequent to the preys' demise, they may eat the victim head first, followed by the viscera , with the meat eaten lastly. Like other raptors who most regularly take birds, Cooper's hawk was profiled in a study as an "attacker" rather than a "searcher" (i.e. mammal -hunters such as Buteos ). "Attackers" such as Accipiters and large falcons usually had lower average hunting success rates, which averaged among the attacker species at 27%, due to the difficulty of capturing the prey. 33% of 45 observed hunts in a study in Missouri were successful. In Terre Haute, Indiana , about 23% of attacks by male Cooper's hawks and 20% by females were successful and were far more prone to being carried out in relatively open areas than those of nearby sharp-shinned hawk. Post-fledgling parties of hawks in Wisconsin were seen to hunt in sibling groups of 2–4, mainly pursuing chipmunks , and were observed to succeed in 56% of 18 hunting attempts. During the first six weeks after the young hatch, in New York, it was estimated that a male Cooper's hawk would need to procure about 66 prey items over the period. In these first six weeks in California, it was thought a minimum of 62 g (2.2 oz) would be required per nestling per day. Cooper's hawk may consume well over 300 prey species from across the range. This predator is known to consume vertebrate prey almost exclusively. Often smallish or medium-sized birds are the preferred food, but also many small mammals and, in more arid vicinities, lizards are regularly taken. Infrequently, frogs may be eaten, as will (rarely) insects and fish in nearly dry watercourse. Birds in general form about 50–85% of diet. One estimate is that globally birds form about 71.1% of the diet, 17.9% mammals, 8.9% reptiles and 2.1% other prey. Cooper's hawks generally prefers birds that inhabit the ground or shrub level within the local habitats. One estimate claims that most prey of Cooper's hawks weighs from 15 to 166 g (0.53 to 5.86 oz) , with male and female averages of 37.6 and 50.7 g (1.33 and 1.79 oz) . Another estimate was from 30 to 130 g (1.1 to 4.6 oz) for typical prey sizes, or about 5–37% the weight of males and 8–22% the weight of females, respectively. However, subsequent studies, such as those in Indiana , found prey weighing up to 360 g (13 oz) (such as adult pigeons ) can be quite common in the diet of Cooper's hawks. Mean prey weights were roughly 112.6 g (3.97 oz) . In Oregon, the mean prey sizes of Cooper's hawk was 135.5 g (4.78 oz) , with larger prey was taken than in greater proportion than their occurrence in the ecosystem (indicating that they locally search out relatively large prey). In Missouri, mean prey sizes were 112 g (4.0 oz) , averaging between 83.5 and 316.5 g (2.95 and 11.16 oz) amongst the main prey classes. Prey delivered by males averaged an estimated 65.9 g (2.32 oz) , while the average estimated size of prey delivered by females was 227.7 g (8.03 oz) . Overall, in Missouri, prey body masses were estimated to range from 15 to 600 g (0.53 to 21.16 oz) . One study unusually found no strong dimorphism in the foods selected by males and females. Birds are by far the leading prey for Cooper's hawks in most areas. A wide diversity of birds, considerably over 250 species, are known to be taken, constituting more than three-quarters of known prey species for these hawks. A Cooper's hawk is estimated to kill an average of two birds a day, or 700 birds a year. Although prior data mostly reflected the taking of adult birds, a study in Wisconsin revealed that Cooper's hawks may largely take young of the year, mostly fledglings but also not infrequently nestlings, during the breeding season. 74% of ageable bird prey in this study were young of the year. Similarly, in Michigan during summer, immature birds were more than 2.5 times more often delivered to Cooper's hawk nests than adult birds. In one case, a Cooper's hawk was seen to fly away with an entire occupied nest of American goldfinches ( Spinus tristis ). One study determined that birds that nest in the canopy level tended to nest fairly close to this hawk but those with mid-level, shrub level and ground level nests nested farther away, indicating that non-canopy-nesting birds are generally taken during the breeding season. Key to prey selection for Cooper's hawk is the availability and abundance of birds in a given region. Therefore, the extremely numerous American robin ( Turdus migratorius ) appears to be the most widely reported prey species. Robins were the leading prey species in northwestern Oregon , at 19.6% of 281 prey items, Lopez Island , Washington , 23.4% of 107 prey items, in Victoria, British Columbia , at 34.6% of 2896 prey items and prominent but ranked second also in California ( Berkeley and Albany ) food studies, 24.5% of 1057 prey items. The robin is regularly hunted in all seasons due to its commonality in exurban regions, with both adults, at estimated averages of 79 to 81.2 g (2.79 to 2.86 oz) when taken, and young being relatively easy for them to access. Beyond the common robin, nearly all thrushes in North America (excluding one species whose breeding range is largely north of Cooper's range and one rare, little-studied species ) are opportunistically hunted by Cooper's hawks. The closest rival to the robin in being most widely taken as prey for Cooper's hawks may be the common starling ( Sturnus vulgaris ), a non-native bird in North America with mean weights when taken of 79 to 82 g (2.8 to 2.9 oz) . The starling was the main food for these hawks in Ithaca, New York , at 28.2% of 857 prey items, and Terre Haute, Indiana , at 56.5% of 57 prey items, and taken in large but somewhat secondary numbers in Missouri, Michigan , and Victoria, British Columbia. In the urban environment of Terre Haute, it was found that starlings were taken in almost the same proportion as starlings were of all birds observed by researchers (i.e. they were 60% of 2146 individual birds seen). Somewhat over 60% of the bird species known in Cooper's hawks' prey spectrum are passerines (including thrushes and starlings). Other medium-sized to largish-bodied families of passerines tend to be most often selected. In many circumstances, Cooper's hawks will hunt corvids , large, intelligent and social passerines, with the smallish jays being particularly popular. In Missouri, the most often selected prey (12.7% of 259 prey items) was the 89 g (3.1 oz) blue jay ( Cyanocitta cristata ), which also important in northern Florida, i.e. 12.27% of 1100 prey items. Steller's jays ( Cyanocitta stelleri ), at 107 g (3.8 oz) a larger western cousin of the blue jay, are also regularly selected in various studies, such as all studied areas of Oregon and New Mexico , where it was the second most regularly selected of prey species at 11.7% of 316 prey items. California scrub jays ( Aphelocoma californica ) are regular supplemental prey in northern California studies as well. Blue jays and other related species are among the most diligent mobbing birds in response to the presence of a Cooper's hawk although sometimes may let out an alarm call or even imitate a Cooper's calls merely to frighten other birds from a desired food source. It was hypothesized that Steller's jays may be able to effectively confuse a Cooper's hawk by engaging in a chorus of calls at close range. In Arizona , Mexican jays ( Aphelocoma ultramarina ) are known to play a key role in flicker ecology by watching out for Cooper's hawks. Numerous other corvids may be hunted, including most overlapping jays, as well as the Clark's nutcracker ( Nucifraga columbiana ), black-billed magpie ( Pica hudsonius ), possibly yellow-billed magpie ( Pica nuttalli ) and a few species of crow . One black-billed magpie was caught and killed by a Cooper's hawk when attempting to mob the hawk. Incidents of predation have been witnessed on both young and adult American crow ( Corvus brachyrhynchos ), as well as on adult northwestern crow ( Corvus caurinus ). These hawks are also a potential predator of fish crow ( Corvus ossifragus ). However, crows are potentially dangerous prey to Cooper's hawks. Adult American crows are about the same size as a female Cooper's hawk and can potentially cause considerable damage to a lone raptor during group mobbing , being capable of inflicting damage with both their feet and bill. In at least one case, a murder of American crows was observed to drive a Cooper's hawk to the ground and possibly seriously injure it, although the fate of the hawk was not certain. Cases of missing toes on Cooper's hawks are thought to have possibly come from failed predation of crows. At least a dozen species of icterid are known to be hunted by Cooper's hawks as well. Common, widespread icterids such as red-winged blackbirds ( Agelaius phoeniceus ) and common grackles ( Quiscalus quiscula ) are fairly frequent prey for these hawks. Cooper's hawks nesting near red-winged blackbird colonies may at times live almost entirely off of female blackbirds. In the Black Hills , although prey species were seldom identified, evidence showed that most regularly selected prey were assorted icterids. Even meadowlarks , such as the 93 g (3.3 oz) eastern meadowlark ( Sturnella magna ) which was the third most often selected prey in Ithaca, New York, and bobolinks ( Dolichonyx oryzivorus ) are taken despite their preference for grasslands well outside the typical habitats of Cooper's hawks. Other passerines families (i.e. outside thrushes, corvids and icterids) tend to not be as large-bodied and, although by no means neglected, are seldom equal in overall dietary importance ( biomass ). About 15 species of tyrant flycatcher , several species each of vireo , swallows , tits , nuthatches , wrens , mimids , about a dozen species of finch , cardinalids and a huge diversity of American sparrows and New World warblers (nearly 30 species each) are known to be taken by Cooper's hawks. A lower diversity are taken of shrikes , larks , penduline tits , aegithalids , treecreepers , dippers , silky-flycatchers and longspurs . The more numerous native passerines, such as northern cardinals ( Cardinalis cardinalis ) and northern mockingbirds ( Mimus polyglottos ), have good reason to fear these hawks as they are widely and regularly taken as are even common birds of less than half their size (around 20 g (0.71 oz) ), such as song sparrows ( Melospiza melodia ), dark-eyed juncos ( Junco hiemalis ) and house finches ( Haemorhous mexicanus ). During harsh late winter weather in Wisconsin, Cooper's hawks were recorded to eke out an existence living largely off of pine siskins ( Spinus pinus ). In modern terms, certainly the most commonly taken small bird would be the non-native, 29 g (1.0 oz) house sparrow ( Passer domesticus ). Although not known to be taken profusely in all studied urban locales, house sparrows were the leading prey in a study from Michigan , were nearly a third of observed delivered prey at nests in Victoria, British Columbia (although were outnumbered by robins in prey remains) and reportedly were the leading prey in Milwaukee and in Grand Forks, North Dakota . Flycatchers are not hugely significant in Cooper's hawk's foods, but the local effect of the hawks on populations can be considerable. For example, willow flycatchers ( Empidonax traillii ) in California suffered a 76% rate of nest predation, among which Cooper's hawks were a considerable contributor, and dusky flycatchers ( Empidonax oberholseri ) experienced a rate of 96% predation elsewhere in California, with 25% attributable to Cooper's. Similar determent to the local nesting attempts of other small passerines such as warblers has also been reported. Chickadees seem to regard Cooper's hawks as a moderate threat based on their anti-predator response, with smaller raptors (which are presumably more dangerous) such as sharp-shinned hawks and small owls evoking a rather more aggressive response by chickadees. While usually the smallest avian prey selected by Cooper's hawks are various warblers (presumably taken mainly by male hawks), down to the size of the 7 g (0.25 oz) Wilson's warbler ( Cardellina pusilla ), even smaller passerines are known to be hunted. The smallest known avian prey species have included the 6.8 g (0.24 oz) verdin ( Auriparus flaviceps ), the 6.3 g (0.22 oz) ruby-crowned kinglet ( Regulus calendula ) and the 5.3 g (0.19 oz) bushtit ( Psaltriparus minimus ). Even smaller birds, the hummingbirds , are essentially immune to Cooper's hawks (due to their own extreme agility) and were seen to incidentally benefit from nesting close to the hawks in California, due to a low risk of predators approaching while the hawks are present. Outside of passerines, almost certainly the most important avian prey type is the pigeon and dove family. Especially for those living in urban areas, Cooper's hawks have seemed to take to living heavily off of doves , particularly the abundant and widely found mourning dove ( Zenaida macroura ), at 119 g (4.2 oz) . Mourning doves appear to be hunted regularly in almost any part of the two species' mutual range. In Tucson , recent data shows that Cooper's hawks are living almost exclusively on doves. Among 151 prey items there, mourning doves were 20.5% by number and 27.5% of the biomass, Inca doves ( Columbina inca ) were 18.5% by number and 12.2% of the biomass and white-winged dove ( Zenaida asiatica ) 17.2% by number and 27.1% of the biomass. In Terre Haute, Indiana , mourning doves and rock doves were 14% and 21% of the diet, respectively. In northern California, mourning doves were the main prey species, making up 25.6% of 1057 prey items. There is even evidence that bluebirds have perceived the change in preference of Cooper's hawks to more profitable prey such as doves in developed areas and show less inhibition to the hawk's presence. In the more rural north Florida , again the mourning dove leads the prey selection, accounting for 16.5% of 1100 prey items. Another popular prey family is the woodpeckers . A rather numerous and widely distributed species, the 132 g (4.7 oz) northern flicker ( Colaptes auratus ), is a particular dietary staple of Cooper's hawks, being about the third most widely reported prey species. The flicker was the main prey in northern New Mexico , at 22.5% of 316 prey items, and in southern Wisconsin, at 22% of 77 prey items. Flickers are common prey elsewhere as well, such as in Ithaca, New York . Medium-sized woodpeckers, such as red-headed woodpeckers ( Melanerpes erythrocephalus ) and red-bellied woodpeckers ( Melanerpes carolinus ) were important secondary prey in different parts of the range. In South Carolina , it was found that 15% of the red-headed woodpeckers in a study population were killed by hawks. All told, about 20 species (almost all in North America but for a couple poorly-studied species) of woodpecker are known to be taken, ranging from the smallest, the 25.6 g (0.90 oz) downy woodpecker ( Picoides pubescens ), to the largest, the 287 g (10.1 oz) pileated woodpecker ( Dryocopus pileatus ). The response of woodpeckers to a sighted Cooper's hawks varies, with evidence showing that downy woodpecker and flickers would behave more boldly and themselves may scold the hawk if part of a mixed flock but, if alone, the woodpecker will typically try to flee. Despite the regularity of predation of woodpeckers that are in the open, a study in British Columbia shows indicated Cooper's hawks seldom prey upon woodpecker nests, perhaps due to being unable to access their secluded, smallish nest holes, with the study showing that the most regular predators of such nests were various mammals (from deermice to bears ). Certainly the most controversial aspect of Cooper's hawks are their predations upon galliforms . By far the most regularly selected types are New World quails . Coveys of quails that attempt to evade predators by running into thick vegetation (which can allow them to successfully escape many predators) often find that Cooper's hawks are undeterred by this, as the hawks may chase them either on the wing or on foot into thickets. However, one grouse was seen to successfully evade a hunting Cooper's hawk by diving belly first into about a foot of snow. Cooper's hawks are often regarded as perhaps the most regular natural predator of northern bobwhites ( Colinus virginianus ). Indeed, the rate of predation by Cooper's does appear to exceed that committed by other species of hawk as well as that by large owls. For instance, during winter in Wisconsin, Cooper's hawks were thought to kill 3.4–12.5% of the local bobwhite population. However, the bobwhite appears to be a secondary prey species in all known studies and there is no evidence that Cooper's hawk predation alone can deplete bobwhite populations, unlike causes directly contributable to man such as overhunting and habitat destruction . In Washington state, female Cooper's hawks took many California quails ( Callipepla californica ), which were estimated to constitute 47% of the prey selected by female hawks, but there was far too little impact overall to affect the quail's overall population. In the rural areas outside of Tucson , Gambel's quail ( Callipepla gambelii ) were found to be the most regularly selected prey species, at 15.2% of 79 prey items. A study of pellets in northwestern Mexico to determine if the local Cooper's hawks were regularly taking Montezuma quail ( Cyrtonyx montezumae ), finding that only one pellet consisted entirely of quail, the other pellets showing that hawks were mainly taking other prey, mostly doves. Most regularly found galliforms in North America (including well-established exotics such as chukars ( Alectoris chukar ) and common pheasants ( Phasianus colchicus )) are known to fall prey occasionally to Cooper's hawks. These include assorted native grouse , including even the grassland -dwelling species (but excluding the more northerly distributed ptarmigans ). Juveniles usually are the more vulnerable and more regularly taken of non-quail galliforms by Cooper's hawks, but the hawks can take adults quite regularly despite the prey's relatively large size. Adult ruffed grouse ( Bonasa umbellus ), weighing an estimated mean of 619 g (1.365 lb) when taken, are not infrequently exploited as prey, while adult sooty grouse ( Dendragapus fuliginosus ), estimated to weigh 1,050 g (2.31 lb) when taken have also been known to be taken repeatedly. Adult male sharp-tailed grouse ( Tympanuchus phasianellus ), which average 1,031 g (2.273 lb) , are also known have been successfully preyed upon by Cooper's hawks. Even more impressive accounts show adult common pheasant estimated to weigh up to 1,158 g (2.553 lb) can be preyed upon by Cooper's hawks. One wild turkey ( Meleagris gallopavo ) taken in Florida was cited with a weight of 5,336 g (11.764 lb) , which is the size of an adult. However, given that this is of enormous size relative to a Cooper's hawk, it would require verification that the turkey was this large and was taken alive by the hawk. Not unexpectedly, turkey poults are known to fall prey to Cooper's hawks. Beyond aforementioned families and orders, other types of birds are taken relatively infrequently. Usually moderate to low numbers of water birds are taken of any variety. About 5 species each of duck and heron , a dozen species of shorebird and a smaller assortment of grebes and rails are known in the prey spectrum. Even among water birds, nonetheless, a wide diversity may be taken, from the tiny 22.9 g (0.81 oz) least sandpiper ( Calidris minutilla ) to an adult mallard ( Anas platyrhynchos ) estimated to weigh 1,150 g (2.54 lb) when taken. Adult ducks and herons of roughly equal weight to Cooper's hawks and other largish adult water birds including ring-billed gulls ( Larus delewarensis ) and American coots ( Fulica americana ) are sometimes tackled by these hawks. Particularly frequency was recorded of 312.7 g (11.03 oz) cattle egrets ( Bubulcus ibis ) in north Florida, where the egrets were the fourth most regularly recorded prey species. Assorted families of land birds are fairly rare as reported in food studies, including some nightjars , trogons , swifts , kingfishers , parrots and assorted other raptorial birds. A lower diversity of species and lower overall numbers of mammals are taken relative to bird prey but mammalian prey can be locally important. Chipmunks are often regularly hunted in various regions, though only about one-third of North American chipmunks are known in the prey spectrum. High balances of the relatively large 96 g (3.4 oz) eastern chipmunk ( Tamias striatus ) were found in studies from New York, Michigan and Wisconsin. The eastern chipmunk appeared to dominate the foods of Cooper's hawks in the Green Ridge State Forest in Maryland , at 49.1% of 57 prey items and mammals altogether made up an exceptional 66.9% of the foods. In the western United States, fewer chipmunks are identifiable but such prey is fairly commonly detected. High balances of chipmunks were found in food studies from Oregon, especially in eastern Oregon where chipmunks (unidentified to species) were the leading prey type, at 22.5% of 120 prey items. The most common chipmunk prey in Oregon is probably the 89.3 g (3.15 oz) Townsend's chipmunk ( Neotamias townsendii ) but Cooper's hawks may take chipmunks down to the size of the 48 g (1.7 oz) least chipmunk ( Neotamias minimus ). Mammals distantly related to chipmunks, such as ground squirrels (including antelope squirrels ) can be taken in locally high volume. Golden-mantled ground squirrels ( Callospermophilus lateralis ) were the second most important prey in eastern Oregon at 16.6%. Thirteen-lined ground squirrels ( Ictidomys tridecemlineatus ) were the second most common prey species in a study from Wisconsin and also important in the diet in North Dakota (where they were the most significant contributor of biomass, constituting 23.4%). Golden-mantled and thirteen-lined ground squirrels are fairly small for ground squirrels, the earlier averaging 166 g (5.9 oz) , the latter of similar size. A few larger ground squirrels may be hunted, such as California ground squirrels ( Otospermophilus beecheyi ) and rock squirrels ( Otospermophilus variegatus ), both averaging over 600 g (1.3 lb) in adults, albeit infrequently. Tree squirrels are widely taken but secondary prey for Cooper's hawks. The smallish, roughly 200 g (7.1 oz) American red squirrel ( Tamiasciurus hudsonicus ) are not infrequent prey in northerly locations. About 36 red squirrels were recorded in the foods of Cooper's hawk in Ithaca, New York and these squirrels appear to have specific alarm calls that are provoked by these hawks, however the rate of predation by Cooper's appears to be low relative to other predators overall. Reported when taking red squirrels, male Cooper's hawks, being relatively small, may tear the prey into pieces that can be transported by them to the nest. Numerous other tree squirrels are taken occasionally by Cooper's hawks. Sizes of tree squirrels taken by Cooper's hawks were studied in Missouri. Eastern gray squirrels ( Sciurus carolinensis ) were taken of up to adult size but fox squirrels ( Sciurus niger ) were only taken as juveniles, as the adults, sometimes scaling up to 1,350 g (2.98 lb) , were apparently too formidable for Cooper's. The estimated weights of both the gray and fox squirrels taken in Missouri was 450 g (16 oz) , with the gray contributing 10.9% of the biomass. About 20 non-sciurid rodent species may be taken by Coopers hawks but are rarely significant in the foods. Both American species of flying squirrels , woodrats , commoner Peromyscus mice, some species of vole and lemming , cotton rats , jumping mice , kangaroo rats and non-native rodents may all be prey occasionally, although most species of these are fairly nocturnal and thus of limited access. Few of these types of rodents are taken frequently enough to warrant much individual mention. Unidentified woodrats, at a mean estimated mass of 256.6 g (9.05 oz) were significant to the biomass of Cooper's hawks in northwestern Oregon. In North Dakota, Peromyscus mice made up an unusually high 13.5% of the foods. In the city of Burnaby , when bird feeders began to attract black rats ( Rattus rattus ), Cooper's hawk's came to locally take significant numbers of both young and adult rats. The first verified predation by a Cooper's hawk on a brown rat ( Rattus norvegicus ) was recently reported, also in British Columbia. One broad study found a somewhat unexpected correlation was found positively relating the previous summer's rodent density to the number of Cooper's hawks. This could be coincidental as rodent populations are probably driven by acorn production in the year prior to the rodent increases, and many of the birds taken regularly by Cooper's are also partially acorn dependent. Occasionally, Cooper's hawks may capture profitable mammalian prey such as rabbits and hares . Mainly, predation has been reported on the cottontail rabbits . Strong numbers of mountain cottontail ( Sylvilagus nuttallii ), averaging about 716 g (1.579 lb) when taken, were reported in northwestern Oregon (7.82% and fifth most regular prey species). In the rural vicinity of Tucson, cottontail rabbits were the second most regularly selected type of prey, at 12.7%. Fairly strong numbers of cottontails were also reported in New Mexico and Durango . In Missouri, the widely found eastern cottontail ( Sylvilagus floridanus ) was the most significant contributor of biomass, making up 14.5% of the total biomass. On average, in Missouri, the body mass of eastern cottontails caught was 600 g (1.3 lb) , indicating juvenile eastern cottontails are usually caught. However, there are several known cases of adult eastern cottontails falling prey to Cooper's hawks, including cottontails estimated to weigh from 1,100 to 1,290 g (2.43 to 2.84 lb) . Various species of non-cottontail leporids may occasionally be caught, including young black-tailed jackrabbits ( Lepus californicus ), pygmy rabbits ( Brachylagus idahoensis ) as well as fairly large numbers of feral European rabbits ( Oryctolagus cuniculus ) in Victoria, British Columbia . Mammals of other orders are taken quite infrequently, with a low volume of shrews and moles reported. Cooper's hawks are considered a potential predator of the smaller species of weasel and were recorded in Florida to kill a striped skunk ( Mephitis mephitis ) kit estimated to weigh about 661 g (1.457 lb) . Occasionally, Cooper's hawks are known to hunt bats. They are said to usually capture bats on the wing rather than search them out. Findings were that in Carlsbad Caverns that Cooper's (and also sharp-shinned) hawks were the most efficient avian predators of bats near the cave entrance (rating as more successful than most Buteo hawks and particularly more so than larger and less agile raptors like red-tailed hawks and large owls ). Per observation in Carlsbad, due to their agility, Cooper's can match the evasive flight of a bat and may be successful in about 90% of observed pursuits. Apart from their well-documented predation of Mexican free-tailed bats ( Tadarida brasiliensis ), quite little is known about which bat species Cooper's hawk's may prey upon and at what level do the local hawks depend on such prey. Apart from caves, sometimes Cooper's hawks have been seen to capture bats in urbanized areas. In some areas, respectable numbers of reptiles may be hunted. All told, nearly 30 species of reptile may be hunted by Cooper's hawks. In the eastern part of the range, even in biodiverse locations for reptilian species such as Florida, a very low volume of such prey are reportedly taken by Cooper's hawks. In Arkansas , a small sample of road-killed Cooper's hawks showed that small reptiles were more common than birds amongst the stomach contents, with Bougainville's skinks ( Lerista bougainvillii ) and ring-necked snakes ( Diadophis punctatus ) constituting about 40% of the diet. Strong detection of reptilian prey is known in more western locations, especially farther south. In fact, of avian predators in one Californian study's estimation, Cooper's hawks showed the most reliance on lizards locally, but that Cooper's was not locally common in the study area so had relatively limited impact. In California, it was found that 69% of the diet was reptiles, most of which were assorted lizards (led by whiptail lizards , nearly 2.8 kg (6.2 lb) of which were estimated to be found in one nest). In rural areas outside of Tucson, a fairly strong presence of (unidentified to species) spiny lizards , at 13% of 77 prey items, although overall in all areas of the Tucson metropolitan, reptiles constituted a lower 8% of the total 228 prey items. In Durango , reptiles were a pronounced part of Cooper's hawk diet. Here, the most frequently identified prey species was the Mexican Plateau horned lizard ( Phrynosoma orbiculare ) (11.5% of 191 prey items), followed by the northern flicker and thirdly the crevice spiny lizard ( Sceloporus poinsettia ) (10.47%, plus other unidentified spiny lizards making up a further 4.2% of the diet). In Arizona, spiny lizards were similarly detected to have a strong prey-predator relationship with Cooper's hawks as well. Most lizards encountered and hunted by Cooper's hawks are fairly small but, despite being more scarcely selected, snake prey may show greater size variation. Snakes known to be taken have ranged in size from the 6 g (0.21 oz) redbelly snake ( Storeria occipitomaculata ) to the a young black rat snake ( Pantherophis obsoletus ), estimated to weigh 200 g (7.1 oz) , and the gopher snake ( Pituophis catenifer ) (adults of the latter two snake species can average roughly 890 g (1.96 lb) for both species and may be too formidable for these hawks). Unlike with reptiles, there is little evidence that Cooper's hawk regularly hunts amphibians in any area, despite a few species being known in the prey spectrum. While some authors have posited that as much as 2.1% of Cooper's hawks' global prey consists of invertebrates , prevailing food studies tend to find scant to none evidence of such prey; however, a truly exceptional case of Cooper's hawks found dead in Arkansas showed that beetles and moths / butterflies each represented 12.5% of detected prey items. Of special interest is how Cooper's hawks live along the other two Accipiters native to North America. Little distinguishes outright the distribution, habitat, ecology and prey spectrum of sharp-shinned hawks from Cooper's hawks. Throughout the range of Cooper's hawk, sharp-shins may be found breeding, migrating and wintering in similar areas. So too is there much overlap between the ranges of Cooper's hawks and northern goshawks , such as throughout southern Canada, the western United States, the Upper Midwest (and sometimes in the Northeastern United States) and during times of passage. In general, sharp-shinned hawks tend to use younger and denser stands of trees than do Cooper's. Meanwhile, goshawks tend to favor old-growth forest area with taller and older trees and generally lower tree densities. However, all three species prefer fairly enclosed canopies over their nesting areas, i.e. canopy coverage are generally thought to need to be at least at 60–70%. A particular opportunity was taken to study the three Accipiters ecology when living near one another in Oregon. Unusually, nests were not consistently well spaced between the species, and 2 sharp-shin nests were approximately 300 m (980 ft) from active Cooper's nests, while 5 Cooper's nests were 300 to 450 m (980 to 1,480 ft) from active goshawk nests. However, the patch habitat and dietary behavior of each species was still fairly partitioned. Here, for sharp-shinned hawks, the tree stands averaged 22–50 years old and had a mean density of 1180 trees per hectare (ha), while Cooper's stands averaged 30–70 years old and had a mean of 907 trees per ha while the goshawk used in oldest and most open stands, with trees of an average age of 150 years, and a mean of 482 trees per ha. The data from the Jemez Mountains of New Mexico was largely corresponding with the goshawk occurring in areas with a median of 781 trees per ha, Cooper's in areas with a median of 1229 trees per ha and the sharp-shins in a median of 1482 tree per ha. In the New Mexico data, goshawks used the largest trees with the lowest median canopy coverage (77.4% vs 78.4% for Cooper' s and 83.1% for sharp-shins). In a study from northern Utah, Cooper's hawks were intermediate in most habitat characteristics, being at median elevation ( 1,782 m (5,846 ft) ), nest height ( 8 m (26 ft) against 6 m (20 ft) for sharp-shins and 12 m (39 ft) for goshawk) and in areas of intermediate branch density. However, Cooper's nests were the closest in Utah to areas disturbed by humans ( 147 m (482 ft) against 161 m (528 ft) for sharp-shinned and 250 m (820 ft) for goshawk), also closest to water ( 220 m (720 ft) against 444 m (1,457 ft) in sharp-shins and 394 m (1,293 ft) for goshawk). There is often some level of distinction in habitat between Cooper's and the sharp-shinned hawk. Compared to sharp-shinned hawks in Wisconsin and Oregon, Cooper's hawks use woods with fewer conifers, less dense stands of trees and stands with taller trees. Often, sharp-shinned hawk nests are lower in the trees and placed in much denser vegetation (often even the sharp-shins with their smaller frames themselves accidentally strike against branches while attempting to enter the nest), to hide the nest more sufficiently against predators. The habitat used by the two species in Missouri was less distinct (i.e. similar tree species used). However, the sharp-shinned hawk nests in Missouri were at much higher elevations, i.e. 343 m (1,125 ft) above sea level, than those of Cooper's (which were at a mean elevation of 151.3 m (496 ft) ; more surprisingly the stand density was higher here for Cooper's, at a mean of 935.7 trees per ha than those used by sharp-shins, at a mean of 599.3 trees per ha. There was some level of temporal differences between the two species in study in Indiana, where Cooper's hawks were generally active in the early morning but sharp-shinned hawks did not become active until later in the morning (hypothetically to avoid more severe interguild predation by large owls due to its smaller size). In northern New Jersey, compared to nesting goshawks, Cooper's hawks used flatter lands that were closer to roads, other openings and human habitations. However, canopy coverage averaged high in New Jersey data for Cooper's, at 89.1%. Cooper's hawk has a mean home range size that was comparable to the roughly half as large-bodied Eurasian sparrowhawk , at 1,190 ha (2,900 acres) for Cooper's and 835 ha (2,060 acres) for the sparrowhawk. However, data shows that in North America, the Accipiters home range size corresponded to the birds' body size, i.e. 2,600 ha (6,400 acres) mean for the goshawk and 458 ha (1,130 acres) mean for the sharp-shinned hawk. The aforementioned Oregon studies also studied at length the dietary differences between the three American Accipiters . Cooper's hawks prey sizes were intermediate in keeping with body size, at around 135 g (4.8 oz) versus a mean prey size of 306.6 g (10.81 oz) for the goshawk in eastern Oregon and 12.8 and 28.4 g (0.45 and 1.00 oz) for sharp-shins in northwestern and eastern Oregon, respectively. The amount of mammals in the diet in Oregon also increased with the body size of the species. The diets of the three species were also studied in the Chiricahua Mountains of Arizona. There was some diet overlap in preferred prey for Cooper's hawks with both other Accipiters . In the case of the goshawk and Cooper's, both hawks regularly took Steller's jays and band-tailed pigeons ( Patagioenas fasciata ). With the sharp-shinned hawk, Cooper's locally also shared a liking for American robins and black-headed grosbeaks ( Pheucticus melanocephalus ). However, unlike either other Accipiter in the Chiricahuas, Cooper's hawks regularly took chipmunks and lizards as well. Furthermore, the nests of Cooper's and goshawks were fairly evenly spaced, at about 1.6 km (0.99 mi) apart, indicating that they maintain exclusive territories (almost as if within the same species), while sharp-shinned hawk nests were closer to goshawk nests but in much denser habitats. When chickens were experimentally exposed to each of the three American Accipiters , they reacted the most aggressively to the sharp-shinned hawk (as they pose little to no threat to adult poultry), intermediately to Cooper's and with strong attempts to evade and escape when exposed to the goshawk, which is very capable and ready to dispatch adult poultry. Many studies have contrasted the diet of Cooper's and sharp-shinned hawk in other areas as well, with the sharp-shinned hawk much more regularly selecting birds weighing under about 28 g (0.99 oz) , a fair amount overlap in birds of 28 to 40 g (0.99 to 1.41 oz) and 40 to 75 g (1.4 to 2.6 oz) weight classes but birds over this weight range are increasingly more often taken almost exclusively by Cooper's. Also, the sharp-shinned hawk appears to hunt more so birds that dwell at the canopy level in the woodlands (as opposed to ground to shrub height-dwelling birds) within the forest and prefers to attack in heavier cover than Cooper's seemingly. The ecology of Cooper's hawks has also been studied in contrast to other diurnal raptors as well. In the raptor guild within southern Michigan, the overall food breadth and size was studied against red-tailed hawks , red-shouldered hawks and American kestrels . Here, although the food niche breadth (mean number of prey species per study site) of Cooper's was relatively low at 1.79, Cooper's hawk had the largest mean prey sizes at 67.4 g (2.38 oz) , which was considerably higher than even the much larger red-tailed hawk (mean prey mass of 43.4 g (1.53 oz) ). In southern Wisconsin, the food niche breadth was rather higher for Cooper's at 6.9 and the mean prey mass, at 109.9 g (3.88 oz) , was second only to the red-tailed hawk's. In the Wisconsin data, the red-shouldered, the broad-winged and rough-legged hawks ( Buteo lagopus ) as well as the northern harrier , peregrine falcon ( Falco peregrinus ) and the American kestrel all had lower mean prey masses. Much farther south in Durango, Mexico, while there was overlap in the class of prey selected by Cooper's hawks with the other studied raptor species, American kestrels, red-tailed and zone-tailed hawks ( Buteo albonotatus ), there was minimal overlap in which prey species were usually selected, especially given the difference in habitat usage. Furthermore, in Durango, while Cooper's and the Buteo hawks all took appreciable numbers of adult cotton rats , kestrels selected only young cotton rats. In a study in western Maryland, Cooper's hawks used more mature woodland with a more developed understory and more extensive ground cover than the other woodland nesting hawks, the broad-winged and red-shouldered hawks. While red-tailed hawks nested fairly high in the Maryland data in isolated pines somewhat out of the interior forest, Cooper's nests were at similar height in forest and slightly higher than those of red-shouldered hawks and much higher than those of broad-winged hawks. In what was probably a case of defense of their hunting ground, a female Cooper's hawk was recorded to attack and drive off (without physical contact) a larger peregrine falcon from a perch during winter in Ontario. Cooper's hawk is usually a top predator in the daytime but is not immune from attack by other predators. The most common predator of this species is almost certainly the great horned owl ( Bubo virginianus ). This rather large owl (averaging more than three times heavier than a Cooper's hawk) is known to regularly track down fledglings and adults as well as raid the nests of other birds of prey. Many records show great horned owls will visit the nests of birds of prey and pick off the young nightly until the prey resource is exhausted (i.e. all young or sometimes adult birds of prey are killed). Furthermore, given the opportunity, great horned owls readily expropriate the nests built by the raptors they kill as their own. Given its preference for secluded wooded spots near woodland openings, Cooper's hawks are frequently the subject of unwanted attention from horned owls. Both the young, especially around the time they leave the nest or are recently fledged, and adult Cooper's hawks are vulnerable to these owls. While little data has been collected on the overall effect great horned owls have on Cooper's hawk populations, it is known that for the larger, more formidable goshawk that as many as 40% of radiotagged juveniles within a study appeared to meet their demise via horned owls. Due to their threat level, the calls of great horned owls provoke a strong response from Cooper's hawks and banders and researchers usually use stimuli of great horned owls to attract a mobbing Cooper's hawks. Reportedly, Cooper's hawks will temporarily tolerate and possibly even cooperate with crows when one or the other spots a great horned owl in the daytime, both species appearing to join forces to mob the threatening owl out of the vicinity. In one case, after a great horned owl pair failed to successfully breed in a nest built by other Cooper's hawks, a pair of Cooper's who tried to nest was supplanted by horned owls, possibly of the same pair who had previously failed. Other natural predators of Cooper's hawks that are known are mainly larger diurnal birds of prey. In some cases, their larger cousins, northern goshawks, will prey on Cooper's hawks. Widely but somewhat scarcely, red-tailed hawks have been known to prey on Cooper's hawk, while a single instance is known of a Cooper's falling prey to a golden eagle ( Aquila chrysaetos ). Less is known about the range of nest predators. Among all known predators, only the raccoon ( Procyon lotor ) can be considered to rival the great horned owl as the most severe threat to nesting attempts, probably consuming mostly nestlings and eggs but also perhaps some older hawks. American crows are known to rob nests of Cooper's hawks as well, especially when the parents have been displaced by the crow's severe mobbing. Smaller diurnal birds of prey are, in turn, threatened by Cooper's hawks. This is especially the case with the American kestrel. After some regional declines, a radiotagging study in Pennsylvania found that of 19 kestrels, 26% were killed by avian predators, with the suspected culprit in a majority of the cases being Cooper's hawks. Some resources have gone as far as to blame the kestrels decline directly on Cooper's hawk predation but subsequent data from the U.S. Breeding Bird Survey and the National Audubon Society Christmas Bird Count appear to discount this theory, instead linking the overall declines to inadvertent human causes. Cooper's hawk are also counted as a predator of merlins ( Falco columbarius ). The only confirmed accipitrid that Cooper's hawk have been known to prey upon is their smaller cousins, the sharp-shinned hawks. However, in the southeast , Cooper's hawks was counted among the potential, but not yet confirmed, predators of swallow-tailed kites ( Elanoides forficatus ) and nesting kites appear to engage in anti-predator behavior towards Cooper's hawks. Furthermore, Cooper's hawks that came into the vicinity were considered potential predators and mobbed as such by nesting gray hawks . Even more so than diurnal raptors, a wide diversity of owls are known to fall prey to Cooper's hawks. Despite the temporal differences of their activity, the intensive hunting methods of Cooper's hawks may allow them to access roosting owls more readily than other types of hawks. Small owls that Cooper's hawk have been known to prey upon have included flammulated owls ( Psiloscops flammeolus ), eastern screech-owls ( Megascops asio ), western screech-owls ( Megascops kennicottii ), whiskered screech-owl ( Megascops trichopsis ), elf owl ( Micrathene whitneyi ), northern pygmy owl ( Glaucidium gnoma ), ferruginous pygmy owl ( Glaucidium brasilianum ), burrowing owl ( Athene cunicularia ), boreal owl ( Aegolius funereus ) and northern saw-whet owl ( Aegolius acadicus ). Medium to large-sized owls are sometimes also prey for Cooper's hawks have been known to include long-eared owl ( Asio otus ) and perhaps the rather large spotted owl ( Strix occidentalis ). Most impressively, an instance was observed where a Cooper's hawk appeared to have preyed upon an adult of the rather larger (averaging about 787 g (1.735 lb) ) barred owl ( Strix varia ). There is also a record of a barred owl preying on a Cooper's hawk as well. Cooper's hawks are known as bold and aggressive predators. Given their dietary habits, these hawks bore a poor reputation well into the 20th century, with one account describing the species as "noxious", an "avian outlaw" and "a relentless tyrant and murderer of small birds". Another describes the species as "bloodthirsty" and a "villain". Early accounts underestimated the opportunistic nature of Cooper's hawks' hunting behavior and provided little insight into the actual effect the hawks have on their prey. The maximum hunting range was estimated at 5.3 km 2 (2.0 sq mi) in Michigan and 2 km 2 (0.77 sq mi) in Wyoming . In another Michigan study, most Cooper's hawks were found to be flying 0.8 to 1.2 km (0.50 to 0.75 mi) from their wooded nests to hunt on agricultural ground. Males in New York usually covered more than 0.8 km (0.50 mi) , sometimes up to 3 km (1.9 mi) , during hunting efforts when flying away from the nest area. Due to scattered prey availability in North Florida , females were nearly nomadic, wandering anywhere where food could be accessed (i.e. chicken farms , feedlots , bird feeders , etc.), while males were more typically devoted to hunting on their regular home range. During hunts, Cooper's hawks rely on agile, twisting flights between bouts of perching and scanning, their flight suddenly picking up speed upon approach to the prey. Hunting hawks typically use forest edge , open woodland and fencelines and such while hunting. In southwestern Tennessee , the preferred hunting habitats in the non-breeding season were forest, then woodland edge , then lastly open country . Near Stevens Point in Wisconsin, males prefer to hunt in quiet woods while females preferred to stay within 100 m (330 ft) of the nest making males a more common sight. This differed strongly in Tucson where hawks while hunting mostly in manmade environments such as residential areas, regional parks , and golf courses more so than they were prevalent in the environment, though usually where there were large (albeit usually non-native) trees. Cooper's hawk does attack birds attracted to bird feeders with a fair amount of frequency. However, data from Indiana showed that birds using bird feeders were at no greater risk of attack than those in random transects, and the effect Cooper's can have on feeder birds may be at times exaggerated. If it sees birds when flying, a hunting hawk does not fly directly to them but instead circles around to available trees and bushes often perching for a few moments before launching its attack. If birds become aware of it, the hawk will tend to quickly gain height in hopes of intercepting some prey. It was found compared to some other North American raptors who are more likely to watch for prey on the ground and/or in the open, that Cooper's hawk had a rather enlarged binocular field . During hunts, these hawks may suddenly alight when detecting an available mammal. Sometimes, Cooper's hawks will engage in tandem hunts with one dashing around after the prey while another waits on the other side of a tree trunk or wooded thicket. Many birds are caught when they inadvertently fly around a tree where a hawk is inconspicuously perched. Young Cooper's are impetuous about crashing into bushes after prey, sometimes even into thorny cover such as barberries, whereas adults are said to be more "prudent". They may chase prey into cover or from bush to bush. The first instance of non-piratical scavenging on carrion was recorded when a Cooper's hawk was seen eating at a white-tailed deer ( Odocoileus virginianus ) carcass. When hunting bats, they can follow all twists and turns, and may succeed in capture in up to 90% of hunts. Much like goshawk, sometimes Cooper's hawks will capture rabbits by pursuing on the ground, half-running, half-flying. Other on-foot hunting efforts, especially when chasing quail , have been detected as well. When hunting sparrows , Cooper's hawks may make multiple passes on a bush before success and the efforts can take up to 45 minutes. During hunts of rock doves ( Columba livia) in urban areas, Cooper's hawks have been seen to engage in open air stoops to capture the prey. An unusual harrier -like flight was seen in be engaged in by a Cooper's hawk before an attack on aquatic prey in a marsh . Most prey is killed by repeatedly kneading the talons, with the kneading sometimes going on even after death, although in some cases birds are plucked while still alive. Despite its gracile appearance, Cooper's hawk, like the northern goshawk, is extremely powerful for its size and presumably able to capture larger prey relative to its size than other raptors such as falcons and Buteos (including red-tailed hawks ( Buteo jamaicensis )) due to its unusually high-speed foot velocity and resulting impact during prey captures. At times, after capture, Cooper's hawk have been seen to hold still living prey underwater, presumably trying to drown it. Subsequent to the preys' demise, they may eat the victim head first, followed by the viscera , with the meat eaten lastly. Like other raptors who most regularly take birds, Cooper's hawk was profiled in a study as an "attacker" rather than a "searcher" (i.e. mammal -hunters such as Buteos ). "Attackers" such as Accipiters and large falcons usually had lower average hunting success rates, which averaged among the attacker species at 27%, due to the difficulty of capturing the prey. 33% of 45 observed hunts in a study in Missouri were successful. In Terre Haute, Indiana , about 23% of attacks by male Cooper's hawks and 20% by females were successful and were far more prone to being carried out in relatively open areas than those of nearby sharp-shinned hawk. Post-fledgling parties of hawks in Wisconsin were seen to hunt in sibling groups of 2–4, mainly pursuing chipmunks , and were observed to succeed in 56% of 18 hunting attempts. During the first six weeks after the young hatch, in New York, it was estimated that a male Cooper's hawk would need to procure about 66 prey items over the period. In these first six weeks in California, it was thought a minimum of 62 g (2.2 oz) would be required per nestling per day. Cooper's hawk may consume well over 300 prey species from across the range. This predator is known to consume vertebrate prey almost exclusively. Often smallish or medium-sized birds are the preferred food, but also many small mammals and, in more arid vicinities, lizards are regularly taken. Infrequently, frogs may be eaten, as will (rarely) insects and fish in nearly dry watercourse. Birds in general form about 50–85% of diet. One estimate is that globally birds form about 71.1% of the diet, 17.9% mammals, 8.9% reptiles and 2.1% other prey. Cooper's hawks generally prefers birds that inhabit the ground or shrub level within the local habitats. One estimate claims that most prey of Cooper's hawks weighs from 15 to 166 g (0.53 to 5.86 oz) , with male and female averages of 37.6 and 50.7 g (1.33 and 1.79 oz) . Another estimate was from 30 to 130 g (1.1 to 4.6 oz) for typical prey sizes, or about 5–37% the weight of males and 8–22% the weight of females, respectively. However, subsequent studies, such as those in Indiana , found prey weighing up to 360 g (13 oz) (such as adult pigeons ) can be quite common in the diet of Cooper's hawks. Mean prey weights were roughly 112.6 g (3.97 oz) . In Oregon, the mean prey sizes of Cooper's hawk was 135.5 g (4.78 oz) , with larger prey was taken than in greater proportion than their occurrence in the ecosystem (indicating that they locally search out relatively large prey). In Missouri, mean prey sizes were 112 g (4.0 oz) , averaging between 83.5 and 316.5 g (2.95 and 11.16 oz) amongst the main prey classes. Prey delivered by males averaged an estimated 65.9 g (2.32 oz) , while the average estimated size of prey delivered by females was 227.7 g (8.03 oz) . Overall, in Missouri, prey body masses were estimated to range from 15 to 600 g (0.53 to 21.16 oz) . One study unusually found no strong dimorphism in the foods selected by males and females. Birds are by far the leading prey for Cooper's hawks in most areas. A wide diversity of birds, considerably over 250 species, are known to be taken, constituting more than three-quarters of known prey species for these hawks. A Cooper's hawk is estimated to kill an average of two birds a day, or 700 birds a year. Although prior data mostly reflected the taking of adult birds, a study in Wisconsin revealed that Cooper's hawks may largely take young of the year, mostly fledglings but also not infrequently nestlings, during the breeding season. 74% of ageable bird prey in this study were young of the year. Similarly, in Michigan during summer, immature birds were more than 2.5 times more often delivered to Cooper's hawk nests than adult birds. In one case, a Cooper's hawk was seen to fly away with an entire occupied nest of American goldfinches ( Spinus tristis ). One study determined that birds that nest in the canopy level tended to nest fairly close to this hawk but those with mid-level, shrub level and ground level nests nested farther away, indicating that non-canopy-nesting birds are generally taken during the breeding season. Key to prey selection for Cooper's hawk is the availability and abundance of birds in a given region. Therefore, the extremely numerous American robin ( Turdus migratorius ) appears to be the most widely reported prey species. Robins were the leading prey species in northwestern Oregon , at 19.6% of 281 prey items, Lopez Island , Washington , 23.4% of 107 prey items, in Victoria, British Columbia , at 34.6% of 2896 prey items and prominent but ranked second also in California ( Berkeley and Albany ) food studies, 24.5% of 1057 prey items. The robin is regularly hunted in all seasons due to its commonality in exurban regions, with both adults, at estimated averages of 79 to 81.2 g (2.79 to 2.86 oz) when taken, and young being relatively easy for them to access. Beyond the common robin, nearly all thrushes in North America (excluding one species whose breeding range is largely north of Cooper's range and one rare, little-studied species ) are opportunistically hunted by Cooper's hawks. The closest rival to the robin in being most widely taken as prey for Cooper's hawks may be the common starling ( Sturnus vulgaris ), a non-native bird in North America with mean weights when taken of 79 to 82 g (2.8 to 2.9 oz) . The starling was the main food for these hawks in Ithaca, New York , at 28.2% of 857 prey items, and Terre Haute, Indiana , at 56.5% of 57 prey items, and taken in large but somewhat secondary numbers in Missouri, Michigan , and Victoria, British Columbia. In the urban environment of Terre Haute, it was found that starlings were taken in almost the same proportion as starlings were of all birds observed by researchers (i.e. they were 60% of 2146 individual birds seen). Somewhat over 60% of the bird species known in Cooper's hawks' prey spectrum are passerines (including thrushes and starlings). Other medium-sized to largish-bodied families of passerines tend to be most often selected. In many circumstances, Cooper's hawks will hunt corvids , large, intelligent and social passerines, with the smallish jays being particularly popular. In Missouri, the most often selected prey (12.7% of 259 prey items) was the 89 g (3.1 oz) blue jay ( Cyanocitta cristata ), which also important in northern Florida, i.e. 12.27% of 1100 prey items. Steller's jays ( Cyanocitta stelleri ), at 107 g (3.8 oz) a larger western cousin of the blue jay, are also regularly selected in various studies, such as all studied areas of Oregon and New Mexico , where it was the second most regularly selected of prey species at 11.7% of 316 prey items. California scrub jays ( Aphelocoma californica ) are regular supplemental prey in northern California studies as well. Blue jays and other related species are among the most diligent mobbing birds in response to the presence of a Cooper's hawk although sometimes may let out an alarm call or even imitate a Cooper's calls merely to frighten other birds from a desired food source. It was hypothesized that Steller's jays may be able to effectively confuse a Cooper's hawk by engaging in a chorus of calls at close range. In Arizona , Mexican jays ( Aphelocoma ultramarina ) are known to play a key role in flicker ecology by watching out for Cooper's hawks. Numerous other corvids may be hunted, including most overlapping jays, as well as the Clark's nutcracker ( Nucifraga columbiana ), black-billed magpie ( Pica hudsonius ), possibly yellow-billed magpie ( Pica nuttalli ) and a few species of crow . One black-billed magpie was caught and killed by a Cooper's hawk when attempting to mob the hawk. Incidents of predation have been witnessed on both young and adult American crow ( Corvus brachyrhynchos ), as well as on adult northwestern crow ( Corvus caurinus ). These hawks are also a potential predator of fish crow ( Corvus ossifragus ). However, crows are potentially dangerous prey to Cooper's hawks. Adult American crows are about the same size as a female Cooper's hawk and can potentially cause considerable damage to a lone raptor during group mobbing , being capable of inflicting damage with both their feet and bill. In at least one case, a murder of American crows was observed to drive a Cooper's hawk to the ground and possibly seriously injure it, although the fate of the hawk was not certain. Cases of missing toes on Cooper's hawks are thought to have possibly come from failed predation of crows. At least a dozen species of icterid are known to be hunted by Cooper's hawks as well. Common, widespread icterids such as red-winged blackbirds ( Agelaius phoeniceus ) and common grackles ( Quiscalus quiscula ) are fairly frequent prey for these hawks. Cooper's hawks nesting near red-winged blackbird colonies may at times live almost entirely off of female blackbirds. In the Black Hills , although prey species were seldom identified, evidence showed that most regularly selected prey were assorted icterids. Even meadowlarks , such as the 93 g (3.3 oz) eastern meadowlark ( Sturnella magna ) which was the third most often selected prey in Ithaca, New York, and bobolinks ( Dolichonyx oryzivorus ) are taken despite their preference for grasslands well outside the typical habitats of Cooper's hawks. Other passerines families (i.e. outside thrushes, corvids and icterids) tend to not be as large-bodied and, although by no means neglected, are seldom equal in overall dietary importance ( biomass ). About 15 species of tyrant flycatcher , several species each of vireo , swallows , tits , nuthatches , wrens , mimids , about a dozen species of finch , cardinalids and a huge diversity of American sparrows and New World warblers (nearly 30 species each) are known to be taken by Cooper's hawks. A lower diversity are taken of shrikes , larks , penduline tits , aegithalids , treecreepers , dippers , silky-flycatchers and longspurs . The more numerous native passerines, such as northern cardinals ( Cardinalis cardinalis ) and northern mockingbirds ( Mimus polyglottos ), have good reason to fear these hawks as they are widely and regularly taken as are even common birds of less than half their size (around 20 g (0.71 oz) ), such as song sparrows ( Melospiza melodia ), dark-eyed juncos ( Junco hiemalis ) and house finches ( Haemorhous mexicanus ). During harsh late winter weather in Wisconsin, Cooper's hawks were recorded to eke out an existence living largely off of pine siskins ( Spinus pinus ). In modern terms, certainly the most commonly taken small bird would be the non-native, 29 g (1.0 oz) house sparrow ( Passer domesticus ). Although not known to be taken profusely in all studied urban locales, house sparrows were the leading prey in a study from Michigan , were nearly a third of observed delivered prey at nests in Victoria, British Columbia (although were outnumbered by robins in prey remains) and reportedly were the leading prey in Milwaukee and in Grand Forks, North Dakota . Flycatchers are not hugely significant in Cooper's hawk's foods, but the local effect of the hawks on populations can be considerable. For example, willow flycatchers ( Empidonax traillii ) in California suffered a 76% rate of nest predation, among which Cooper's hawks were a considerable contributor, and dusky flycatchers ( Empidonax oberholseri ) experienced a rate of 96% predation elsewhere in California, with 25% attributable to Cooper's. Similar determent to the local nesting attempts of other small passerines such as warblers has also been reported. Chickadees seem to regard Cooper's hawks as a moderate threat based on their anti-predator response, with smaller raptors (which are presumably more dangerous) such as sharp-shinned hawks and small owls evoking a rather more aggressive response by chickadees. While usually the smallest avian prey selected by Cooper's hawks are various warblers (presumably taken mainly by male hawks), down to the size of the 7 g (0.25 oz) Wilson's warbler ( Cardellina pusilla ), even smaller passerines are known to be hunted. The smallest known avian prey species have included the 6.8 g (0.24 oz) verdin ( Auriparus flaviceps ), the 6.3 g (0.22 oz) ruby-crowned kinglet ( Regulus calendula ) and the 5.3 g (0.19 oz) bushtit ( Psaltriparus minimus ). Even smaller birds, the hummingbirds , are essentially immune to Cooper's hawks (due to their own extreme agility) and were seen to incidentally benefit from nesting close to the hawks in California, due to a low risk of predators approaching while the hawks are present. Outside of passerines, almost certainly the most important avian prey type is the pigeon and dove family. Especially for those living in urban areas, Cooper's hawks have seemed to take to living heavily off of doves , particularly the abundant and widely found mourning dove ( Zenaida macroura ), at 119 g (4.2 oz) . Mourning doves appear to be hunted regularly in almost any part of the two species' mutual range. In Tucson , recent data shows that Cooper's hawks are living almost exclusively on doves. Among 151 prey items there, mourning doves were 20.5% by number and 27.5% of the biomass, Inca doves ( Columbina inca ) were 18.5% by number and 12.2% of the biomass and white-winged dove ( Zenaida asiatica ) 17.2% by number and 27.1% of the biomass. In Terre Haute, Indiana , mourning doves and rock doves were 14% and 21% of the diet, respectively. In northern California, mourning doves were the main prey species, making up 25.6% of 1057 prey items. There is even evidence that bluebirds have perceived the change in preference of Cooper's hawks to more profitable prey such as doves in developed areas and show less inhibition to the hawk's presence. In the more rural north Florida , again the mourning dove leads the prey selection, accounting for 16.5% of 1100 prey items. Another popular prey family is the woodpeckers . A rather numerous and widely distributed species, the 132 g (4.7 oz) northern flicker ( Colaptes auratus ), is a particular dietary staple of Cooper's hawks, being about the third most widely reported prey species. The flicker was the main prey in northern New Mexico , at 22.5% of 316 prey items, and in southern Wisconsin, at 22% of 77 prey items. Flickers are common prey elsewhere as well, such as in Ithaca, New York . Medium-sized woodpeckers, such as red-headed woodpeckers ( Melanerpes erythrocephalus ) and red-bellied woodpeckers ( Melanerpes carolinus ) were important secondary prey in different parts of the range. In South Carolina , it was found that 15% of the red-headed woodpeckers in a study population were killed by hawks. All told, about 20 species (almost all in North America but for a couple poorly-studied species) of woodpecker are known to be taken, ranging from the smallest, the 25.6 g (0.90 oz) downy woodpecker ( Picoides pubescens ), to the largest, the 287 g (10.1 oz) pileated woodpecker ( Dryocopus pileatus ). The response of woodpeckers to a sighted Cooper's hawks varies, with evidence showing that downy woodpecker and flickers would behave more boldly and themselves may scold the hawk if part of a mixed flock but, if alone, the woodpecker will typically try to flee. Despite the regularity of predation of woodpeckers that are in the open, a study in British Columbia shows indicated Cooper's hawks seldom prey upon woodpecker nests, perhaps due to being unable to access their secluded, smallish nest holes, with the study showing that the most regular predators of such nests were various mammals (from deermice to bears ). Certainly the most controversial aspect of Cooper's hawks are their predations upon galliforms . By far the most regularly selected types are New World quails . Coveys of quails that attempt to evade predators by running into thick vegetation (which can allow them to successfully escape many predators) often find that Cooper's hawks are undeterred by this, as the hawks may chase them either on the wing or on foot into thickets. However, one grouse was seen to successfully evade a hunting Cooper's hawk by diving belly first into about a foot of snow. Cooper's hawks are often regarded as perhaps the most regular natural predator of northern bobwhites ( Colinus virginianus ). Indeed, the rate of predation by Cooper's does appear to exceed that committed by other species of hawk as well as that by large owls. For instance, during winter in Wisconsin, Cooper's hawks were thought to kill 3.4–12.5% of the local bobwhite population. However, the bobwhite appears to be a secondary prey species in all known studies and there is no evidence that Cooper's hawk predation alone can deplete bobwhite populations, unlike causes directly contributable to man such as overhunting and habitat destruction . In Washington state, female Cooper's hawks took many California quails ( Callipepla californica ), which were estimated to constitute 47% of the prey selected by female hawks, but there was far too little impact overall to affect the quail's overall population. In the rural areas outside of Tucson , Gambel's quail ( Callipepla gambelii ) were found to be the most regularly selected prey species, at 15.2% of 79 prey items. A study of pellets in northwestern Mexico to determine if the local Cooper's hawks were regularly taking Montezuma quail ( Cyrtonyx montezumae ), finding that only one pellet consisted entirely of quail, the other pellets showing that hawks were mainly taking other prey, mostly doves. Most regularly found galliforms in North America (including well-established exotics such as chukars ( Alectoris chukar ) and common pheasants ( Phasianus colchicus )) are known to fall prey occasionally to Cooper's hawks. These include assorted native grouse , including even the grassland -dwelling species (but excluding the more northerly distributed ptarmigans ). Juveniles usually are the more vulnerable and more regularly taken of non-quail galliforms by Cooper's hawks, but the hawks can take adults quite regularly despite the prey's relatively large size. Adult ruffed grouse ( Bonasa umbellus ), weighing an estimated mean of 619 g (1.365 lb) when taken, are not infrequently exploited as prey, while adult sooty grouse ( Dendragapus fuliginosus ), estimated to weigh 1,050 g (2.31 lb) when taken have also been known to be taken repeatedly. Adult male sharp-tailed grouse ( Tympanuchus phasianellus ), which average 1,031 g (2.273 lb) , are also known have been successfully preyed upon by Cooper's hawks. Even more impressive accounts show adult common pheasant estimated to weigh up to 1,158 g (2.553 lb) can be preyed upon by Cooper's hawks. One wild turkey ( Meleagris gallopavo ) taken in Florida was cited with a weight of 5,336 g (11.764 lb) , which is the size of an adult. However, given that this is of enormous size relative to a Cooper's hawk, it would require verification that the turkey was this large and was taken alive by the hawk. Not unexpectedly, turkey poults are known to fall prey to Cooper's hawks. Beyond aforementioned families and orders, other types of birds are taken relatively infrequently. Usually moderate to low numbers of water birds are taken of any variety. About 5 species each of duck and heron , a dozen species of shorebird and a smaller assortment of grebes and rails are known in the prey spectrum. Even among water birds, nonetheless, a wide diversity may be taken, from the tiny 22.9 g (0.81 oz) least sandpiper ( Calidris minutilla ) to an adult mallard ( Anas platyrhynchos ) estimated to weigh 1,150 g (2.54 lb) when taken. Adult ducks and herons of roughly equal weight to Cooper's hawks and other largish adult water birds including ring-billed gulls ( Larus delewarensis ) and American coots ( Fulica americana ) are sometimes tackled by these hawks. Particularly frequency was recorded of 312.7 g (11.03 oz) cattle egrets ( Bubulcus ibis ) in north Florida, where the egrets were the fourth most regularly recorded prey species. Assorted families of land birds are fairly rare as reported in food studies, including some nightjars , trogons , swifts , kingfishers , parrots and assorted other raptorial birds. Birds are by far the leading prey for Cooper's hawks in most areas. A wide diversity of birds, considerably over 250 species, are known to be taken, constituting more than three-quarters of known prey species for these hawks. A Cooper's hawk is estimated to kill an average of two birds a day, or 700 birds a year. Although prior data mostly reflected the taking of adult birds, a study in Wisconsin revealed that Cooper's hawks may largely take young of the year, mostly fledglings but also not infrequently nestlings, during the breeding season. 74% of ageable bird prey in this study were young of the year. Similarly, in Michigan during summer, immature birds were more than 2.5 times more often delivered to Cooper's hawk nests than adult birds. In one case, a Cooper's hawk was seen to fly away with an entire occupied nest of American goldfinches ( Spinus tristis ). One study determined that birds that nest in the canopy level tended to nest fairly close to this hawk but those with mid-level, shrub level and ground level nests nested farther away, indicating that non-canopy-nesting birds are generally taken during the breeding season. Key to prey selection for Cooper's hawk is the availability and abundance of birds in a given region. Therefore, the extremely numerous American robin ( Turdus migratorius ) appears to be the most widely reported prey species. Robins were the leading prey species in northwestern Oregon , at 19.6% of 281 prey items, Lopez Island , Washington , 23.4% of 107 prey items, in Victoria, British Columbia , at 34.6% of 2896 prey items and prominent but ranked second also in California ( Berkeley and Albany ) food studies, 24.5% of 1057 prey items. The robin is regularly hunted in all seasons due to its commonality in exurban regions, with both adults, at estimated averages of 79 to 81.2 g (2.79 to 2.86 oz) when taken, and young being relatively easy for them to access. Beyond the common robin, nearly all thrushes in North America (excluding one species whose breeding range is largely north of Cooper's range and one rare, little-studied species ) are opportunistically hunted by Cooper's hawks. The closest rival to the robin in being most widely taken as prey for Cooper's hawks may be the common starling ( Sturnus vulgaris ), a non-native bird in North America with mean weights when taken of 79 to 82 g (2.8 to 2.9 oz) . The starling was the main food for these hawks in Ithaca, New York , at 28.2% of 857 prey items, and Terre Haute, Indiana , at 56.5% of 57 prey items, and taken in large but somewhat secondary numbers in Missouri, Michigan , and Victoria, British Columbia. In the urban environment of Terre Haute, it was found that starlings were taken in almost the same proportion as starlings were of all birds observed by researchers (i.e. they were 60% of 2146 individual birds seen). Somewhat over 60% of the bird species known in Cooper's hawks' prey spectrum are passerines (including thrushes and starlings). Other medium-sized to largish-bodied families of passerines tend to be most often selected. In many circumstances, Cooper's hawks will hunt corvids , large, intelligent and social passerines, with the smallish jays being particularly popular. In Missouri, the most often selected prey (12.7% of 259 prey items) was the 89 g (3.1 oz) blue jay ( Cyanocitta cristata ), which also important in northern Florida, i.e. 12.27% of 1100 prey items. Steller's jays ( Cyanocitta stelleri ), at 107 g (3.8 oz) a larger western cousin of the blue jay, are also regularly selected in various studies, such as all studied areas of Oregon and New Mexico , where it was the second most regularly selected of prey species at 11.7% of 316 prey items. California scrub jays ( Aphelocoma californica ) are regular supplemental prey in northern California studies as well. Blue jays and other related species are among the most diligent mobbing birds in response to the presence of a Cooper's hawk although sometimes may let out an alarm call or even imitate a Cooper's calls merely to frighten other birds from a desired food source. It was hypothesized that Steller's jays may be able to effectively confuse a Cooper's hawk by engaging in a chorus of calls at close range. In Arizona , Mexican jays ( Aphelocoma ultramarina ) are known to play a key role in flicker ecology by watching out for Cooper's hawks. Numerous other corvids may be hunted, including most overlapping jays, as well as the Clark's nutcracker ( Nucifraga columbiana ), black-billed magpie ( Pica hudsonius ), possibly yellow-billed magpie ( Pica nuttalli ) and a few species of crow . One black-billed magpie was caught and killed by a Cooper's hawk when attempting to mob the hawk. Incidents of predation have been witnessed on both young and adult American crow ( Corvus brachyrhynchos ), as well as on adult northwestern crow ( Corvus caurinus ). These hawks are also a potential predator of fish crow ( Corvus ossifragus ). However, crows are potentially dangerous prey to Cooper's hawks. Adult American crows are about the same size as a female Cooper's hawk and can potentially cause considerable damage to a lone raptor during group mobbing , being capable of inflicting damage with both their feet and bill. In at least one case, a murder of American crows was observed to drive a Cooper's hawk to the ground and possibly seriously injure it, although the fate of the hawk was not certain. Cases of missing toes on Cooper's hawks are thought to have possibly come from failed predation of crows. At least a dozen species of icterid are known to be hunted by Cooper's hawks as well. Common, widespread icterids such as red-winged blackbirds ( Agelaius phoeniceus ) and common grackles ( Quiscalus quiscula ) are fairly frequent prey for these hawks. Cooper's hawks nesting near red-winged blackbird colonies may at times live almost entirely off of female blackbirds. In the Black Hills , although prey species were seldom identified, evidence showed that most regularly selected prey were assorted icterids. Even meadowlarks , such as the 93 g (3.3 oz) eastern meadowlark ( Sturnella magna ) which was the third most often selected prey in Ithaca, New York, and bobolinks ( Dolichonyx oryzivorus ) are taken despite their preference for grasslands well outside the typical habitats of Cooper's hawks. Other passerines families (i.e. outside thrushes, corvids and icterids) tend to not be as large-bodied and, although by no means neglected, are seldom equal in overall dietary importance ( biomass ). About 15 species of tyrant flycatcher , several species each of vireo , swallows , tits , nuthatches , wrens , mimids , about a dozen species of finch , cardinalids and a huge diversity of American sparrows and New World warblers (nearly 30 species each) are known to be taken by Cooper's hawks. A lower diversity are taken of shrikes , larks , penduline tits , aegithalids , treecreepers , dippers , silky-flycatchers and longspurs . The more numerous native passerines, such as northern cardinals ( Cardinalis cardinalis ) and northern mockingbirds ( Mimus polyglottos ), have good reason to fear these hawks as they are widely and regularly taken as are even common birds of less than half their size (around 20 g (0.71 oz) ), such as song sparrows ( Melospiza melodia ), dark-eyed juncos ( Junco hiemalis ) and house finches ( Haemorhous mexicanus ). During harsh late winter weather in Wisconsin, Cooper's hawks were recorded to eke out an existence living largely off of pine siskins ( Spinus pinus ). In modern terms, certainly the most commonly taken small bird would be the non-native, 29 g (1.0 oz) house sparrow ( Passer domesticus ). Although not known to be taken profusely in all studied urban locales, house sparrows were the leading prey in a study from Michigan , were nearly a third of observed delivered prey at nests in Victoria, British Columbia (although were outnumbered by robins in prey remains) and reportedly were the leading prey in Milwaukee and in Grand Forks, North Dakota . Flycatchers are not hugely significant in Cooper's hawk's foods, but the local effect of the hawks on populations can be considerable. For example, willow flycatchers ( Empidonax traillii ) in California suffered a 76% rate of nest predation, among which Cooper's hawks were a considerable contributor, and dusky flycatchers ( Empidonax oberholseri ) experienced a rate of 96% predation elsewhere in California, with 25% attributable to Cooper's. Similar determent to the local nesting attempts of other small passerines such as warblers has also been reported. Chickadees seem to regard Cooper's hawks as a moderate threat based on their anti-predator response, with smaller raptors (which are presumably more dangerous) such as sharp-shinned hawks and small owls evoking a rather more aggressive response by chickadees. While usually the smallest avian prey selected by Cooper's hawks are various warblers (presumably taken mainly by male hawks), down to the size of the 7 g (0.25 oz) Wilson's warbler ( Cardellina pusilla ), even smaller passerines are known to be hunted. The smallest known avian prey species have included the 6.8 g (0.24 oz) verdin ( Auriparus flaviceps ), the 6.3 g (0.22 oz) ruby-crowned kinglet ( Regulus calendula ) and the 5.3 g (0.19 oz) bushtit ( Psaltriparus minimus ). Even smaller birds, the hummingbirds , are essentially immune to Cooper's hawks (due to their own extreme agility) and were seen to incidentally benefit from nesting close to the hawks in California, due to a low risk of predators approaching while the hawks are present. Outside of passerines, almost certainly the most important avian prey type is the pigeon and dove family. Especially for those living in urban areas, Cooper's hawks have seemed to take to living heavily off of doves , particularly the abundant and widely found mourning dove ( Zenaida macroura ), at 119 g (4.2 oz) . Mourning doves appear to be hunted regularly in almost any part of the two species' mutual range. In Tucson , recent data shows that Cooper's hawks are living almost exclusively on doves. Among 151 prey items there, mourning doves were 20.5% by number and 27.5% of the biomass, Inca doves ( Columbina inca ) were 18.5% by number and 12.2% of the biomass and white-winged dove ( Zenaida asiatica ) 17.2% by number and 27.1% of the biomass. In Terre Haute, Indiana , mourning doves and rock doves were 14% and 21% of the diet, respectively. In northern California, mourning doves were the main prey species, making up 25.6% of 1057 prey items. There is even evidence that bluebirds have perceived the change in preference of Cooper's hawks to more profitable prey such as doves in developed areas and show less inhibition to the hawk's presence. In the more rural north Florida , again the mourning dove leads the prey selection, accounting for 16.5% of 1100 prey items. Another popular prey family is the woodpeckers . A rather numerous and widely distributed species, the 132 g (4.7 oz) northern flicker ( Colaptes auratus ), is a particular dietary staple of Cooper's hawks, being about the third most widely reported prey species. The flicker was the main prey in northern New Mexico , at 22.5% of 316 prey items, and in southern Wisconsin, at 22% of 77 prey items. Flickers are common prey elsewhere as well, such as in Ithaca, New York . Medium-sized woodpeckers, such as red-headed woodpeckers ( Melanerpes erythrocephalus ) and red-bellied woodpeckers ( Melanerpes carolinus ) were important secondary prey in different parts of the range. In South Carolina , it was found that 15% of the red-headed woodpeckers in a study population were killed by hawks. All told, about 20 species (almost all in North America but for a couple poorly-studied species) of woodpecker are known to be taken, ranging from the smallest, the 25.6 g (0.90 oz) downy woodpecker ( Picoides pubescens ), to the largest, the 287 g (10.1 oz) pileated woodpecker ( Dryocopus pileatus ). The response of woodpeckers to a sighted Cooper's hawks varies, with evidence showing that downy woodpecker and flickers would behave more boldly and themselves may scold the hawk if part of a mixed flock but, if alone, the woodpecker will typically try to flee. Despite the regularity of predation of woodpeckers that are in the open, a study in British Columbia shows indicated Cooper's hawks seldom prey upon woodpecker nests, perhaps due to being unable to access their secluded, smallish nest holes, with the study showing that the most regular predators of such nests were various mammals (from deermice to bears ). Certainly the most controversial aspect of Cooper's hawks are their predations upon galliforms . By far the most regularly selected types are New World quails . Coveys of quails that attempt to evade predators by running into thick vegetation (which can allow them to successfully escape many predators) often find that Cooper's hawks are undeterred by this, as the hawks may chase them either on the wing or on foot into thickets. However, one grouse was seen to successfully evade a hunting Cooper's hawk by diving belly first into about a foot of snow. Cooper's hawks are often regarded as perhaps the most regular natural predator of northern bobwhites ( Colinus virginianus ). Indeed, the rate of predation by Cooper's does appear to exceed that committed by other species of hawk as well as that by large owls. For instance, during winter in Wisconsin, Cooper's hawks were thought to kill 3.4–12.5% of the local bobwhite population. However, the bobwhite appears to be a secondary prey species in all known studies and there is no evidence that Cooper's hawk predation alone can deplete bobwhite populations, unlike causes directly contributable to man such as overhunting and habitat destruction . In Washington state, female Cooper's hawks took many California quails ( Callipepla californica ), which were estimated to constitute 47% of the prey selected by female hawks, but there was far too little impact overall to affect the quail's overall population. In the rural areas outside of Tucson , Gambel's quail ( Callipepla gambelii ) were found to be the most regularly selected prey species, at 15.2% of 79 prey items. A study of pellets in northwestern Mexico to determine if the local Cooper's hawks were regularly taking Montezuma quail ( Cyrtonyx montezumae ), finding that only one pellet consisted entirely of quail, the other pellets showing that hawks were mainly taking other prey, mostly doves. Most regularly found galliforms in North America (including well-established exotics such as chukars ( Alectoris chukar ) and common pheasants ( Phasianus colchicus )) are known to fall prey occasionally to Cooper's hawks. These include assorted native grouse , including even the grassland -dwelling species (but excluding the more northerly distributed ptarmigans ). Juveniles usually are the more vulnerable and more regularly taken of non-quail galliforms by Cooper's hawks, but the hawks can take adults quite regularly despite the prey's relatively large size. Adult ruffed grouse ( Bonasa umbellus ), weighing an estimated mean of 619 g (1.365 lb) when taken, are not infrequently exploited as prey, while adult sooty grouse ( Dendragapus fuliginosus ), estimated to weigh 1,050 g (2.31 lb) when taken have also been known to be taken repeatedly. Adult male sharp-tailed grouse ( Tympanuchus phasianellus ), which average 1,031 g (2.273 lb) , are also known have been successfully preyed upon by Cooper's hawks. Even more impressive accounts show adult common pheasant estimated to weigh up to 1,158 g (2.553 lb) can be preyed upon by Cooper's hawks. One wild turkey ( Meleagris gallopavo ) taken in Florida was cited with a weight of 5,336 g (11.764 lb) , which is the size of an adult. However, given that this is of enormous size relative to a Cooper's hawk, it would require verification that the turkey was this large and was taken alive by the hawk. Not unexpectedly, turkey poults are known to fall prey to Cooper's hawks. Beyond aforementioned families and orders, other types of birds are taken relatively infrequently. Usually moderate to low numbers of water birds are taken of any variety. About 5 species each of duck and heron , a dozen species of shorebird and a smaller assortment of grebes and rails are known in the prey spectrum. Even among water birds, nonetheless, a wide diversity may be taken, from the tiny 22.9 g (0.81 oz) least sandpiper ( Calidris minutilla ) to an adult mallard ( Anas platyrhynchos ) estimated to weigh 1,150 g (2.54 lb) when taken. Adult ducks and herons of roughly equal weight to Cooper's hawks and other largish adult water birds including ring-billed gulls ( Larus delewarensis ) and American coots ( Fulica americana ) are sometimes tackled by these hawks. Particularly frequency was recorded of 312.7 g (11.03 oz) cattle egrets ( Bubulcus ibis ) in north Florida, where the egrets were the fourth most regularly recorded prey species. Assorted families of land birds are fairly rare as reported in food studies, including some nightjars , trogons , swifts , kingfishers , parrots and assorted other raptorial birds. A lower diversity of species and lower overall numbers of mammals are taken relative to bird prey but mammalian prey can be locally important. Chipmunks are often regularly hunted in various regions, though only about one-third of North American chipmunks are known in the prey spectrum. High balances of the relatively large 96 g (3.4 oz) eastern chipmunk ( Tamias striatus ) were found in studies from New York, Michigan and Wisconsin. The eastern chipmunk appeared to dominate the foods of Cooper's hawks in the Green Ridge State Forest in Maryland , at 49.1% of 57 prey items and mammals altogether made up an exceptional 66.9% of the foods. In the western United States, fewer chipmunks are identifiable but such prey is fairly commonly detected. High balances of chipmunks were found in food studies from Oregon, especially in eastern Oregon where chipmunks (unidentified to species) were the leading prey type, at 22.5% of 120 prey items. The most common chipmunk prey in Oregon is probably the 89.3 g (3.15 oz) Townsend's chipmunk ( Neotamias townsendii ) but Cooper's hawks may take chipmunks down to the size of the 48 g (1.7 oz) least chipmunk ( Neotamias minimus ). Mammals distantly related to chipmunks, such as ground squirrels (including antelope squirrels ) can be taken in locally high volume. Golden-mantled ground squirrels ( Callospermophilus lateralis ) were the second most important prey in eastern Oregon at 16.6%. Thirteen-lined ground squirrels ( Ictidomys tridecemlineatus ) were the second most common prey species in a study from Wisconsin and also important in the diet in North Dakota (where they were the most significant contributor of biomass, constituting 23.4%). Golden-mantled and thirteen-lined ground squirrels are fairly small for ground squirrels, the earlier averaging 166 g (5.9 oz) , the latter of similar size. A few larger ground squirrels may be hunted, such as California ground squirrels ( Otospermophilus beecheyi ) and rock squirrels ( Otospermophilus variegatus ), both averaging over 600 g (1.3 lb) in adults, albeit infrequently. Tree squirrels are widely taken but secondary prey for Cooper's hawks. The smallish, roughly 200 g (7.1 oz) American red squirrel ( Tamiasciurus hudsonicus ) are not infrequent prey in northerly locations. About 36 red squirrels were recorded in the foods of Cooper's hawk in Ithaca, New York and these squirrels appear to have specific alarm calls that are provoked by these hawks, however the rate of predation by Cooper's appears to be low relative to other predators overall. Reported when taking red squirrels, male Cooper's hawks, being relatively small, may tear the prey into pieces that can be transported by them to the nest. Numerous other tree squirrels are taken occasionally by Cooper's hawks. Sizes of tree squirrels taken by Cooper's hawks were studied in Missouri. Eastern gray squirrels ( Sciurus carolinensis ) were taken of up to adult size but fox squirrels ( Sciurus niger ) were only taken as juveniles, as the adults, sometimes scaling up to 1,350 g (2.98 lb) , were apparently too formidable for Cooper's. The estimated weights of both the gray and fox squirrels taken in Missouri was 450 g (16 oz) , with the gray contributing 10.9% of the biomass. About 20 non-sciurid rodent species may be taken by Coopers hawks but are rarely significant in the foods. Both American species of flying squirrels , woodrats , commoner Peromyscus mice, some species of vole and lemming , cotton rats , jumping mice , kangaroo rats and non-native rodents may all be prey occasionally, although most species of these are fairly nocturnal and thus of limited access. Few of these types of rodents are taken frequently enough to warrant much individual mention. Unidentified woodrats, at a mean estimated mass of 256.6 g (9.05 oz) were significant to the biomass of Cooper's hawks in northwestern Oregon. In North Dakota, Peromyscus mice made up an unusually high 13.5% of the foods. In the city of Burnaby , when bird feeders began to attract black rats ( Rattus rattus ), Cooper's hawk's came to locally take significant numbers of both young and adult rats. The first verified predation by a Cooper's hawk on a brown rat ( Rattus norvegicus ) was recently reported, also in British Columbia. One broad study found a somewhat unexpected correlation was found positively relating the previous summer's rodent density to the number of Cooper's hawks. This could be coincidental as rodent populations are probably driven by acorn production in the year prior to the rodent increases, and many of the birds taken regularly by Cooper's are also partially acorn dependent. Occasionally, Cooper's hawks may capture profitable mammalian prey such as rabbits and hares . Mainly, predation has been reported on the cottontail rabbits . Strong numbers of mountain cottontail ( Sylvilagus nuttallii ), averaging about 716 g (1.579 lb) when taken, were reported in northwestern Oregon (7.82% and fifth most regular prey species). In the rural vicinity of Tucson, cottontail rabbits were the second most regularly selected type of prey, at 12.7%. Fairly strong numbers of cottontails were also reported in New Mexico and Durango . In Missouri, the widely found eastern cottontail ( Sylvilagus floridanus ) was the most significant contributor of biomass, making up 14.5% of the total biomass. On average, in Missouri, the body mass of eastern cottontails caught was 600 g (1.3 lb) , indicating juvenile eastern cottontails are usually caught. However, there are several known cases of adult eastern cottontails falling prey to Cooper's hawks, including cottontails estimated to weigh from 1,100 to 1,290 g (2.43 to 2.84 lb) . Various species of non-cottontail leporids may occasionally be caught, including young black-tailed jackrabbits ( Lepus californicus ), pygmy rabbits ( Brachylagus idahoensis ) as well as fairly large numbers of feral European rabbits ( Oryctolagus cuniculus ) in Victoria, British Columbia . Mammals of other orders are taken quite infrequently, with a low volume of shrews and moles reported. Cooper's hawks are considered a potential predator of the smaller species of weasel and were recorded in Florida to kill a striped skunk ( Mephitis mephitis ) kit estimated to weigh about 661 g (1.457 lb) . Occasionally, Cooper's hawks are known to hunt bats. They are said to usually capture bats on the wing rather than search them out. Findings were that in Carlsbad Caverns that Cooper's (and also sharp-shinned) hawks were the most efficient avian predators of bats near the cave entrance (rating as more successful than most Buteo hawks and particularly more so than larger and less agile raptors like red-tailed hawks and large owls ). Per observation in Carlsbad, due to their agility, Cooper's can match the evasive flight of a bat and may be successful in about 90% of observed pursuits. Apart from their well-documented predation of Mexican free-tailed bats ( Tadarida brasiliensis ), quite little is known about which bat species Cooper's hawk's may prey upon and at what level do the local hawks depend on such prey. Apart from caves, sometimes Cooper's hawks have been seen to capture bats in urbanized areas. In some areas, respectable numbers of reptiles may be hunted. All told, nearly 30 species of reptile may be hunted by Cooper's hawks. In the eastern part of the range, even in biodiverse locations for reptilian species such as Florida, a very low volume of such prey are reportedly taken by Cooper's hawks. In Arkansas , a small sample of road-killed Cooper's hawks showed that small reptiles were more common than birds amongst the stomach contents, with Bougainville's skinks ( Lerista bougainvillii ) and ring-necked snakes ( Diadophis punctatus ) constituting about 40% of the diet. Strong detection of reptilian prey is known in more western locations, especially farther south. In fact, of avian predators in one Californian study's estimation, Cooper's hawks showed the most reliance on lizards locally, but that Cooper's was not locally common in the study area so had relatively limited impact. In California, it was found that 69% of the diet was reptiles, most of which were assorted lizards (led by whiptail lizards , nearly 2.8 kg (6.2 lb) of which were estimated to be found in one nest). In rural areas outside of Tucson, a fairly strong presence of (unidentified to species) spiny lizards , at 13% of 77 prey items, although overall in all areas of the Tucson metropolitan, reptiles constituted a lower 8% of the total 228 prey items. In Durango , reptiles were a pronounced part of Cooper's hawk diet. Here, the most frequently identified prey species was the Mexican Plateau horned lizard ( Phrynosoma orbiculare ) (11.5% of 191 prey items), followed by the northern flicker and thirdly the crevice spiny lizard ( Sceloporus poinsettia ) (10.47%, plus other unidentified spiny lizards making up a further 4.2% of the diet). In Arizona, spiny lizards were similarly detected to have a strong prey-predator relationship with Cooper's hawks as well. Most lizards encountered and hunted by Cooper's hawks are fairly small but, despite being more scarcely selected, snake prey may show greater size variation. Snakes known to be taken have ranged in size from the 6 g (0.21 oz) redbelly snake ( Storeria occipitomaculata ) to the a young black rat snake ( Pantherophis obsoletus ), estimated to weigh 200 g (7.1 oz) , and the gopher snake ( Pituophis catenifer ) (adults of the latter two snake species can average roughly 890 g (1.96 lb) for both species and may be too formidable for these hawks). Unlike with reptiles, there is little evidence that Cooper's hawk regularly hunts amphibians in any area, despite a few species being known in the prey spectrum. While some authors have posited that as much as 2.1% of Cooper's hawks' global prey consists of invertebrates , prevailing food studies tend to find scant to none evidence of such prey; however, a truly exceptional case of Cooper's hawks found dead in Arkansas showed that beetles and moths / butterflies each represented 12.5% of detected prey items. Of special interest is how Cooper's hawks live along the other two Accipiters native to North America. Little distinguishes outright the distribution, habitat, ecology and prey spectrum of sharp-shinned hawks from Cooper's hawks. Throughout the range of Cooper's hawk, sharp-shins may be found breeding, migrating and wintering in similar areas. So too is there much overlap between the ranges of Cooper's hawks and northern goshawks , such as throughout southern Canada, the western United States, the Upper Midwest (and sometimes in the Northeastern United States) and during times of passage. In general, sharp-shinned hawks tend to use younger and denser stands of trees than do Cooper's. Meanwhile, goshawks tend to favor old-growth forest area with taller and older trees and generally lower tree densities. However, all three species prefer fairly enclosed canopies over their nesting areas, i.e. canopy coverage are generally thought to need to be at least at 60–70%. A particular opportunity was taken to study the three Accipiters ecology when living near one another in Oregon. Unusually, nests were not consistently well spaced between the species, and 2 sharp-shin nests were approximately 300 m (980 ft) from active Cooper's nests, while 5 Cooper's nests were 300 to 450 m (980 to 1,480 ft) from active goshawk nests. However, the patch habitat and dietary behavior of each species was still fairly partitioned. Here, for sharp-shinned hawks, the tree stands averaged 22–50 years old and had a mean density of 1180 trees per hectare (ha), while Cooper's stands averaged 30–70 years old and had a mean of 907 trees per ha while the goshawk used in oldest and most open stands, with trees of an average age of 150 years, and a mean of 482 trees per ha. The data from the Jemez Mountains of New Mexico was largely corresponding with the goshawk occurring in areas with a median of 781 trees per ha, Cooper's in areas with a median of 1229 trees per ha and the sharp-shins in a median of 1482 tree per ha. In the New Mexico data, goshawks used the largest trees with the lowest median canopy coverage (77.4% vs 78.4% for Cooper' s and 83.1% for sharp-shins). In a study from northern Utah, Cooper's hawks were intermediate in most habitat characteristics, being at median elevation ( 1,782 m (5,846 ft) ), nest height ( 8 m (26 ft) against 6 m (20 ft) for sharp-shins and 12 m (39 ft) for goshawk) and in areas of intermediate branch density. However, Cooper's nests were the closest in Utah to areas disturbed by humans ( 147 m (482 ft) against 161 m (528 ft) for sharp-shinned and 250 m (820 ft) for goshawk), also closest to water ( 220 m (720 ft) against 444 m (1,457 ft) in sharp-shins and 394 m (1,293 ft) for goshawk). There is often some level of distinction in habitat between Cooper's and the sharp-shinned hawk. Compared to sharp-shinned hawks in Wisconsin and Oregon, Cooper's hawks use woods with fewer conifers, less dense stands of trees and stands with taller trees. Often, sharp-shinned hawk nests are lower in the trees and placed in much denser vegetation (often even the sharp-shins with their smaller frames themselves accidentally strike against branches while attempting to enter the nest), to hide the nest more sufficiently against predators. The habitat used by the two species in Missouri was less distinct (i.e. similar tree species used). However, the sharp-shinned hawk nests in Missouri were at much higher elevations, i.e. 343 m (1,125 ft) above sea level, than those of Cooper's (which were at a mean elevation of 151.3 m (496 ft) ; more surprisingly the stand density was higher here for Cooper's, at a mean of 935.7 trees per ha than those used by sharp-shins, at a mean of 599.3 trees per ha. There was some level of temporal differences between the two species in study in Indiana, where Cooper's hawks were generally active in the early morning but sharp-shinned hawks did not become active until later in the morning (hypothetically to avoid more severe interguild predation by large owls due to its smaller size). In northern New Jersey, compared to nesting goshawks, Cooper's hawks used flatter lands that were closer to roads, other openings and human habitations. However, canopy coverage averaged high in New Jersey data for Cooper's, at 89.1%. Cooper's hawk has a mean home range size that was comparable to the roughly half as large-bodied Eurasian sparrowhawk , at 1,190 ha (2,900 acres) for Cooper's and 835 ha (2,060 acres) for the sparrowhawk. However, data shows that in North America, the Accipiters home range size corresponded to the birds' body size, i.e. 2,600 ha (6,400 acres) mean for the goshawk and 458 ha (1,130 acres) mean for the sharp-shinned hawk. The aforementioned Oregon studies also studied at length the dietary differences between the three American Accipiters . Cooper's hawks prey sizes were intermediate in keeping with body size, at around 135 g (4.8 oz) versus a mean prey size of 306.6 g (10.81 oz) for the goshawk in eastern Oregon and 12.8 and 28.4 g (0.45 and 1.00 oz) for sharp-shins in northwestern and eastern Oregon, respectively. The amount of mammals in the diet in Oregon also increased with the body size of the species. The diets of the three species were also studied in the Chiricahua Mountains of Arizona. There was some diet overlap in preferred prey for Cooper's hawks with both other Accipiters . In the case of the goshawk and Cooper's, both hawks regularly took Steller's jays and band-tailed pigeons ( Patagioenas fasciata ). With the sharp-shinned hawk, Cooper's locally also shared a liking for American robins and black-headed grosbeaks ( Pheucticus melanocephalus ). However, unlike either other Accipiter in the Chiricahuas, Cooper's hawks regularly took chipmunks and lizards as well. Furthermore, the nests of Cooper's and goshawks were fairly evenly spaced, at about 1.6 km (0.99 mi) apart, indicating that they maintain exclusive territories (almost as if within the same species), while sharp-shinned hawk nests were closer to goshawk nests but in much denser habitats. When chickens were experimentally exposed to each of the three American Accipiters , they reacted the most aggressively to the sharp-shinned hawk (as they pose little to no threat to adult poultry), intermediately to Cooper's and with strong attempts to evade and escape when exposed to the goshawk, which is very capable and ready to dispatch adult poultry. Many studies have contrasted the diet of Cooper's and sharp-shinned hawk in other areas as well, with the sharp-shinned hawk much more regularly selecting birds weighing under about 28 g (0.99 oz) , a fair amount overlap in birds of 28 to 40 g (0.99 to 1.41 oz) and 40 to 75 g (1.4 to 2.6 oz) weight classes but birds over this weight range are increasingly more often taken almost exclusively by Cooper's. Also, the sharp-shinned hawk appears to hunt more so birds that dwell at the canopy level in the woodlands (as opposed to ground to shrub height-dwelling birds) within the forest and prefers to attack in heavier cover than Cooper's seemingly. The ecology of Cooper's hawks has also been studied in contrast to other diurnal raptors as well. In the raptor guild within southern Michigan, the overall food breadth and size was studied against red-tailed hawks , red-shouldered hawks and American kestrels . Here, although the food niche breadth (mean number of prey species per study site) of Cooper's was relatively low at 1.79, Cooper's hawk had the largest mean prey sizes at 67.4 g (2.38 oz) , which was considerably higher than even the much larger red-tailed hawk (mean prey mass of 43.4 g (1.53 oz) ). In southern Wisconsin, the food niche breadth was rather higher for Cooper's at 6.9 and the mean prey mass, at 109.9 g (3.88 oz) , was second only to the red-tailed hawk's. In the Wisconsin data, the red-shouldered, the broad-winged and rough-legged hawks ( Buteo lagopus ) as well as the northern harrier , peregrine falcon ( Falco peregrinus ) and the American kestrel all had lower mean prey masses. Much farther south in Durango, Mexico, while there was overlap in the class of prey selected by Cooper's hawks with the other studied raptor species, American kestrels, red-tailed and zone-tailed hawks ( Buteo albonotatus ), there was minimal overlap in which prey species were usually selected, especially given the difference in habitat usage. Furthermore, in Durango, while Cooper's and the Buteo hawks all took appreciable numbers of adult cotton rats , kestrels selected only young cotton rats. In a study in western Maryland, Cooper's hawks used more mature woodland with a more developed understory and more extensive ground cover than the other woodland nesting hawks, the broad-winged and red-shouldered hawks. While red-tailed hawks nested fairly high in the Maryland data in isolated pines somewhat out of the interior forest, Cooper's nests were at similar height in forest and slightly higher than those of red-shouldered hawks and much higher than those of broad-winged hawks. In what was probably a case of defense of their hunting ground, a female Cooper's hawk was recorded to attack and drive off (without physical contact) a larger peregrine falcon from a perch during winter in Ontario. Cooper's hawk is usually a top predator in the daytime but is not immune from attack by other predators. The most common predator of this species is almost certainly the great horned owl ( Bubo virginianus ). This rather large owl (averaging more than three times heavier than a Cooper's hawk) is known to regularly track down fledglings and adults as well as raid the nests of other birds of prey. Many records show great horned owls will visit the nests of birds of prey and pick off the young nightly until the prey resource is exhausted (i.e. all young or sometimes adult birds of prey are killed). Furthermore, given the opportunity, great horned owls readily expropriate the nests built by the raptors they kill as their own. Given its preference for secluded wooded spots near woodland openings, Cooper's hawks are frequently the subject of unwanted attention from horned owls. Both the young, especially around the time they leave the nest or are recently fledged, and adult Cooper's hawks are vulnerable to these owls. While little data has been collected on the overall effect great horned owls have on Cooper's hawk populations, it is known that for the larger, more formidable goshawk that as many as 40% of radiotagged juveniles within a study appeared to meet their demise via horned owls. Due to their threat level, the calls of great horned owls provoke a strong response from Cooper's hawks and banders and researchers usually use stimuli of great horned owls to attract a mobbing Cooper's hawks. Reportedly, Cooper's hawks will temporarily tolerate and possibly even cooperate with crows when one or the other spots a great horned owl in the daytime, both species appearing to join forces to mob the threatening owl out of the vicinity. In one case, after a great horned owl pair failed to successfully breed in a nest built by other Cooper's hawks, a pair of Cooper's who tried to nest was supplanted by horned owls, possibly of the same pair who had previously failed. Other natural predators of Cooper's hawks that are known are mainly larger diurnal birds of prey. In some cases, their larger cousins, northern goshawks, will prey on Cooper's hawks. Widely but somewhat scarcely, red-tailed hawks have been known to prey on Cooper's hawk, while a single instance is known of a Cooper's falling prey to a golden eagle ( Aquila chrysaetos ). Less is known about the range of nest predators. Among all known predators, only the raccoon ( Procyon lotor ) can be considered to rival the great horned owl as the most severe threat to nesting attempts, probably consuming mostly nestlings and eggs but also perhaps some older hawks. American crows are known to rob nests of Cooper's hawks as well, especially when the parents have been displaced by the crow's severe mobbing. Smaller diurnal birds of prey are, in turn, threatened by Cooper's hawks. This is especially the case with the American kestrel. After some regional declines, a radiotagging study in Pennsylvania found that of 19 kestrels, 26% were killed by avian predators, with the suspected culprit in a majority of the cases being Cooper's hawks. Some resources have gone as far as to blame the kestrels decline directly on Cooper's hawk predation but subsequent data from the U.S. Breeding Bird Survey and the National Audubon Society Christmas Bird Count appear to discount this theory, instead linking the overall declines to inadvertent human causes. Cooper's hawk are also counted as a predator of merlins ( Falco columbarius ). The only confirmed accipitrid that Cooper's hawk have been known to prey upon is their smaller cousins, the sharp-shinned hawks. However, in the southeast , Cooper's hawks was counted among the potential, but not yet confirmed, predators of swallow-tailed kites ( Elanoides forficatus ) and nesting kites appear to engage in anti-predator behavior towards Cooper's hawks. Furthermore, Cooper's hawks that came into the vicinity were considered potential predators and mobbed as such by nesting gray hawks . Even more so than diurnal raptors, a wide diversity of owls are known to fall prey to Cooper's hawks. Despite the temporal differences of their activity, the intensive hunting methods of Cooper's hawks may allow them to access roosting owls more readily than other types of hawks. Small owls that Cooper's hawk have been known to prey upon have included flammulated owls ( Psiloscops flammeolus ), eastern screech-owls ( Megascops asio ), western screech-owls ( Megascops kennicottii ), whiskered screech-owl ( Megascops trichopsis ), elf owl ( Micrathene whitneyi ), northern pygmy owl ( Glaucidium gnoma ), ferruginous pygmy owl ( Glaucidium brasilianum ), burrowing owl ( Athene cunicularia ), boreal owl ( Aegolius funereus ) and northern saw-whet owl ( Aegolius acadicus ). Medium to large-sized owls are sometimes also prey for Cooper's hawks have been known to include long-eared owl ( Asio otus ) and perhaps the rather large spotted owl ( Strix occidentalis ). Most impressively, an instance was observed where a Cooper's hawk appeared to have preyed upon an adult of the rather larger (averaging about 787 g (1.735 lb) ) barred owl ( Strix varia ). There is also a record of a barred owl preying on a Cooper's hawk as well. Cooper's hawk is a solitary bird apart from breeding and rare aggregations during migration. This species usually is considered monogamous. However, pairings of two males (1 young, 1 adult) with a single female have been recorded at least three times. In Grand Forks, North Dakota , a single male has been recorded to successfully mate with two nearby females, with similar records from New Mexico. However, the breeding efforts in Grand Forks were found to be disproportionately producing males, seven to one. A Wisconsin study determined 19.3% of nestlings in a Milwaukee study area were from extra-pair couplings and that 34% of all broods included at least 1 extra-pair young. Despite their generally monogamous breeding system, Cooper's hawks are often rather inconsistent regarding breeding for life (as many other birds of prey do). While males are more or less devoted to same breeding sites throughout lifetime, 23% of adult females in Wisconsin moved to differ nesting grounds from 0.8 to 14.6 km (0.50 to 9.07 mi) away, averaging 2.6 km (1.6 mi) , in subsequent years. Meanwhile, in Arizona, 3% of males and 10% of females displayed yearly breeding dispersal. However, in the urbanized areas of Tucson, evidence indicates that mate fidelity is higher than elsewhere. In Tucson, it was found that the mean distance of the mated pairs was only 473.4 m (1,553 ft) during the non-breeding season and 36 interactions were recorded almost all in the core range, indicating an unusually close perennial typical pair bond here. The rate of dispersal to a different breeding ground was a much higher at 68% in north Florida. Data in Wisconsin shows that pairs line up in correspondence with their size, i.e. larger female Cooper's hawks mate with large males and smaller females with smaller males. The data indicated that larger pairs tend to have earlier laying dates, larger broods and more recruits than smaller ones. Relatively large body mass may be a heritable trait. However, no correlation was found between the age of the pair and apparent breeding site quality and time of breeding or annual productivity (though older females may lay slightly earlier than yearlings in most cases). In Arizona, birds of each sex were found to usually pair with like-age individuals. Pairs frequently high circle together. Either sex or the pair together perform in courtship , sometimes over an open field. Courting usually occurs on bright, sunny days, in midmorning. During sky-dances by males, the wings are raised high over back in a wide arch with slow, rhythmic flapping, similar to the flight of a nighthawk , with exaggerated down strokes. Often, much like the northern goshawk, the displaying male flares his undertail coverts. Sometimes frequently for a month or so, the pair will perform as such. When perching together, the male usually keeps on a perch at least 1 m (3.3 ft) away from his unpredictable larger mate. The bowing display reported in Wisconsin, usually (but not always) done by the male, may be a sign to the other mate of their readiness to nest build. Breeding may begin as early as February in the southern part of range, but, for the most part, the breeding season is from April to July. In central New York, the male arrives in nesting woods by March, initially defending an area of 100 m (330 ft) or so. Both members of pair arrive by early March in Wisconsin and, in both Pennsylvania and Wisconsin, nest building and copulation is often complete within the month of March. Generally both members of a pair remain on the breeding ground vicinity year-around in Arizona, New Mexico and even in British Columbia. In Michigan, the density average was 1 pair per 1,554 ha (3,840 acres) . In North Dakota, 10–12 pairs were found on 23,310 ha (57,600 acres) . 1 nest per 734 ha (1,810 acres) in central Wisconsin, 1 nest per 2,321 ha (5,740 acres) in northwestern Oregon and 1 nest per 2,200 ha (5,400 acres) in eastern Oregon. Minimal distance between active nests is seldom less than 0.7 to 1 km (0.43 to 0.62 mi) . Distance between active nest on average was 1.6 km (0.99 mi) in both California and Arizona, 2.4 km (1.5 mi) in New York, 1 km (0.62 mi) in Kansas, 5 km (3.1 mi) in western Oregon and 3.5 km (2.2 mi) in eastern Oregon and 1.6 km (0.99 mi) in central Wisconsin. Mean distance between active nests in Illinois was 5.3 km (3.3 mi) . Rather small areas may be defended where hunting occurs near the nest. Typical home range sizes for Cooper's hawks are between 400 and 1,800 ha (990 and 4,450 acres) . Home range for a Wisconsin male hawk is around 193 to 571 ha (480 to 1,410 acres) during breeding and about 732 ha (1,810 acres) during non-breeding. Exceptionally close active and successful nests were recorded only 160 m (520 ft) apart in Albuquerque and 270 m (890 ft) in Victoria, British Columbia. Male home ranges in Tucson (sample size 9) averaged 65.5 ha (162 acres) , being smaller than in Wisconsin due to better prey concentrations (doves), however juvenile males in rural Tucson areas covered a home range of 771 ha (1,910 acres) . Breeding hawks in Oshkosh, Wisconsin had an average home range of 238 ha (590 acres) . In southwest Tennessee, a male Cooper's hawk had a home range size of 331 ha (820 acres) and 4 females had an average range of 869 ha (2,150 acres) . Slightly smaller home ranges were found for urban males in a California study, at a mean of 481 ha (1,190 acres) , than in non-developed areas here, which showed a mean of 609 ha (1,500 acres) . Huge male home ranges were found for breeding ones in New Mexico, at 1,206 ha (2,980 acres) , and in north Florida, at 1,460 ha (3,600 acres) , probably due to dispersed prey resources. Home ranges of females tend to constrict with age. An exceptionally pronounced case of this was in north Florida, where first year female home ranges went from up to about 932 km 2 (360 sq mi) down to as little as 4 km 2 (1.5 sq mi) . In central New York, the nest sites of various other woodland birds were surprisingly close to those of Cooper's hawks, though some of the nest were occupied by other birds of prey that are not regularly threatened by these hawks (though flickers, one of the birds most at threat by the hawks, were fairly dispersed away from the hawk's nests). As in most accipitrids, copulation is brief (averaging about 4.5 seconds) and frequent (at around 0.9 per hour), with total copulations averaging per season about 372. This species builds a bulky platform nest, usually 61 to 76 cm (24 to 30 in) across and 15 to 45 cm (5.9 to 17.7 in) deep. Often the nest is shallower in conifers (i.e. 15 to 20 cm (5.9 to 7.9 in) deep in New York) and deeper in broad-leafed trees (averaging 43 cm (17 in) in New York). Nests average larger in the eastern part of the range than in the west, perhaps in keeping with the eastern hawks' larger average body sizes. While sticks are almost always used, one unusual Florida nest was observed to be made largely of Spanish moss ( Tillandsia usneoides ). Often nests are lined by Cooper's pair with bark or odd bits of greenery. The male grabs at bark like prey, while the female, if participating, may tear off bark with her bill; the piles of bark may be up to 3 inches deep by the time eggs are laid, though green spray is added considerably less often than other species of hawks such as Buteo . One male, unusually, was seen to be engaging in nest building while helping parent an active brood in mid-summer. Nest are often located at 8 to 15.1 m (26 to 50 ft) above the ground in the main fork or horizontal branch close to the trunk, though are sometimes up to 20 m (66 ft) above the ground, and in trees usually of 21 to 52 cm (8.3 to 20.5 in) in diameter. Usually nest sites are within plots of woodland of at least 4 to 8 ha (9.9 to 19.8 acres) in size, with a canopy coverage usually over 64%, but can be much smaller in some urban vicinities. One unusual nest in North Dakota was in dense shrub rather than a tree and it even successfully produced fledglings. Another unconventional nesting area in North Dakota in the Little Missouri National Grassland and was recorded to have unusually open canopy, at a mean of 55%, and to be in a rather steep sloped area. An unusual nest site in Wisconsin was on a grapevine . Water access is of secondary import. Pine plantations are popular nesting sites across several parts of the range. In Tucson, 70.8% of 48 nests were found to be non-native Eucalyptus trees. Native white pine ( Pinus strobus ) was preferred in Massachusetts , at 58% of 48 nests, and in Pennsylvania, at 78% of 18 studied nests, and the most used tree in a study from Wisconsin as well, at 35% of 82 nests. Shortleaf pine ( Pinus echinata ), another native was preferred in Missouri (at 51% of 43 nests) and in Illinois (at 81% of 16 nests). Deciduous trees may be preferred elsewhere in the east, such as American beech ( Fagus grandifolia ) in New York (39% of 36 nests), oaks in Maryland (66%) and laurel oak ( Quercus laurifolia ) in north Florida (81% of 77 nests). Douglas firs ( Pseudotsuga menziesii ) were preferred in northwest Oregon (94% of 18 nests) and also in northeast Oregon as well as in British Columbia (34% of 64 nests), often where mistletoe parasitizes the tree (64% of 31 in the overall state of Oregon were on mistletoe). Ponderosa pine ( Pinus ponderosa ) were preferred in eastern Oregon (53% of 15 nests) as well as in New Mexico. In the enormous redwood forests of California, all Cooper's hawk nests were in more modestly sized native tan-oaks ( Notholithocarpus densiflorus ). It has historically taken to almost be a rule that Cooper's hawk uses a new nest site each year. Exceptionally, though, pairs have used the same nests for up to 4 years, though mostly records show up to 2 to 3 years of use when a nest is reused. As much as 59% of 17 nests (New Mexico) or 66.7% of 12 nests (southern Illinois) may be reused in the following year but this is not usual. In north Florida, 21% of nests were reused in a subsequent year, while in New York, it was around 10%. New nests are often near prior nests, at a mean distance between them of around 170 m (560 ft) in Wisconsin. In Alberta, a female was reported to use a grove of trees over two consecutive years as a nest site, be absent for one year and then returned to nest in the same grove the subsequent year. Nest building usually takes about two weeks. However, if a clutch is lost, a pair may repair and use another nest within four days. A majority of 385 nests (40–60% annually) in Wisconsin built on pre-existing structures. At times, the material is put on the residue of a crow's nest, squirrel's drey or even a woodrat tree nest. In Tucson, nest building was recorded during winter, exceptionally. When grass is found to be incorporated in nest structure, it is an indication that Cooper's is using a nest built by crows as they have never themselves been known to use grass. Oregon nests frequently incorporate mistletoe into the nest, more so those built by pairs with mature females rather than juvenile females. Their nest structure requires about 4.8 support branches. Data is conflicting on whether it is the male or the female who selects the nest site. Males were found to do 70% of the nest building in Wisconsin but the female does not consistently take a secondary role. Mostly, the male gathers nesting materials within 100 to 200 m (330 to 660 ft) of the nest. The male snaps off twigs with his feet to build with, though smaller twigs may be carried in the bill. After an early duet, at as early as 5:30, the male may start nest building at around 6:30. Later in the day, he will hunt, though females also hunt at this stage, much of her food is brought by him. South-facing nests are thought to be avoided, possibly due to solar irradiance reducing soil moisture, tree density and shading or possibly due to the more deciduous local nature of north-facing nest sites. When using a prior years nest, the female reportedly selects and repairs it. Egg laying in New York is between after April 24 to June 26 (about 50% from May 10 to 20) with similar dates in New England and also from Ohio to Minnesota. Similar laying dates were also found for Ontario as well as in British Columbia, but more laying date variation was found for the latter province. Data shows that mean egg laying times in Wisconsin may be shifting earlier by up to 4–5 days in different years, but the current mean is 1.3 days. Similar shifts may be occurring in New York state as well. From New Jersey to Virginia, egg laying may be from April 7 to May 23 (about 52% from April 29 to May 11), with similar dates on the opposite coast, from Washington state to California. From Florida to Baja California, egg-laying can began as early February, but, despite the lower latitude, known records show most are between mid-April and early May and can even run into June. Similar egg-laying dates, peaking around late April, are known in Arizona. The mean clutch initiation, in 57 clutches from North Dakota was mid-May and, though pairs arrive more than a month before that, the mean dates are consistently 2–3 weeks later in nests at other similar latitude in British Columbia and Wisconsin. It was determined in Maryland that egg-laying and other mean dates rival or are even later than the longer distance migrating broad-winged hawk, and are much later in general than other Buteo hawks here. Dates of egg laying and other behaviors were also found to average slightly later than the even further migrating Buteo , the Swainson's hawk ( Buteo swainsonii ). The clutch size averages anywhere from about three to five. Female egg laying is individually consistent from year-to-year, with a variance of a day or two. Often about 3–5 eggs are laid every other day, though can be up to 2 days between the 4th and 5th eggs. Clutch sizes fell historically from a mean of 3.5 (1929–1945) to 3.1 (1946–1948) and 2.7 (1949–1967) during the use of DDT then back up to 3.3 in 1967–1976 after DDT was banned. 7 of 266 clutches in early museum records were 6 egg clutches while one 7 egg clutch was recorded in Arizona. Records of 2 egg clutches may usually be laid by yearling females. The mean clutch size in 72 clutches was 3.5 and 3.33 in 46 clutches in central Arizona. Clutch sizes were similar in Ontario, at around a mean of 3.4, and in North Dakota, at 3.5. In southern Illinois, the mean clutch size is 4.1. The average clutch size in Wisconsin Cooper's hawks was 4.3, with a little varying range of 3.9 to 4.8 over 6 years. The clutch size in Wisconsin is on average 1–3 eggs smaller in immature females. There was no strong differences in Wisconsin in clutch sizes between urban and rural locations. In British Columbia, the mean clutch size was a particularly high 4.43. A clutch of 5 may be laid in 10 days and hatch in a span of about 3 days. Some authors suspect that clutch size is functionally reliant on habitat quality. The eggs are pale sky blue, fading to dirty white, with a smooth texture. However, an occasional set is reported as lightly spotted. It is reported by some authorities that the spotted eggs are laid by a female that does so each year, however others opine that these are misidentified eggs that were laid by broad-winged hawks. The eggs may measure 43 to 54 mm (1.7 to 2.1 in) in height by 34 to 42 mm (1.3 to 1.7 in) by diameter (averaging 47 mm to 49.1 mm × 37.6 mm to 38.7 mm (1.85 in to 1.93 in × 1.48 in to 1.52 in) in 121 from Ohio and 137 from New York, respectively). California eggs averaged 47.5 mm × 37.6 mm (1.87 in × 1.48 in) in a count of 82. The average weight of eggs is 43 g (1.5 oz) (with a range of 36 to 52 g (1.3 to 1.8 oz) ). Incubation starts with the laying of the third egg. Evidence shows that pairs may be able to successfully delay breeding somewhat if it is unusually harsh and snowy early spring. The female mainly incubates (including throughout nighttime) though the male may substitute for 10–30 minutes after he brings his mate food, often doing so for about 2 to 3 times a day. The male usually roosts nearby during incubation, when he begins calling, she may join for 5–10 minutes before quickly flying back. By the third week, she may leave the nest only to take food or to defecate. Incubation lasts for 34–36 days, but sometimes may be down to 30 days. Eggs may be discarded by the mother after hatching but those that never hatch are left in place. The female sleeps on the nest until the young are 2 weeks old. The young were photographed to sleep at night directly under her body until there is not enough room to do so. The male is rarely present at nest longer than 3–4 seconds after hatching but at least once was recorded staying for 3 minutes when coming with prey after the female stops heavily brooding. Most prey deliveries are intercepted by the female slightly away from the nest. However, often the male does not perch far away, averaging about 765 m (2,510 ft) , away from the nest during nesting to fledging stages, and occasionally as close as 120 m (390 ft) . The nest may be crowded while the nestlings grow, and the female may expand platform with additional sticks. Usually the male Cooper's hawk removes the head and viscera of prey before bringing it, then taking it to plucking stumps, although often the plucking is done right where prey is killed. Rate of feeding depends on brood size but is dictated in part by the availability and size of prey. Only 2 to 3 food deliveries daily are usually necessary during incubation but the male has to hunt constantly once the young are large, rarely plucking and no longer decapitating prey. Peak deliveries are typically needed in about the 4th week. 6–9 deliveries a day are usually necessary for broods of 3 to 5. New Mexican nests with adult females had 95 prey deliveries in 120 hours of observations, whereas nest with younger females (i.e. second years), there were 65 prey deliveries were observed in 120 hours, or 694 fewer prey individuals per square kilometer than nests on territories of adult females. The parents are non-aggressive usually when the nest area is breached but the female may dive and call if a person climbs directly to their nest, sometimes also the male, often doing so silently. The reaction to human intrusion varies among individuals and probably with stage of nesting, hatch date, and probably prior experience. Generally, individuals rarely strike humans. Prolonged visits to the nest by humans, i.e. more than 30 minutes or around an hour, can cause temporary nest abandonment, and can be the cause of up to 1.2% of nest failures. During early incubation, the female often quietly flushes if a person comes up to nest tree or knocks on it but will sometimes call if someone climbs to the nest. After 2 weeks, she may begin to make "half-hearted" dives at the climber. After 3 or 4 weeks, some females still quietly flush but others grow increasingly aggressive with much variance in temperament. The aggressiveness increases around hatching, decreases for the first couple weeks after hatching, then quickly increases after 3 weeks. All dives at climbers are mock ones to early on but after the young are about 3 weeks old, either one of the pair may actually hit and draw blood from the climbers. Despite a reputation as a "somewhat aggressive" or even as being a hawk with a "very aggressive defense" towards humans in nest defense, the actual rate of attacks even at peak times seems to be very low and the reputation is thought to be fairly unearned. Various researchers consider this species less aggressive to intruders than either of the other North American Accipiter , and some even less so than red-shouldered hawks as well. Anti-predator behavior by parent Cooper's hawks against crows, red-tailed hawks and eastern gray squirrels were observed in Wisconsin to be surprisingly six times more often carried out by the male rather than the female. Female defensive attacks are sufficiently forceful enough to drive away more formidable predators such as bobcats ( Lynx rufus ) from the nest area. When large quadrupeds walk under the nest, the female may utter a semi-alarm call but does not leave the nest. Sex ratio can skew towards male in eggs, nestlings and fledglings in about 54–60% in nests of Cooper's hawks in the region of Milwaukee. However the sex ratio corrected over time in the urban area to an even amount, though it is still skewed outside the city (skewed broods towards males occur in cases where the females may become too costly to bring up, needing longer development stages and more foods). There are similar cases of male skewed ratios recorded now in southwestern cities (i.e. Tucson and Albuquerque). Due to the female usually only beginning incubation with the third egg, the first three eggs often hatch on the same day, while the fourth and fifth eggs often hatch one (rarely up to three) day later. New hatchling young average about 28 g (0.99 oz) in body mass and are about 9 cm (3.5 in) in total length. Hatchlings are covered in white natal down with blue-gray eyes and are tan to pink on many of the bareparts. While growth is slow for about three days, sexual dimorphism by size may begin by to be measurable by about seven days of age. At about 10 days, the nestlings begin to engage in rather feeble standing and wing flapping. The bill (at around 11 days) grows about twice as fast as the tarsus (at around 22 days). At 13 days, the nestlings stretch their legs and often yawn, and at 16 days can be aggressive if the nest is breached by people. Down first becomes deep and fluffy around two weeks, the following week first feathers among dense down, feather production accelerates but growth slows in the fourth week after which both increase for the fifth week. By 16–18 days, the nestlings preen well, starts to rip at prey and flap well. Within first two weeks, the young Cooper's hawks begin to defecate over nest edge but often soil the edge of nest. At three weeks often begin to stand up and feed by themselves and often begin to mantle prey away from each other. The young grow is rapid for the period when they are 17 days old to about 23 days, growth then slows down abruptly before they nearly pause growth to feather out and then thereafter become fully grown. At the age of three weeks a female nestling may stand and be able to fully feed herself. Sometimes smaller, more agile male nest mates may snatch several bits of meat from their larger sister as if taking food from the mother. Siblicide rarely has been proven for this species, and may occur "accidentally" at times. Sometimes a younger sibling that has died from other means may be eaten by the siblings or by the parents. In one case, an entire brood of 4 nestlings from 2.5 to 3.5 weeks old were found dead in the nest, apparently having died due to exposure after consistent heavy rains. Normal departure from nest is 30 days (up to 27 days) for males and 34 days for females, but averaged sooner in Oregon, at 27–30 days. Response to the parents after the young Cooper's becoming branchers depends on their hunger levels. Snyder and Wiley recorded feeding rates of 0.267 per hour for a brood of 2 and 0.564 per hour for a brood of 4. In New York and Wisconsin, the sex ratio of broods roughly even, but slightly male biased in Wisconsin (53.5% or 137 against 119). Food may be brought to the nest for the first ten days after the young leave it, as the young often return to rest on it or even to sun from it. Largely, the young are quiet until they leave the nest when they begin their loud, persistent hunger calls. Around this stage, the young hawks will frequently engage in play with sticks and pinecones. After they are about eight weeks old, they may start to hunt for themselves, but are usually still reliant on parents for food. The young Cooper's hawks are frequently loud, voracious and aggressive in procuring food from the parents. The parents soon seem to lose interest in feeding the young. Fledgling occurs at 27–34 days (males averaging earlier), but the young may often returns to nest and are not fully feathered until about 50–54 days. The siblings often stay within 4 m (13 ft) of each other even after leaving their parents range. Siblings before long-distance dispersal may hunt together, although may too steal prey from one another. Juveniles Cooper's hawks in mostly urban areas of Arizona wandered somewhat randomly it seems until they were about 2.5–3 months old, when they settled on a wintering ground, averaging 9.7 km (6.0 mi) for females and averaging 7.4 km (4.6 mi) in males away from their respective natal sites. From their initial natal site to the site where they ultimately breed, in Wisconsin the average young male Cooper's hawk settled 7.2 km (4.5 mi) away from their nest of origin and the average young female 27.6 km (17.1 mi) away. Attempts to average mean dispersal distances within another study found farther than expected dispersal distances for Cooper's hawks from across the range. These were estimated at 43 km (27 mi) . Greater dispersal distances by female juveniles are probably meant to limit the likelihood of inbreeding. In one instance, a grandson Cooper's mated with his grandmother over 3 years while there were two instances known of full siblings mating in Victoria, British Columbia. Cooper's hawks usually first breed at 2 years old but yearlings can often be reported to average at 6 to 22% of the breeding populations in short 3–6-year studies. Longer-term studies of 16–25 years of large urban populations within Milwaukee, Wisconsin, Tucson, Arizona and Victoria, British Columbia, show yearling females average 16–25% of the breeding population but that breeding by yearling male was uncommon to non-existent. Similarly, 79% more females bred in their first year in study in New Mexico than did males. Despite the considerable number of breeding young females, in Oregon, they averaged about 1 egg smaller and nearly a fledgling smaller than their older female counterparts; while results in Albuquerque were even more skewed towards breeding success for older females. Many studies found no yearling males to be breeding with various populations but 7% of 184 males in Tucson were yearlings over several years of study (78% of which were paired with immature females). Only one breeding male in both Victoria, British Columbia (579 sample size) and in Albuquerque (sample size 305) were yearling while 4.8% of 123 in Milwaukee were yearlings (92% of which were paired with an adult female). In New Mexico, males sometimes bred in their first year where there were rich prey concentrations, but had 37% higher mean annual mortality than those who did not breed until mature plumaged. New Mexican data showed that 14% of 20 males bred in their first year and 71% in their second year while 93% of the local female bred in their first year. In addition to Tucson, other cases of successful breeding by pairs of immatures reported in varied areas such as Indiana and New York. Considerable numbers of juvenile Cooper's hawks breeding may be historically associated with high turnover within populations. Evidence from the Milwaukee area shows a significant reduction in more recent decades of two-year old or younger breeding hawks, which was indicative of a recovering population. The average of 117 successful laid clutches was 4.18 eggs laid, 3.53 nestlings in successfully hatched clutches and 3.08 young in 26 successfully fledged broods in the Northeastern United States and southeastern Canada . Nesting success in western Pennsylvania in 32 successful nests was 3.2 fledglings; in 6 nests within Michigan, a mean of 3 in all nests got to fledge (4.3 eggs, 3 hatchlings on average); in Wisconsin, 3.5 fledglings were produced from successful nests (68.6% of 83 nests produced at least 1 fledgling); a mean of 2 fledged from 11 nests in Maryland and 2.23 fledglings per 41 successful nests in Arizona. In Illinois, in all breeding attempts (not just successful ones), the mean number of fledglings was 2.8. 81% of New York nests produced fledged young and 75% did so in Pennsylvania. Nesting success rates in western wildland areas may be lower such as in Utah, where 53.5% of nests fledged young, with many of the failures attributable to owl predation. Data from Oregon showed that 74% hatched and 61.4–69% successfully fledged, a much lower rate of nest success than goshawks, at 90.4%, and, surprisingly, than sharp-shinned hawks, at 91.7%. However, in the Oregon data, the number of eggs hatched was higher in Cooper's at 74% than in sharp-shinned hawks, at 69.4% (but not than the goshawk's). In Wisconsin in 2019, all of the eggs in a clutch of seven hatched and all of the young fledged. In North Dakota , better habitat such as upland forest showed much higher breeding success levels (at least 1 fledgling in 86% of 26 nests) than in poorer habitats such as narrow riparian strips, in which 1 fledgling was produced in 57% of 44 nests. Younger forest in North Dakota was surprisingly preferred, with the average estimated age of trees used by Cooper's at 59.9 against a random tree age in the area of 74.6. It was found that adult female who mated with males who provisioned food at a higher rate produced 1.6 more fledglings on average. Yearling females in northeastern Oregon tended to use younger successional stands than older females and tended to have lower productivity in clutch size and brood counts. Among 70 studied male hawks in Wisconsin, the number of fledged young produced in their lifetime was similar in males who did not breed until they were two years old (mean of 8.8 fledglings) compared to those who started breeding as yearlings (mean of 8.7 fledglings), with the most successful studied male having started breeding in his second year and had produced 32 fledglings by the time he was nine years of age. In Arizona and New Mexico, 23% of nests failed altogether and 56.5% of 23 nests in Wisconsin failed during incubation. A high genetic diversity, or allele level, was found in the nestlings of the urbanized population of Tucson, ensuring a hardy local population despite historic concerns about the parasite levels of nestlings in these populations. Cooper's hawks can be a long-living bird. Some authors credit lifespans of up to 8 years of age in the wild. The oldest recorded bird recorded among migrants that bred in Oregon was 10 years and 5 months old. The oldest recorded breeding bird was a 12-year-old female in British Columbia while the oldest recorded wild bird was 20 years, 5 months old, banded in migration. However, the mean age at death recorded in 136 banded Cooper's hawks was 16.3 months. It was estimated for the species that the mortality rate in the first year of life for these hawk is 71–78% while it about 34–37% in the subsequent years. An annual survival rate of 75% was recorded for juvenile males in Tucson while the survival rate for juvenile female here was 64%. The survival rate for Tucson adults was between 69 and 88%. 75% was considered the survival rate of wintering Cooper's hawks in Indiana and southern Illinois but mean mortality between adults and juveniles was estimated to possibly average up to 46.4%. The annual survival rate in Albuquerque was 27–38% for female immatures. No correlation was found to body size or habitat in female survivorship but those in Wisconsin who changed nest sites annually may have had slightly higher survival rates than those who reused a same nest site. The opposite trend was reported for north Florida, wherein females who reused a nest site seemed to have higher survival rates. Historic survival rates (1925–1940) as reported were much lower, with extensive persecution causing an annual mortality that was estimated at 44%. Regular natural causes of mortality in Cooper's hawk, mainly of their young, include hypothermia , windstorms and tree collapses . Clashes between members of the same sex can be lethal, especially those between two males. Although Cooper's hawks are not known to prey on venomous snakes , one was found dead from envenomation next to a burrow holding both a copperhead ( Agkistrodon contortrix ) and an eastern diamondback rattlesnake ( Crotalus adamanteus ). Hunting accidents can frequently cause injury, especially in the form of potentially hobbling bone fractures , or sometimes can kill Cooper's hawks, especially those living in urban areas. In Indiana and Illinois, mortality from collisions were somewhat more prevalent in Cooper's hawks than in sharp-shinned hawks but instances of predation on immature sharp-shins were three times more prevalent than predations on immature Cooper's. Despite the risks of urban living, evidence indicates that urban Cooper's seem to be relatively successful, have moderate to low annual survival and reproduce prolifically. Cooper's hawks are known to be vulnerable to West Nile virus with some regularity but sometimes are able to survive despite the viral antibodies being found. Some mortality from West Nile has been reported, unsurprisingly. Fatal infections of the herpes virus have been recorded at least twice in Cooper's hawks. Cooper's hawks, along with great horned owls , had the greatest seroprevalence of Avipoxvirus among several raptorial birds in Illinois. An extremely high amount of Trichomoniasis was found in nestlings in southeast Arizona. The bacteria was recorded in 95% of urban Cooper's hawk nestlings (though only 8% of non-urban ones) and caused about 50% of recorded nestling deaths, probably roughly doubling the nestling mortality rate compared to the non-urban areas. Adults are less vulnerable to Trichomoniasis infections but there was no variability to be found by sex, time of year or by location. In Wisconsin and British Columbia only 2.7% of 145 studied nestlings had Trichomoniasis . A high balance of the bacterial disease Mycoplasma gallisepticum , common to birds who frequent bird feeders , was found in Cooper's hawks (transmitted from their prey) studied in Illinois (the highest of any six raptor species studied) however effective antibodies were found and no external infection was noted. A high balance of bacterial flora were found the airways of 10 Cooper's hawks, including many with Salmonella (rarely fatal in hawks but can compromise their condition). 91% of 47 tested adults in Wisconsin had Leucocytozoon toddi and 62% had Haemoproteus but only 12% of 33 nestlings there had parasites. A similar blood parasite infection rate was found in northern New York (and California) as well. Compared to sharp-shinned hawks, while migrating off Lake Ontario , Cooper's hawks were found to have higher white blood cell counts ( heterophiles , monocytes , and eosinophils ) that may have made them more vulnerable to blood parasitism. Haematozoa infection rates were also higher in adults than they were in nestlings in Arizona. Blood parasites were recorded to be higher for later migrating Cooper's hawks in northern New York but were, on the contrary, higher in earlier migrating hawks in Marin County, California . Even rare parasites such as Sarcocystis may be found in wild Cooper's hawks, being apparently more prevalent in juvenile hawks and slightly more often afflicting females rather than males. Helminths were quite diverse in Cooper's hawks from Florida. In Minnesota and Wisconsin, several helminths were recorded and there was one instance of a tissue reaction from Serratospiculum as well as a case was reported of related Serratospiculoides in an injured Cooper's hawk in Yellowstone National Park . Cooper's hawk is a solitary bird apart from breeding and rare aggregations during migration. This species usually is considered monogamous. However, pairings of two males (1 young, 1 adult) with a single female have been recorded at least three times. In Grand Forks, North Dakota , a single male has been recorded to successfully mate with two nearby females, with similar records from New Mexico. However, the breeding efforts in Grand Forks were found to be disproportionately producing males, seven to one. A Wisconsin study determined 19.3% of nestlings in a Milwaukee study area were from extra-pair couplings and that 34% of all broods included at least 1 extra-pair young. Despite their generally monogamous breeding system, Cooper's hawks are often rather inconsistent regarding breeding for life (as many other birds of prey do). While males are more or less devoted to same breeding sites throughout lifetime, 23% of adult females in Wisconsin moved to differ nesting grounds from 0.8 to 14.6 km (0.50 to 9.07 mi) away, averaging 2.6 km (1.6 mi) , in subsequent years. Meanwhile, in Arizona, 3% of males and 10% of females displayed yearly breeding dispersal. However, in the urbanized areas of Tucson, evidence indicates that mate fidelity is higher than elsewhere. In Tucson, it was found that the mean distance of the mated pairs was only 473.4 m (1,553 ft) during the non-breeding season and 36 interactions were recorded almost all in the core range, indicating an unusually close perennial typical pair bond here. The rate of dispersal to a different breeding ground was a much higher at 68% in north Florida. Data in Wisconsin shows that pairs line up in correspondence with their size, i.e. larger female Cooper's hawks mate with large males and smaller females with smaller males. The data indicated that larger pairs tend to have earlier laying dates, larger broods and more recruits than smaller ones. Relatively large body mass may be a heritable trait. However, no correlation was found between the age of the pair and apparent breeding site quality and time of breeding or annual productivity (though older females may lay slightly earlier than yearlings in most cases). In Arizona, birds of each sex were found to usually pair with like-age individuals. Pairs frequently high circle together. Either sex or the pair together perform in courtship , sometimes over an open field. Courting usually occurs on bright, sunny days, in midmorning. During sky-dances by males, the wings are raised high over back in a wide arch with slow, rhythmic flapping, similar to the flight of a nighthawk , with exaggerated down strokes. Often, much like the northern goshawk, the displaying male flares his undertail coverts. Sometimes frequently for a month or so, the pair will perform as such. When perching together, the male usually keeps on a perch at least 1 m (3.3 ft) away from his unpredictable larger mate. The bowing display reported in Wisconsin, usually (but not always) done by the male, may be a sign to the other mate of their readiness to nest build. Breeding may begin as early as February in the southern part of range, but, for the most part, the breeding season is from April to July. In central New York, the male arrives in nesting woods by March, initially defending an area of 100 m (330 ft) or so. Both members of pair arrive by early March in Wisconsin and, in both Pennsylvania and Wisconsin, nest building and copulation is often complete within the month of March. Generally both members of a pair remain on the breeding ground vicinity year-around in Arizona, New Mexico and even in British Columbia. In Michigan, the density average was 1 pair per 1,554 ha (3,840 acres) . In North Dakota, 10–12 pairs were found on 23,310 ha (57,600 acres) . 1 nest per 734 ha (1,810 acres) in central Wisconsin, 1 nest per 2,321 ha (5,740 acres) in northwestern Oregon and 1 nest per 2,200 ha (5,400 acres) in eastern Oregon. Minimal distance between active nests is seldom less than 0.7 to 1 km (0.43 to 0.62 mi) . Distance between active nest on average was 1.6 km (0.99 mi) in both California and Arizona, 2.4 km (1.5 mi) in New York, 1 km (0.62 mi) in Kansas, 5 km (3.1 mi) in western Oregon and 3.5 km (2.2 mi) in eastern Oregon and 1.6 km (0.99 mi) in central Wisconsin. Mean distance between active nests in Illinois was 5.3 km (3.3 mi) . Rather small areas may be defended where hunting occurs near the nest. Typical home range sizes for Cooper's hawks are between 400 and 1,800 ha (990 and 4,450 acres) . Home range for a Wisconsin male hawk is around 193 to 571 ha (480 to 1,410 acres) during breeding and about 732 ha (1,810 acres) during non-breeding. Exceptionally close active and successful nests were recorded only 160 m (520 ft) apart in Albuquerque and 270 m (890 ft) in Victoria, British Columbia. Male home ranges in Tucson (sample size 9) averaged 65.5 ha (162 acres) , being smaller than in Wisconsin due to better prey concentrations (doves), however juvenile males in rural Tucson areas covered a home range of 771 ha (1,910 acres) . Breeding hawks in Oshkosh, Wisconsin had an average home range of 238 ha (590 acres) . In southwest Tennessee, a male Cooper's hawk had a home range size of 331 ha (820 acres) and 4 females had an average range of 869 ha (2,150 acres) . Slightly smaller home ranges were found for urban males in a California study, at a mean of 481 ha (1,190 acres) , than in non-developed areas here, which showed a mean of 609 ha (1,500 acres) . Huge male home ranges were found for breeding ones in New Mexico, at 1,206 ha (2,980 acres) , and in north Florida, at 1,460 ha (3,600 acres) , probably due to dispersed prey resources. Home ranges of females tend to constrict with age. An exceptionally pronounced case of this was in north Florida, where first year female home ranges went from up to about 932 km 2 (360 sq mi) down to as little as 4 km 2 (1.5 sq mi) . In central New York, the nest sites of various other woodland birds were surprisingly close to those of Cooper's hawks, though some of the nest were occupied by other birds of prey that are not regularly threatened by these hawks (though flickers, one of the birds most at threat by the hawks, were fairly dispersed away from the hawk's nests). As in most accipitrids, copulation is brief (averaging about 4.5 seconds) and frequent (at around 0.9 per hour), with total copulations averaging per season about 372. This species builds a bulky platform nest, usually 61 to 76 cm (24 to 30 in) across and 15 to 45 cm (5.9 to 17.7 in) deep. Often the nest is shallower in conifers (i.e. 15 to 20 cm (5.9 to 7.9 in) deep in New York) and deeper in broad-leafed trees (averaging 43 cm (17 in) in New York). Nests average larger in the eastern part of the range than in the west, perhaps in keeping with the eastern hawks' larger average body sizes. While sticks are almost always used, one unusual Florida nest was observed to be made largely of Spanish moss ( Tillandsia usneoides ). Often nests are lined by Cooper's pair with bark or odd bits of greenery. The male grabs at bark like prey, while the female, if participating, may tear off bark with her bill; the piles of bark may be up to 3 inches deep by the time eggs are laid, though green spray is added considerably less often than other species of hawks such as Buteo . One male, unusually, was seen to be engaging in nest building while helping parent an active brood in mid-summer. Nest are often located at 8 to 15.1 m (26 to 50 ft) above the ground in the main fork or horizontal branch close to the trunk, though are sometimes up to 20 m (66 ft) above the ground, and in trees usually of 21 to 52 cm (8.3 to 20.5 in) in diameter. Usually nest sites are within plots of woodland of at least 4 to 8 ha (9.9 to 19.8 acres) in size, with a canopy coverage usually over 64%, but can be much smaller in some urban vicinities. One unusual nest in North Dakota was in dense shrub rather than a tree and it even successfully produced fledglings. Another unconventional nesting area in North Dakota in the Little Missouri National Grassland and was recorded to have unusually open canopy, at a mean of 55%, and to be in a rather steep sloped area. An unusual nest site in Wisconsin was on a grapevine . Water access is of secondary import. Pine plantations are popular nesting sites across several parts of the range. In Tucson, 70.8% of 48 nests were found to be non-native Eucalyptus trees. Native white pine ( Pinus strobus ) was preferred in Massachusetts , at 58% of 48 nests, and in Pennsylvania, at 78% of 18 studied nests, and the most used tree in a study from Wisconsin as well, at 35% of 82 nests. Shortleaf pine ( Pinus echinata ), another native was preferred in Missouri (at 51% of 43 nests) and in Illinois (at 81% of 16 nests). Deciduous trees may be preferred elsewhere in the east, such as American beech ( Fagus grandifolia ) in New York (39% of 36 nests), oaks in Maryland (66%) and laurel oak ( Quercus laurifolia ) in north Florida (81% of 77 nests). Douglas firs ( Pseudotsuga menziesii ) were preferred in northwest Oregon (94% of 18 nests) and also in northeast Oregon as well as in British Columbia (34% of 64 nests), often where mistletoe parasitizes the tree (64% of 31 in the overall state of Oregon were on mistletoe). Ponderosa pine ( Pinus ponderosa ) were preferred in eastern Oregon (53% of 15 nests) as well as in New Mexico. In the enormous redwood forests of California, all Cooper's hawk nests were in more modestly sized native tan-oaks ( Notholithocarpus densiflorus ). It has historically taken to almost be a rule that Cooper's hawk uses a new nest site each year. Exceptionally, though, pairs have used the same nests for up to 4 years, though mostly records show up to 2 to 3 years of use when a nest is reused. As much as 59% of 17 nests (New Mexico) or 66.7% of 12 nests (southern Illinois) may be reused in the following year but this is not usual. In north Florida, 21% of nests were reused in a subsequent year, while in New York, it was around 10%. New nests are often near prior nests, at a mean distance between them of around 170 m (560 ft) in Wisconsin. In Alberta, a female was reported to use a grove of trees over two consecutive years as a nest site, be absent for one year and then returned to nest in the same grove the subsequent year. Nest building usually takes about two weeks. However, if a clutch is lost, a pair may repair and use another nest within four days. A majority of 385 nests (40–60% annually) in Wisconsin built on pre-existing structures. At times, the material is put on the residue of a crow's nest, squirrel's drey or even a woodrat tree nest. In Tucson, nest building was recorded during winter, exceptionally. When grass is found to be incorporated in nest structure, it is an indication that Cooper's is using a nest built by crows as they have never themselves been known to use grass. Oregon nests frequently incorporate mistletoe into the nest, more so those built by pairs with mature females rather than juvenile females. Their nest structure requires about 4.8 support branches. Data is conflicting on whether it is the male or the female who selects the nest site. Males were found to do 70% of the nest building in Wisconsin but the female does not consistently take a secondary role. Mostly, the male gathers nesting materials within 100 to 200 m (330 to 660 ft) of the nest. The male snaps off twigs with his feet to build with, though smaller twigs may be carried in the bill. After an early duet, at as early as 5:30, the male may start nest building at around 6:30. Later in the day, he will hunt, though females also hunt at this stage, much of her food is brought by him. South-facing nests are thought to be avoided, possibly due to solar irradiance reducing soil moisture, tree density and shading or possibly due to the more deciduous local nature of north-facing nest sites. When using a prior years nest, the female reportedly selects and repairs it. Egg laying in New York is between after April 24 to June 26 (about 50% from May 10 to 20) with similar dates in New England and also from Ohio to Minnesota. Similar laying dates were also found for Ontario as well as in British Columbia, but more laying date variation was found for the latter province. Data shows that mean egg laying times in Wisconsin may be shifting earlier by up to 4–5 days in different years, but the current mean is 1.3 days. Similar shifts may be occurring in New York state as well. From New Jersey to Virginia, egg laying may be from April 7 to May 23 (about 52% from April 29 to May 11), with similar dates on the opposite coast, from Washington state to California. From Florida to Baja California, egg-laying can began as early February, but, despite the lower latitude, known records show most are between mid-April and early May and can even run into June. Similar egg-laying dates, peaking around late April, are known in Arizona. The mean clutch initiation, in 57 clutches from North Dakota was mid-May and, though pairs arrive more than a month before that, the mean dates are consistently 2–3 weeks later in nests at other similar latitude in British Columbia and Wisconsin. It was determined in Maryland that egg-laying and other mean dates rival or are even later than the longer distance migrating broad-winged hawk, and are much later in general than other Buteo hawks here. Dates of egg laying and other behaviors were also found to average slightly later than the even further migrating Buteo , the Swainson's hawk ( Buteo swainsonii ). The clutch size averages anywhere from about three to five. Female egg laying is individually consistent from year-to-year, with a variance of a day or two. Often about 3–5 eggs are laid every other day, though can be up to 2 days between the 4th and 5th eggs. Clutch sizes fell historically from a mean of 3.5 (1929–1945) to 3.1 (1946–1948) and 2.7 (1949–1967) during the use of DDT then back up to 3.3 in 1967–1976 after DDT was banned. 7 of 266 clutches in early museum records were 6 egg clutches while one 7 egg clutch was recorded in Arizona. Records of 2 egg clutches may usually be laid by yearling females. The mean clutch size in 72 clutches was 3.5 and 3.33 in 46 clutches in central Arizona. Clutch sizes were similar in Ontario, at around a mean of 3.4, and in North Dakota, at 3.5. In southern Illinois, the mean clutch size is 4.1. The average clutch size in Wisconsin Cooper's hawks was 4.3, with a little varying range of 3.9 to 4.8 over 6 years. The clutch size in Wisconsin is on average 1–3 eggs smaller in immature females. There was no strong differences in Wisconsin in clutch sizes between urban and rural locations. In British Columbia, the mean clutch size was a particularly high 4.43. A clutch of 5 may be laid in 10 days and hatch in a span of about 3 days. Some authors suspect that clutch size is functionally reliant on habitat quality. The eggs are pale sky blue, fading to dirty white, with a smooth texture. However, an occasional set is reported as lightly spotted. It is reported by some authorities that the spotted eggs are laid by a female that does so each year, however others opine that these are misidentified eggs that were laid by broad-winged hawks. The eggs may measure 43 to 54 mm (1.7 to 2.1 in) in height by 34 to 42 mm (1.3 to 1.7 in) by diameter (averaging 47 mm to 49.1 mm × 37.6 mm to 38.7 mm (1.85 in to 1.93 in × 1.48 in to 1.52 in) in 121 from Ohio and 137 from New York, respectively). California eggs averaged 47.5 mm × 37.6 mm (1.87 in × 1.48 in) in a count of 82. The average weight of eggs is 43 g (1.5 oz) (with a range of 36 to 52 g (1.3 to 1.8 oz) ). Incubation starts with the laying of the third egg. Evidence shows that pairs may be able to successfully delay breeding somewhat if it is unusually harsh and snowy early spring. The female mainly incubates (including throughout nighttime) though the male may substitute for 10–30 minutes after he brings his mate food, often doing so for about 2 to 3 times a day. The male usually roosts nearby during incubation, when he begins calling, she may join for 5–10 minutes before quickly flying back. By the third week, she may leave the nest only to take food or to defecate. Incubation lasts for 34–36 days, but sometimes may be down to 30 days. Eggs may be discarded by the mother after hatching but those that never hatch are left in place. The female sleeps on the nest until the young are 2 weeks old. The young were photographed to sleep at night directly under her body until there is not enough room to do so. The male is rarely present at nest longer than 3–4 seconds after hatching but at least once was recorded staying for 3 minutes when coming with prey after the female stops heavily brooding. Most prey deliveries are intercepted by the female slightly away from the nest. However, often the male does not perch far away, averaging about 765 m (2,510 ft) , away from the nest during nesting to fledging stages, and occasionally as close as 120 m (390 ft) . The nest may be crowded while the nestlings grow, and the female may expand platform with additional sticks. Usually the male Cooper's hawk removes the head and viscera of prey before bringing it, then taking it to plucking stumps, although often the plucking is done right where prey is killed. Rate of feeding depends on brood size but is dictated in part by the availability and size of prey. Only 2 to 3 food deliveries daily are usually necessary during incubation but the male has to hunt constantly once the young are large, rarely plucking and no longer decapitating prey. Peak deliveries are typically needed in about the 4th week. 6–9 deliveries a day are usually necessary for broods of 3 to 5. New Mexican nests with adult females had 95 prey deliveries in 120 hours of observations, whereas nest with younger females (i.e. second years), there were 65 prey deliveries were observed in 120 hours, or 694 fewer prey individuals per square kilometer than nests on territories of adult females. The parents are non-aggressive usually when the nest area is breached but the female may dive and call if a person climbs directly to their nest, sometimes also the male, often doing so silently. The reaction to human intrusion varies among individuals and probably with stage of nesting, hatch date, and probably prior experience. Generally, individuals rarely strike humans. Prolonged visits to the nest by humans, i.e. more than 30 minutes or around an hour, can cause temporary nest abandonment, and can be the cause of up to 1.2% of nest failures. During early incubation, the female often quietly flushes if a person comes up to nest tree or knocks on it but will sometimes call if someone climbs to the nest. After 2 weeks, she may begin to make "half-hearted" dives at the climber. After 3 or 4 weeks, some females still quietly flush but others grow increasingly aggressive with much variance in temperament. The aggressiveness increases around hatching, decreases for the first couple weeks after hatching, then quickly increases after 3 weeks. All dives at climbers are mock ones to early on but after the young are about 3 weeks old, either one of the pair may actually hit and draw blood from the climbers. Despite a reputation as a "somewhat aggressive" or even as being a hawk with a "very aggressive defense" towards humans in nest defense, the actual rate of attacks even at peak times seems to be very low and the reputation is thought to be fairly unearned. Various researchers consider this species less aggressive to intruders than either of the other North American Accipiter , and some even less so than red-shouldered hawks as well. Anti-predator behavior by parent Cooper's hawks against crows, red-tailed hawks and eastern gray squirrels were observed in Wisconsin to be surprisingly six times more often carried out by the male rather than the female. Female defensive attacks are sufficiently forceful enough to drive away more formidable predators such as bobcats ( Lynx rufus ) from the nest area. When large quadrupeds walk under the nest, the female may utter a semi-alarm call but does not leave the nest. Sex ratio can skew towards male in eggs, nestlings and fledglings in about 54–60% in nests of Cooper's hawks in the region of Milwaukee. However the sex ratio corrected over time in the urban area to an even amount, though it is still skewed outside the city (skewed broods towards males occur in cases where the females may become too costly to bring up, needing longer development stages and more foods). There are similar cases of male skewed ratios recorded now in southwestern cities (i.e. Tucson and Albuquerque). Due to the female usually only beginning incubation with the third egg, the first three eggs often hatch on the same day, while the fourth and fifth eggs often hatch one (rarely up to three) day later. New hatchling young average about 28 g (0.99 oz) in body mass and are about 9 cm (3.5 in) in total length. Hatchlings are covered in white natal down with blue-gray eyes and are tan to pink on many of the bareparts. While growth is slow for about three days, sexual dimorphism by size may begin by to be measurable by about seven days of age. At about 10 days, the nestlings begin to engage in rather feeble standing and wing flapping. The bill (at around 11 days) grows about twice as fast as the tarsus (at around 22 days). At 13 days, the nestlings stretch their legs and often yawn, and at 16 days can be aggressive if the nest is breached by people. Down first becomes deep and fluffy around two weeks, the following week first feathers among dense down, feather production accelerates but growth slows in the fourth week after which both increase for the fifth week. By 16–18 days, the nestlings preen well, starts to rip at prey and flap well. Within first two weeks, the young Cooper's hawks begin to defecate over nest edge but often soil the edge of nest. At three weeks often begin to stand up and feed by themselves and often begin to mantle prey away from each other. The young grow is rapid for the period when they are 17 days old to about 23 days, growth then slows down abruptly before they nearly pause growth to feather out and then thereafter become fully grown. At the age of three weeks a female nestling may stand and be able to fully feed herself. Sometimes smaller, more agile male nest mates may snatch several bits of meat from their larger sister as if taking food from the mother. Siblicide rarely has been proven for this species, and may occur "accidentally" at times. Sometimes a younger sibling that has died from other means may be eaten by the siblings or by the parents. In one case, an entire brood of 4 nestlings from 2.5 to 3.5 weeks old were found dead in the nest, apparently having died due to exposure after consistent heavy rains. Normal departure from nest is 30 days (up to 27 days) for males and 34 days for females, but averaged sooner in Oregon, at 27–30 days. Response to the parents after the young Cooper's becoming branchers depends on their hunger levels. Snyder and Wiley recorded feeding rates of 0.267 per hour for a brood of 2 and 0.564 per hour for a brood of 4. In New York and Wisconsin, the sex ratio of broods roughly even, but slightly male biased in Wisconsin (53.5% or 137 against 119). Food may be brought to the nest for the first ten days after the young leave it, as the young often return to rest on it or even to sun from it. Largely, the young are quiet until they leave the nest when they begin their loud, persistent hunger calls. Around this stage, the young hawks will frequently engage in play with sticks and pinecones. After they are about eight weeks old, they may start to hunt for themselves, but are usually still reliant on parents for food. The young Cooper's hawks are frequently loud, voracious and aggressive in procuring food from the parents. The parents soon seem to lose interest in feeding the young. Fledgling occurs at 27–34 days (males averaging earlier), but the young may often returns to nest and are not fully feathered until about 50–54 days. The siblings often stay within 4 m (13 ft) of each other even after leaving their parents range. Siblings before long-distance dispersal may hunt together, although may too steal prey from one another. Juveniles Cooper's hawks in mostly urban areas of Arizona wandered somewhat randomly it seems until they were about 2.5–3 months old, when they settled on a wintering ground, averaging 9.7 km (6.0 mi) for females and averaging 7.4 km (4.6 mi) in males away from their respective natal sites. From their initial natal site to the site where they ultimately breed, in Wisconsin the average young male Cooper's hawk settled 7.2 km (4.5 mi) away from their nest of origin and the average young female 27.6 km (17.1 mi) away. Attempts to average mean dispersal distances within another study found farther than expected dispersal distances for Cooper's hawks from across the range. These were estimated at 43 km (27 mi) . Greater dispersal distances by female juveniles are probably meant to limit the likelihood of inbreeding. In one instance, a grandson Cooper's mated with his grandmother over 3 years while there were two instances known of full siblings mating in Victoria, British Columbia. Cooper's hawks usually first breed at 2 years old but yearlings can often be reported to average at 6 to 22% of the breeding populations in short 3–6-year studies. Longer-term studies of 16–25 years of large urban populations within Milwaukee, Wisconsin, Tucson, Arizona and Victoria, British Columbia, show yearling females average 16–25% of the breeding population but that breeding by yearling male was uncommon to non-existent. Similarly, 79% more females bred in their first year in study in New Mexico than did males. Despite the considerable number of breeding young females, in Oregon, they averaged about 1 egg smaller and nearly a fledgling smaller than their older female counterparts; while results in Albuquerque were even more skewed towards breeding success for older females. Many studies found no yearling males to be breeding with various populations but 7% of 184 males in Tucson were yearlings over several years of study (78% of which were paired with immature females). Only one breeding male in both Victoria, British Columbia (579 sample size) and in Albuquerque (sample size 305) were yearling while 4.8% of 123 in Milwaukee were yearlings (92% of which were paired with an adult female). In New Mexico, males sometimes bred in their first year where there were rich prey concentrations, but had 37% higher mean annual mortality than those who did not breed until mature plumaged. New Mexican data showed that 14% of 20 males bred in their first year and 71% in their second year while 93% of the local female bred in their first year. In addition to Tucson, other cases of successful breeding by pairs of immatures reported in varied areas such as Indiana and New York. Considerable numbers of juvenile Cooper's hawks breeding may be historically associated with high turnover within populations. Evidence from the Milwaukee area shows a significant reduction in more recent decades of two-year old or younger breeding hawks, which was indicative of a recovering population. The average of 117 successful laid clutches was 4.18 eggs laid, 3.53 nestlings in successfully hatched clutches and 3.08 young in 26 successfully fledged broods in the Northeastern United States and southeastern Canada . Nesting success in western Pennsylvania in 32 successful nests was 3.2 fledglings; in 6 nests within Michigan, a mean of 3 in all nests got to fledge (4.3 eggs, 3 hatchlings on average); in Wisconsin, 3.5 fledglings were produced from successful nests (68.6% of 83 nests produced at least 1 fledgling); a mean of 2 fledged from 11 nests in Maryland and 2.23 fledglings per 41 successful nests in Arizona. In Illinois, in all breeding attempts (not just successful ones), the mean number of fledglings was 2.8. 81% of New York nests produced fledged young and 75% did so in Pennsylvania. Nesting success rates in western wildland areas may be lower such as in Utah, where 53.5% of nests fledged young, with many of the failures attributable to owl predation. Data from Oregon showed that 74% hatched and 61.4–69% successfully fledged, a much lower rate of nest success than goshawks, at 90.4%, and, surprisingly, than sharp-shinned hawks, at 91.7%. However, in the Oregon data, the number of eggs hatched was higher in Cooper's at 74% than in sharp-shinned hawks, at 69.4% (but not than the goshawk's). In Wisconsin in 2019, all of the eggs in a clutch of seven hatched and all of the young fledged. In North Dakota , better habitat such as upland forest showed much higher breeding success levels (at least 1 fledgling in 86% of 26 nests) than in poorer habitats such as narrow riparian strips, in which 1 fledgling was produced in 57% of 44 nests. Younger forest in North Dakota was surprisingly preferred, with the average estimated age of trees used by Cooper's at 59.9 against a random tree age in the area of 74.6. It was found that adult female who mated with males who provisioned food at a higher rate produced 1.6 more fledglings on average. Yearling females in northeastern Oregon tended to use younger successional stands than older females and tended to have lower productivity in clutch size and brood counts. Among 70 studied male hawks in Wisconsin, the number of fledged young produced in their lifetime was similar in males who did not breed until they were two years old (mean of 8.8 fledglings) compared to those who started breeding as yearlings (mean of 8.7 fledglings), with the most successful studied male having started breeding in his second year and had produced 32 fledglings by the time he was nine years of age. In Arizona and New Mexico, 23% of nests failed altogether and 56.5% of 23 nests in Wisconsin failed during incubation. A high genetic diversity, or allele level, was found in the nestlings of the urbanized population of Tucson, ensuring a hardy local population despite historic concerns about the parasite levels of nestlings in these populations. Cooper's hawks can be a long-living bird. Some authors credit lifespans of up to 8 years of age in the wild. The oldest recorded bird recorded among migrants that bred in Oregon was 10 years and 5 months old. The oldest recorded breeding bird was a 12-year-old female in British Columbia while the oldest recorded wild bird was 20 years, 5 months old, banded in migration. However, the mean age at death recorded in 136 banded Cooper's hawks was 16.3 months. It was estimated for the species that the mortality rate in the first year of life for these hawk is 71–78% while it about 34–37% in the subsequent years. An annual survival rate of 75% was recorded for juvenile males in Tucson while the survival rate for juvenile female here was 64%. The survival rate for Tucson adults was between 69 and 88%. 75% was considered the survival rate of wintering Cooper's hawks in Indiana and southern Illinois but mean mortality between adults and juveniles was estimated to possibly average up to 46.4%. The annual survival rate in Albuquerque was 27–38% for female immatures. No correlation was found to body size or habitat in female survivorship but those in Wisconsin who changed nest sites annually may have had slightly higher survival rates than those who reused a same nest site. The opposite trend was reported for north Florida, wherein females who reused a nest site seemed to have higher survival rates. Historic survival rates (1925–1940) as reported were much lower, with extensive persecution causing an annual mortality that was estimated at 44%. Regular natural causes of mortality in Cooper's hawk, mainly of their young, include hypothermia , windstorms and tree collapses . Clashes between members of the same sex can be lethal, especially those between two males. Although Cooper's hawks are not known to prey on venomous snakes , one was found dead from envenomation next to a burrow holding both a copperhead ( Agkistrodon contortrix ) and an eastern diamondback rattlesnake ( Crotalus adamanteus ). Hunting accidents can frequently cause injury, especially in the form of potentially hobbling bone fractures , or sometimes can kill Cooper's hawks, especially those living in urban areas. In Indiana and Illinois, mortality from collisions were somewhat more prevalent in Cooper's hawks than in sharp-shinned hawks but instances of predation on immature sharp-shins were three times more prevalent than predations on immature Cooper's. Despite the risks of urban living, evidence indicates that urban Cooper's seem to be relatively successful, have moderate to low annual survival and reproduce prolifically. Cooper's hawks are known to be vulnerable to West Nile virus with some regularity but sometimes are able to survive despite the viral antibodies being found. Some mortality from West Nile has been reported, unsurprisingly. Fatal infections of the herpes virus have been recorded at least twice in Cooper's hawks. Cooper's hawks, along with great horned owls , had the greatest seroprevalence of Avipoxvirus among several raptorial birds in Illinois. An extremely high amount of Trichomoniasis was found in nestlings in southeast Arizona. The bacteria was recorded in 95% of urban Cooper's hawk nestlings (though only 8% of non-urban ones) and caused about 50% of recorded nestling deaths, probably roughly doubling the nestling mortality rate compared to the non-urban areas. Adults are less vulnerable to Trichomoniasis infections but there was no variability to be found by sex, time of year or by location. In Wisconsin and British Columbia only 2.7% of 145 studied nestlings had Trichomoniasis . A high balance of the bacterial disease Mycoplasma gallisepticum , common to birds who frequent bird feeders , was found in Cooper's hawks (transmitted from their prey) studied in Illinois (the highest of any six raptor species studied) however effective antibodies were found and no external infection was noted. A high balance of bacterial flora were found the airways of 10 Cooper's hawks, including many with Salmonella (rarely fatal in hawks but can compromise their condition). 91% of 47 tested adults in Wisconsin had Leucocytozoon toddi and 62% had Haemoproteus but only 12% of 33 nestlings there had parasites. A similar blood parasite infection rate was found in northern New York (and California) as well. Compared to sharp-shinned hawks, while migrating off Lake Ontario , Cooper's hawks were found to have higher white blood cell counts ( heterophiles , monocytes , and eosinophils ) that may have made them more vulnerable to blood parasitism. Haematozoa infection rates were also higher in adults than they were in nestlings in Arizona. Blood parasites were recorded to be higher for later migrating Cooper's hawks in northern New York but were, on the contrary, higher in earlier migrating hawks in Marin County, California . Even rare parasites such as Sarcocystis may be found in wild Cooper's hawks, being apparently more prevalent in juvenile hawks and slightly more often afflicting females rather than males. Helminths were quite diverse in Cooper's hawks from Florida. In Minnesota and Wisconsin, several helminths were recorded and there was one instance of a tissue reaction from Serratospiculum as well as a case was reported of related Serratospiculoides in an injured Cooper's hawk in Yellowstone National Park . Cooper's hawks have had an erratic status throughout the 20th into the 21st centuries. Historic data shows a threefold increase, roughly, around 1920. However, mortality rates shot up soon after as some authors consider the annual rate of mortality due largely to legalized direct persecution ( poisoning , "pole trapping" and, especially, shooting ) between 1925 and 1957 could range up to 60.5–77.6% in the most severe years. The amount of hawks shot down within different populations was estimated at 12 to 40%. Migration counts during the 1930s showed a strong downward trend, and an even worse decline for Cooper's hawk was observed during the late 1950s. Most Cooper's hawks reacted to heavy persecution by behaving with more shyness and elusiveness. Much of the human animosity towards Cooper's hawks was due to their hunting of gamebirds such as quail which human hunters themselves coveted. Furthermore, even ornithological writings from these times reveal a strong bias against the hawks for their hunting of admired small birds. However, several studies have determined that Cooper's hawk predation is not detrimental to healthy gamebird population, and that most of the blame must fall directly on overexploitation and habitat destruction of humans themselves, with a more recently quantified causal of changing climate further exacerbating the gamebirds' declines. Human hunting of Cooper's hawk declined when governmental protection of the species was instituted in the late 1960s (nearly two decades after some less controversial birds of prey species were protected in America). However, instead of the expected gradual recovery, in the 1960s to 1970s, the breeding success rate dropped, in almost certain correlation with man's use of chemical biocides , mostly DDT . Raptorial birds which predominantly prey on either birds or fish were severely affected by the DDT biocide. The concentrations of organochlorines like DDT were high in all American Accipiters , averaging at intermediate levels in Cooper's (0.11 mg/kg) but could include the highest known in the Accipiters at up to 1.5 mg/kg. A considerable average reduction in eggshell thickness was measured to average at around 7%. A particularly severe reduction in eggshell thickness was recorded in New York state, at an average of 19.02%. The survival of the species, especially in the eastern part of the continent, was seriously questioned in the 1960s and 1970s. Fewer dramatic ebbs were detected during the height of DDT use in the western part of North America overall, perhaps because of less overall reliance on bird prey. Nonetheless, 11 of 16 eggs in Arizona and New Mexico broke due to this cause. Subsequent to the prohibition of DDT use in North America, the population increased exponentially in the 1980s and 1990s and ultimately was thought to stabilize. Data from Hawk Mountain Sanctuary shows that Cooper's hawk has recovered from DDT more gradually than the sharp-shinned hawk here. In the 1990s, it was estimated that Cooper's hawks may number "well into six figures" due to their regular distribution over 8 million square kilometers. Today, Cooper's hawk is thought to number around 800,000 in the United States and Canada. These estimates were gained cross-referencing the number of hectares per active nest, which was in the range of 101 to 2,326 ha (250 to 5,750 acres) in the western states and 272 to 5,000 ha (670 to 12,360 acres) in the Midwestern and eastern states, as well as data from Christmas Bird Counts and migration counts. Evidence from long-time migration counts at Bake Oven Knob show slight peaks at intervals of 3 to 4 years, however no dramatic declines have been detected since the 1980s. Following their historic decline, Breeding Bird Surveys have tracked strong increases of the breeding population (upward trends from 1.2% in California to 4.4% in Pennsylvania) in six states, with a 2.2% increase overall, and similar trends in multiple other states. In many states (Arizona, California, Florida, Missouri, New Mexico and North Dakota) the numbers are probably similar or greater to those prior to 1945. It is thought that the population of Cooper's hawks in Wisconsin is nearly saturated relative to the landmass of the state, after a rough 25-fold increase since the late 1970s. Based largely on data from well-known populations such as Tucson and Milwaukee, some authors opine that Cooper's hawk may be the most common raptor in American urban areas today, although surely other common raptorial birds such as red-tailed hawks, American kestrels and turkey vultures ( Cathartes aura ) may easily rival them in this regard. Shooting is now a generally insignificant cause of mortality though is still sometimes reported. Despite the declining effect of pesticides on Cooper's hawk's overall population, lingering harmful effect from dieldrin has been indicated in some hawks in British Columbia and recently some hawks have been killed by the pesticide warfarin . Bioaccumulation of pollutants may still have considerable effect on this species. Declines due to pollutants are seemingly occurring for Cooper's hawks living in Vancouver . Recent cases of cyanide poisoning of Cooper's hawks have been reported. Lead poisoning can sometimes threaten Cooper's hawks, through lead bullets left in dead or injured game. Most urban-related mortality for Cooper's hawks is likely to be collisions with manmade objects. These are mostly wire strikes (with or without resulting electrocution ), automobile collisions and window strikes or with other parts of manmade structure while distractingly hunting. 70.8% of diagnosed mortality for Cooper's hawks of yearling age or older in Tucson was from such collisions. In less developed regions, such as much of Montana, the rate of wire collisions and electrocutions was considerably lower for Cooper's hawks than for various other birds of prey who are either larger-bodied and/or use less forested areas. Other studies support that the number of fatal window and wire collisions of urban-living Cooper's hawks is "excessively high". Cooper's hawks found in the vicinity of airports are at risk of bird strike with aircraft, therefore 185 Cooper's were translocated away from these areas (the 5th most frequently translocated raptor species). A similar translocation effort away from the Los Angeles basin around the Los Angeles International Airport translocated 349 Cooper's hawks (about a fifth of all translocated raptors), apparently successfully. Cooper's hawks are sometimes displaced by the placement of wind farms , with studies indicating that Cooper's need about seven years to locally recover from such displacement. Synurbization has been detected in Cooper's hawks as, despite the dangers of various kinds of collisions, it has been found that in favorable urban areas, hawks of the species can seem to breed more closer to one another, gather more food and produce more young on average than those outside such areas. Even New York City has seen (if erratically present) since the late 1990s, a return of nesting Cooper's hawks. Logging may decrease some populations but the overall effect it has on Cooper's hawks is generally considered unknown. As with all Accipiters , Cooper's hawks can presumably only withstand a certain level of loss of habitat before an area becomes essentially unlivable. Studies in Arizona determined that heavily grazed agricultural areas were favored over lightly grazed ones due to greater prey concentrations in the latter habitats. On the contrary, in the early 1990s (while the species was generally recovering), the species was considered to be "state-endangered" in New Jersey, with ongoing harmful effects found for poorly-regulated (or entirely unregulated) logging and land development within 40 to 120 m (130 to 390 ft) of active nests. In the Black Hills , harvesting of ponderosa pines appears to be causing Cooper's and both other species of Accipiter to vacate large parts of the forest. It has been recommended that a buffer zone of at least 200 to 240 m (660 to 790 ft) , with a median estimated space needed of about 525 m (1,722 ft) , should be free from human disturbance or development to retain the protected nests of Cooper's hawks. Studies in New Mexico showed that these hawks are reliant on the conservation of riparian woodlands in much of the southern part of the state. Despite the large, productive and genetically diverse population of Cooper's hawks in Tucson, several authors have hypothesized, controversially, that the city is an ecological trap , due to the unsustainably high turnover for nestlings via Trichomoniasis -related mortality and for adults via frequent lethal collisions. Quite few Cooper's hawks have ever been gathered for use in falconry . This hawk is fairly unpopular in falconry practices due to its high-strung personality and is additionally considered in such captive conditions as given towards "tyrannical", "hysterical" and "demanding" behaviors, even compared to its similarly disposed larger cousin, the northern goshawk , which is fairly popular in falconry. Generally, Cooper's hawks hunt the locally common birds that are available and probably control some birds (such as the more numerous icterids and corvids) that may without the influence of natural predation risk overpopulation and potential harm to ecosystems. However, as an opportunistic natural predator of almost any North American bird smaller than itself, Cooper's hawk may inadvertently deplete populations of rarer, conservation-dependent species. The American kestrel , whose populations have experienced considerable decrease, may be one species which has suffered from the extensive predation of the recovered Cooper's hawk population. However, there is no evidence that Cooper's hawk predation is one of the leading causes of kestrel declines and data seems to indicate it is, at most, a localized threat. Similarly, Cooper's hawks occasionally prey upon other threatened bird species, and, although said predation is not a primary cause of concern, may exacerbate the already worrying condition of many declining North American birds. Some threatened species known to be thusly hunted by these hawks are greater prairie chicken ( Tympanuchus cupido ), lesser prairie chickens ( Tympanuchus pallidicinctus ), red-headed woodpeckers , Bell's vireo ( Vireo bellii ), Florida scrub jay ( Aphelocoma coerulescens ), wood thrush ( Hylocichla mustelina ) (Cooper's being identified as one three major nest predators along with blue jays and raccoons), golden-winged warbler ( Vermivora chrysoptera ), cerulean warbler ( Setophaga cerulea ) and golden-cheeked warbler ( Setophaga chrysoparia ). Cooper's hawks have had an erratic status throughout the 20th into the 21st centuries. Historic data shows a threefold increase, roughly, around 1920. However, mortality rates shot up soon after as some authors consider the annual rate of mortality due largely to legalized direct persecution ( poisoning , "pole trapping" and, especially, shooting ) between 1925 and 1957 could range up to 60.5–77.6% in the most severe years. The amount of hawks shot down within different populations was estimated at 12 to 40%. Migration counts during the 1930s showed a strong downward trend, and an even worse decline for Cooper's hawk was observed during the late 1950s. Most Cooper's hawks reacted to heavy persecution by behaving with more shyness and elusiveness. Much of the human animosity towards Cooper's hawks was due to their hunting of gamebirds such as quail which human hunters themselves coveted. Furthermore, even ornithological writings from these times reveal a strong bias against the hawks for their hunting of admired small birds. However, several studies have determined that Cooper's hawk predation is not detrimental to healthy gamebird population, and that most of the blame must fall directly on overexploitation and habitat destruction of humans themselves, with a more recently quantified causal of changing climate further exacerbating the gamebirds' declines. Human hunting of Cooper's hawk declined when governmental protection of the species was instituted in the late 1960s (nearly two decades after some less controversial birds of prey species were protected in America). However, instead of the expected gradual recovery, in the 1960s to 1970s, the breeding success rate dropped, in almost certain correlation with man's use of chemical biocides , mostly DDT . Raptorial birds which predominantly prey on either birds or fish were severely affected by the DDT biocide. The concentrations of organochlorines like DDT were high in all American Accipiters , averaging at intermediate levels in Cooper's (0.11 mg/kg) but could include the highest known in the Accipiters at up to 1.5 mg/kg. A considerable average reduction in eggshell thickness was measured to average at around 7%. A particularly severe reduction in eggshell thickness was recorded in New York state, at an average of 19.02%. The survival of the species, especially in the eastern part of the continent, was seriously questioned in the 1960s and 1970s. Fewer dramatic ebbs were detected during the height of DDT use in the western part of North America overall, perhaps because of less overall reliance on bird prey. Nonetheless, 11 of 16 eggs in Arizona and New Mexico broke due to this cause. Subsequent to the prohibition of DDT use in North America, the population increased exponentially in the 1980s and 1990s and ultimately was thought to stabilize. Data from Hawk Mountain Sanctuary shows that Cooper's hawk has recovered from DDT more gradually than the sharp-shinned hawk here. In the 1990s, it was estimated that Cooper's hawks may number "well into six figures" due to their regular distribution over 8 million square kilometers. Today, Cooper's hawk is thought to number around 800,000 in the United States and Canada. These estimates were gained cross-referencing the number of hectares per active nest, which was in the range of 101 to 2,326 ha (250 to 5,750 acres) in the western states and 272 to 5,000 ha (670 to 12,360 acres) in the Midwestern and eastern states, as well as data from Christmas Bird Counts and migration counts. Evidence from long-time migration counts at Bake Oven Knob show slight peaks at intervals of 3 to 4 years, however no dramatic declines have been detected since the 1980s. Following their historic decline, Breeding Bird Surveys have tracked strong increases of the breeding population (upward trends from 1.2% in California to 4.4% in Pennsylvania) in six states, with a 2.2% increase overall, and similar trends in multiple other states. In many states (Arizona, California, Florida, Missouri, New Mexico and North Dakota) the numbers are probably similar or greater to those prior to 1945. It is thought that the population of Cooper's hawks in Wisconsin is nearly saturated relative to the landmass of the state, after a rough 25-fold increase since the late 1970s. Based largely on data from well-known populations such as Tucson and Milwaukee, some authors opine that Cooper's hawk may be the most common raptor in American urban areas today, although surely other common raptorial birds such as red-tailed hawks, American kestrels and turkey vultures ( Cathartes aura ) may easily rival them in this regard. Shooting is now a generally insignificant cause of mortality though is still sometimes reported. Despite the declining effect of pesticides on Cooper's hawk's overall population, lingering harmful effect from dieldrin has been indicated in some hawks in British Columbia and recently some hawks have been killed by the pesticide warfarin . Bioaccumulation of pollutants may still have considerable effect on this species. Declines due to pollutants are seemingly occurring for Cooper's hawks living in Vancouver . Recent cases of cyanide poisoning of Cooper's hawks have been reported. Lead poisoning can sometimes threaten Cooper's hawks, through lead bullets left in dead or injured game. Most urban-related mortality for Cooper's hawks is likely to be collisions with manmade objects. These are mostly wire strikes (with or without resulting electrocution ), automobile collisions and window strikes or with other parts of manmade structure while distractingly hunting. 70.8% of diagnosed mortality for Cooper's hawks of yearling age or older in Tucson was from such collisions. In less developed regions, such as much of Montana, the rate of wire collisions and electrocutions was considerably lower for Cooper's hawks than for various other birds of prey who are either larger-bodied and/or use less forested areas. Other studies support that the number of fatal window and wire collisions of urban-living Cooper's hawks is "excessively high". Cooper's hawks found in the vicinity of airports are at risk of bird strike with aircraft, therefore 185 Cooper's were translocated away from these areas (the 5th most frequently translocated raptor species). A similar translocation effort away from the Los Angeles basin around the Los Angeles International Airport translocated 349 Cooper's hawks (about a fifth of all translocated raptors), apparently successfully. Cooper's hawks are sometimes displaced by the placement of wind farms , with studies indicating that Cooper's need about seven years to locally recover from such displacement. Synurbization has been detected in Cooper's hawks as, despite the dangers of various kinds of collisions, it has been found that in favorable urban areas, hawks of the species can seem to breed more closer to one another, gather more food and produce more young on average than those outside such areas. Even New York City has seen (if erratically present) since the late 1990s, a return of nesting Cooper's hawks. Logging may decrease some populations but the overall effect it has on Cooper's hawks is generally considered unknown. As with all Accipiters , Cooper's hawks can presumably only withstand a certain level of loss of habitat before an area becomes essentially unlivable. Studies in Arizona determined that heavily grazed agricultural areas were favored over lightly grazed ones due to greater prey concentrations in the latter habitats. On the contrary, in the early 1990s (while the species was generally recovering), the species was considered to be "state-endangered" in New Jersey, with ongoing harmful effects found for poorly-regulated (or entirely unregulated) logging and land development within 40 to 120 m (130 to 390 ft) of active nests. In the Black Hills , harvesting of ponderosa pines appears to be causing Cooper's and both other species of Accipiter to vacate large parts of the forest. It has been recommended that a buffer zone of at least 200 to 240 m (660 to 790 ft) , with a median estimated space needed of about 525 m (1,722 ft) , should be free from human disturbance or development to retain the protected nests of Cooper's hawks. Studies in New Mexico showed that these hawks are reliant on the conservation of riparian woodlands in much of the southern part of the state. Despite the large, productive and genetically diverse population of Cooper's hawks in Tucson, several authors have hypothesized, controversially, that the city is an ecological trap , due to the unsustainably high turnover for nestlings via Trichomoniasis -related mortality and for adults via frequent lethal collisions. Quite few Cooper's hawks have ever been gathered for use in falconry . This hawk is fairly unpopular in falconry practices due to its high-strung personality and is additionally considered in such captive conditions as given towards "tyrannical", "hysterical" and "demanding" behaviors, even compared to its similarly disposed larger cousin, the northern goshawk , which is fairly popular in falconry. Generally, Cooper's hawks hunt the locally common birds that are available and probably control some birds (such as the more numerous icterids and corvids) that may without the influence of natural predation risk overpopulation and potential harm to ecosystems. However, as an opportunistic natural predator of almost any North American bird smaller than itself, Cooper's hawk may inadvertently deplete populations of rarer, conservation-dependent species. The American kestrel , whose populations have experienced considerable decrease, may be one species which has suffered from the extensive predation of the recovered Cooper's hawk population. However, there is no evidence that Cooper's hawk predation is one of the leading causes of kestrel declines and data seems to indicate it is, at most, a localized threat. Similarly, Cooper's hawks occasionally prey upon other threatened bird species, and, although said predation is not a primary cause of concern, may exacerbate the already worrying condition of many declining North American birds. Some threatened species known to be thusly hunted by these hawks are greater prairie chicken ( Tympanuchus cupido ), lesser prairie chickens ( Tympanuchus pallidicinctus ), red-headed woodpeckers , Bell's vireo ( Vireo bellii ), Florida scrub jay ( Aphelocoma coerulescens ), wood thrush ( Hylocichla mustelina ) (Cooper's being identified as one three major nest predators along with blue jays and raccoons), golden-winged warbler ( Vermivora chrysoptera ), cerulean warbler ( Setophaga cerulea ) and golden-cheeked warbler ( Setophaga chrysoparia ).

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Methylene blue

AU : D 3,7-bis(Dimethylamino)-phenothiazin-5-ium chloride CN(C)c1ccc2c(c1)sc-3cc(=[N+](C)C)ccc3n2.[Cl-] InChI=1S/C16H18N3S.ClH/c1-18(2)11-5-7-13-15(9-11)20-16-10-12(19(3)4)6-8-14(16)17-13;/h5-10H,1-4H3;1H/q+1;/p-1 Y Key:CXKWCBBOMKCUKX-UHFFFAOYSA-M Y Methylthioninium chloride , commonly called methylene blue , is a salt used as a dye and as a medication. As a medication, it is mainly used to treat methemoglobinemia by chemically reducing the ferric iron in hemoglobin to ferrous iron . Specifically, it is used to treat methemoglobin levels that are greater than 30% or in which there are symptoms despite oxygen therapy . It has previously been used for treating cyanide poisoning and urinary tract infections , but this use is no longer recommended. Methylene blue is typically given by injection into a vein . Common side effects include headache and vomiting. While use during pregnancy may harm the baby, not using it in methemoglobinemia is likely more dangerous. Methylene blue was first prepared in 1876, by Heinrich Caro . It is on the World Health Organization's List of Essential Medicines . Methylene blue is employed as a medication for the treatment of methemoglobinemia , which can arise from ingestion of certain pharmaceuticals, toxins, or broad beans in those susceptible. Normally, through the NADH - or NADPH -dependent methemoglobin reductase enzymes, methemoglobin is reduced back to hemoglobin. When large amounts of methemoglobin occur secondary to toxins, methemoglobin reductases are overwhelmed. Methylene blue, when injected intravenously as an antidote, is itself first reduced to leucomethylene blue , which then reduces the heme group from methemoglobin to hemoglobin . Methylene blue can reduce the half life of methemoglobin from hours to minutes. At high doses, however, methylene blue actually induces methemoglobinemia, reversing this pathway. [ dead link ] Since its reduction potential is similar to that of oxygen and can be reduced by components of the electron transport chain , large doses of methylene blue are sometimes used as an antidote to potassium cyanide poisoning, a method first successfully tested in 1933 by Dr. Matilda Moldenhauer Brooks in San Francisco, although first demonstrated by Bo Sahlin of Lund University , in 1926. Methylene blue is used in endoscopic polypectomy as an adjunct to saline or epinephrine , and is used for injection into the submucosa around the polyp to be removed. This allows the submucosal tissue plane to be identified after the polyp is removed, which is useful in determining if more tissue needs to be removed, or if there has been a high risk for perforation. Methylene blue is also used as a dye in chromoendoscopy , and is sprayed onto the mucosa of the gastrointestinal tract in order to identify dysplasia , or pre-cancerous lesions. Intravenously injected methylene blue is readily released into the urine and thus can be used to test the urinary tract for leaks or fistulas . [ citation needed ] In surgeries such as sentinel lymph node dissections, methylene blue can be used to visually trace the lymphatic drainage of tested tissues. Similarly, methylene blue is added to bone cement in orthopedic operations to provide easy discrimination between native bone and cement. Additionally, methylene blue accelerates the hardening of bone cement, increasing the speed at which bone cement can be effectively applied. Methylene blue is used as an aid to visualisation/orientation in a number of medical devices, including a Surgical sealant film , TissuePatch. In fistulas and pilonidal sinuses it is used to identify the tract for complete excision. [ citation needed ] It can also be used during gastrointestinal surgeries (such as bowel resection or gastric bypass ) to test for leaks. [ citation needed ] It is sometimes used in cytopathology , in mixtures including Wright-Giemsa and Diff-Quik . It confers a blue color to both nuclei and cytoplasm, and makes the nuclei more visible. When methylene blue is "polychromed" (oxidized in solution or "ripened" by fungal metabolism, as originally noted in the thesis of Dr. D. L. Romanowsky in the 1890s), it gets serially demethylated and forms all the tri-, di-, mono- and non-methyl intermediates, which are Azure B , Azure A , Azure C , and thionine , respectively. This is the basis of the basophilic part of the spectrum of Romanowski-Giemsa effect. If only synthetic Azure B and Eosin Y is used, it may serve as a standardized Giemsa stain ; but, without methylene blue, the normal neutrophilic granules tend to overstain and look like toxic granules. On the other hand, if methylene blue is used it might help to give the normal look of neutrophil granules and may also enhance the staining of nucleoli and polychromatophilic RBCs (reticulocytes). A traditional application of methylene blue is the intravital or supravital staining of nerve fibers, an effect first described by Paul Ehrlich in 1887. A dilute solution of the dye is either injected into tissue or applied to small freshly removed pieces. The selective blue coloration develops with exposure to air (oxygen) and can be fixed by immersion of the stained specimen in an aqueous solution of ammonium molybdate. Vital methylene blue was formerly much used for examining the innervation of muscle, skin and internal organs. The mechanism of selective dye uptake is incompletely understood; vital staining of nerve fibers in skin is prevented by ouabain , a drug that inhibits the Na/K-ATPase of cell membranes. Methylene blue has been used as a placebo ; physicians would tell their patients to expect their urine to change color and view this as a sign that their condition had improved. This same side effect makes methylene blue difficult to use in traditional placebo-controlled clinical studies , including those testing for its efficacy as a treatment. Isobutyl nitrite is one of the compounds used as poppers , an inhalant drug that induces a brief euphoria . Isobutyl nitrite is known to cause methemoglobinemia . Severe methemoglobinemia may be treated with methylene blue. Another use of methylene blue is to treat ifosfamide neurotoxicity . Methylene blue was first reported for treatment and prophylaxis of ifosfamide neuropsychiatric toxicity in 1994. A toxic metabolite of ifosfamide, chloroacetaldehyde (CAA), disrupts the mitochondrial respiratory chain , leading to an accumulation of nicotinamide adenine dinucleotide hydrogen (NADH). Methylene blue acts as an alternative electron acceptor, and reverses the NADH inhibition of hepatic gluconeogenesis while also inhibiting the transformation of chloroethylamine into chloroacetaldehyde, and inhibits multiple amine oxidase activities, preventing the formation of CAA. The dosing of methylene blue for treatment of ifosfamide neurotoxicity varies, depending upon its use simultaneously as an adjuvant in ifosfamide infusion, versus its use to reverse psychiatric symptoms that manifest after completion of an ifosfamide infusion. Reports suggest that methylene blue up to six doses a day have resulted in improvement of symptoms within 10 minutes to several days. Alternatively, it has been suggested that intravenous methylene blue every six hours for prophylaxis during ifosfamide treatment in people with history of ifosfamide neuropsychiatric toxicity. Prophylactic administration of methylene blue the day before initiation of ifosfamide, and three times daily during ifosfamide chemotherapy has been recommended to lower the occurrence of ifosfamide neurotoxicity. It has also been used in septic shock and anaphylaxis . Methylene blue consistently increases blood pressure in people with vasoplegic syndrome (redistributive shock), but has not been shown to improve delivery of oxygen to tissues or to decrease mortality. Methylene blue has been used in calcium channel blocker toxicity as a rescue therapy for distributive shock unresponsive to first line agents. Evidence for its use in this circumstance is very poor and limited to a handful of case reports. [ excessive citations ]Methylene blue is employed as a medication for the treatment of methemoglobinemia , which can arise from ingestion of certain pharmaceuticals, toxins, or broad beans in those susceptible. Normally, through the NADH - or NADPH -dependent methemoglobin reductase enzymes, methemoglobin is reduced back to hemoglobin. When large amounts of methemoglobin occur secondary to toxins, methemoglobin reductases are overwhelmed. Methylene blue, when injected intravenously as an antidote, is itself first reduced to leucomethylene blue , which then reduces the heme group from methemoglobin to hemoglobin . Methylene blue can reduce the half life of methemoglobin from hours to minutes. At high doses, however, methylene blue actually induces methemoglobinemia, reversing this pathway. [ dead link ]Since its reduction potential is similar to that of oxygen and can be reduced by components of the electron transport chain , large doses of methylene blue are sometimes used as an antidote to potassium cyanide poisoning, a method first successfully tested in 1933 by Dr. Matilda Moldenhauer Brooks in San Francisco, although first demonstrated by Bo Sahlin of Lund University , in 1926. Methylene blue is used in endoscopic polypectomy as an adjunct to saline or epinephrine , and is used for injection into the submucosa around the polyp to be removed. This allows the submucosal tissue plane to be identified after the polyp is removed, which is useful in determining if more tissue needs to be removed, or if there has been a high risk for perforation. Methylene blue is also used as a dye in chromoendoscopy , and is sprayed onto the mucosa of the gastrointestinal tract in order to identify dysplasia , or pre-cancerous lesions. Intravenously injected methylene blue is readily released into the urine and thus can be used to test the urinary tract for leaks or fistulas . [ citation needed ] In surgeries such as sentinel lymph node dissections, methylene blue can be used to visually trace the lymphatic drainage of tested tissues. Similarly, methylene blue is added to bone cement in orthopedic operations to provide easy discrimination between native bone and cement. Additionally, methylene blue accelerates the hardening of bone cement, increasing the speed at which bone cement can be effectively applied. Methylene blue is used as an aid to visualisation/orientation in a number of medical devices, including a Surgical sealant film , TissuePatch. In fistulas and pilonidal sinuses it is used to identify the tract for complete excision. [ citation needed ] It can also be used during gastrointestinal surgeries (such as bowel resection or gastric bypass ) to test for leaks. [ citation needed ] It is sometimes used in cytopathology , in mixtures including Wright-Giemsa and Diff-Quik . It confers a blue color to both nuclei and cytoplasm, and makes the nuclei more visible. When methylene blue is "polychromed" (oxidized in solution or "ripened" by fungal metabolism, as originally noted in the thesis of Dr. D. L. Romanowsky in the 1890s), it gets serially demethylated and forms all the tri-, di-, mono- and non-methyl intermediates, which are Azure B , Azure A , Azure C , and thionine , respectively. This is the basis of the basophilic part of the spectrum of Romanowski-Giemsa effect. If only synthetic Azure B and Eosin Y is used, it may serve as a standardized Giemsa stain ; but, without methylene blue, the normal neutrophilic granules tend to overstain and look like toxic granules. On the other hand, if methylene blue is used it might help to give the normal look of neutrophil granules and may also enhance the staining of nucleoli and polychromatophilic RBCs (reticulocytes). A traditional application of methylene blue is the intravital or supravital staining of nerve fibers, an effect first described by Paul Ehrlich in 1887. A dilute solution of the dye is either injected into tissue or applied to small freshly removed pieces. The selective blue coloration develops with exposure to air (oxygen) and can be fixed by immersion of the stained specimen in an aqueous solution of ammonium molybdate. Vital methylene blue was formerly much used for examining the innervation of muscle, skin and internal organs. The mechanism of selective dye uptake is incompletely understood; vital staining of nerve fibers in skin is prevented by ouabain , a drug that inhibits the Na/K-ATPase of cell membranes. Methylene blue has been used as a placebo ; physicians would tell their patients to expect their urine to change color and view this as a sign that their condition had improved. This same side effect makes methylene blue difficult to use in traditional placebo-controlled clinical studies , including those testing for its efficacy as a treatment. Isobutyl nitrite is one of the compounds used as poppers , an inhalant drug that induces a brief euphoria . Isobutyl nitrite is known to cause methemoglobinemia . Severe methemoglobinemia may be treated with methylene blue. Another use of methylene blue is to treat ifosfamide neurotoxicity . Methylene blue was first reported for treatment and prophylaxis of ifosfamide neuropsychiatric toxicity in 1994. A toxic metabolite of ifosfamide, chloroacetaldehyde (CAA), disrupts the mitochondrial respiratory chain , leading to an accumulation of nicotinamide adenine dinucleotide hydrogen (NADH). Methylene blue acts as an alternative electron acceptor, and reverses the NADH inhibition of hepatic gluconeogenesis while also inhibiting the transformation of chloroethylamine into chloroacetaldehyde, and inhibits multiple amine oxidase activities, preventing the formation of CAA. The dosing of methylene blue for treatment of ifosfamide neurotoxicity varies, depending upon its use simultaneously as an adjuvant in ifosfamide infusion, versus its use to reverse psychiatric symptoms that manifest after completion of an ifosfamide infusion. Reports suggest that methylene blue up to six doses a day have resulted in improvement of symptoms within 10 minutes to several days. Alternatively, it has been suggested that intravenous methylene blue every six hours for prophylaxis during ifosfamide treatment in people with history of ifosfamide neuropsychiatric toxicity. Prophylactic administration of methylene blue the day before initiation of ifosfamide, and three times daily during ifosfamide chemotherapy has been recommended to lower the occurrence of ifosfamide neurotoxicity. It has also been used in septic shock and anaphylaxis . Methylene blue consistently increases blood pressure in people with vasoplegic syndrome (redistributive shock), but has not been shown to improve delivery of oxygen to tissues or to decrease mortality. Methylene blue has been used in calcium channel blocker toxicity as a rescue therapy for distributive shock unresponsive to first line agents. Evidence for its use in this circumstance is very poor and limited to a handful of case reports. [ excessive citations ]Methylene blue is a monoamine oxidase inhibitor (MAOI), and if infused intravenously at doses exceeding 5 mg/kg, may precipitate serious serotonin toxicity, serotonin syndrome , if combined with any selective serotonin reuptake inhibitors (SSRIs) or other serotonin reuptake inhibitor (e.g., duloxetine , sibutramine , venlafaxine , clomipramine , imipramine ). It causes hemolytic anemia in carriers of the G6PD ( favism ) enzymatic deficiency. Methylene blue is a formal derivative of phenothiazine . It is a dark green powder that yields a blue solution in water . The hydrated form has 3 molecules of water per unit of methylene blue. This compound is prepared by oxidation of 4-aminodimethylaniline in the presence of sodium thiosulfate to give the quinonediiminothiosulfonic acid, reaction with dimethylaniline, oxidation to the indamine, and cyclization to give the thiazine: A green electrochemical procedure, using only dimethyl-4-phenylenediamine and sulfide ions has been proposed. The maximum absorption of light is near 670 nm. The specifics of absorption depend on a number of factors, including protonation , adsorption to other materials, and metachromasy - the formation of dimers and higher-order aggregates depending on concentration and other interactions: This compound is prepared by oxidation of 4-aminodimethylaniline in the presence of sodium thiosulfate to give the quinonediiminothiosulfonic acid, reaction with dimethylaniline, oxidation to the indamine, and cyclization to give the thiazine: A green electrochemical procedure, using only dimethyl-4-phenylenediamine and sulfide ions has been proposed. The maximum absorption of light is near 670 nm. The specifics of absorption depend on a number of factors, including protonation , adsorption to other materials, and metachromasy - the formation of dimers and higher-order aggregates depending on concentration and other interactions: Methylene blue is widely used as a redox indicator in analytical chemistry . Solutions of this substance are blue when in an oxidizing environment, but will turn colorless if exposed to a reducing agent. The redox properties can be seen in a classical demonstration of chemical kinetics in general chemistry, the " blue bottle " experiment. Typically, a solution is made of glucose (dextrose), methylene blue, and sodium hydroxide . Upon shaking the bottle, oxygen oxidizes methylene blue, and the solution turns blue. The dextrose will gradually reduce the methylene blue to its colorless, reduced form. Hence, when the dissolved dextrose is entirely consumed, the solution will turn blue again. The redox midpoint potential E 0 ' is +0.01 V. Methylene blue is also a photosensitizer used to create singlet oxygen when exposed to both oxygen and light. It is used in this regard to make organic peroxides by a Diels-Alder reaction which is spin forbidden with normal atmospheric triplet oxygen . [ citation needed ] The formation of methylene blue after the reaction of hydrogen sulfide with dimethyl-p-phenylenediamine and iron(III) at pH 0.4 – 0.7 is used to determine by photometric measurements sulfide concentration in the range 0.020 to 1.50 mg/L (20 ppb to 1.5 ppm). The test is very sensitive and the blue coloration developing upon contact of the reagents with dissolved H 2 S is stable for 60 min. Ready-to-use kits such as the Spectroquant sulfide test facilitate routine analyses. The methylene blue sulfide test is a convenient method often used in soil microbiology to quickly detect in water the metabolic activity of sulfate reducing bacteria (SRB). It must be noted that in this colorimetric test, methylene blue is a product formed by the reaction and not a reagent added to the system. The addition of a strong reducing agent , such as ascorbic acid , to a sulfide-containing solution is sometimes used to prevent sulfide oxidation from atmospheric oxygen. Although it is certainly a sound precaution for the determination of sulfide with an ion selective electrode , it might however hamper the development of the blue color if the freshly formed methylene blue is also reduced, as described here above in the paragraph on redox indicator. Methylene blue is a dye behaving as a redox indicator that is commonly used in the food industry to test the freshness of milk and dairy products. A few drops of methylene blue solution added to a sample of milk should remain blue (oxidized form in the presence of enough dissolved O 2 ), otherwise (discoloration caused by the reduction of methylene blue into its colorless reduced form) the dissolved O 2 concentration in the milk sample is low indicating that the milk is not fresh (already abiotically oxidized by O 2 whose concentration in solution decreases) or could be contaminated by bacteria also consuming the atmospheric O 2 dissolved in the milk. In other words, aerobic conditions should prevail in fresh milk and methylene blue is simply used as an indicator of the dissolved oxygen remaining in the milk. The adsorption of methylene blue serves as an indicator defining the adsorptive capacity of granular activated carbon in water filters. Adsorption of methylene blue is very similar to adsorption of pesticides from water, this quality makes methylene blue serve as a good predictor for filtration qualities of carbon. It is as well a quick method of comparing different batches of activated carbon of the same quality. A color reaction in an acidified, aqueous methylene blue solution containing chloroform can detect anionic surfactants in a water sample. Such a test is known as an MBAS assay (methylene blue active substances assay). The MBAS assay cannot distinguish between specific surfactants, however. Some examples of anionic surfactants are carboxylates , phosphates , sulfates , and sulfonates . [ citation needed ] The methylene blue value is defined as the number of milliliter's standard methylene value solution decolorized 0.1 g of activated carbon (dry basis). Methylene blue value reflects the amount of clay minerals in aggregate samples. In materials science , methylene blue solution is successively added to fine aggregate which is being agitated in water. The presence of free dye solution can be checked with stain test on a filter paper. In biology, methylene blue is used as a dye for a number of different staining procedures, such as Wright's stain and Jenner's stain . Since it is a temporary staining technique, methylene blue can also be used to examine RNA or DNA under the microscope or in a gel: as an example, a solution of methylene blue can be used to stain RNA on hybridization membranes in northern blotting to verify the amount of nucleic acid present. While methylene blue is not as sensitive as ethidium bromide , it is less toxic and it does not intercalate in nucleic acid chains, thus avoiding interference with nucleic acid retention on hybridization membranes or with the hybridization process itself. [ citation needed ] It can also be used as an indicator to determine whether eukaryotic cells such as yeast are alive or dead. The methylene blue is reduced in viable cells, leaving them unstained. However dead cells are unable to reduce the oxidized methylene blue and the cells are stained blue. Methylene blue can interfere with the respiration of the yeast as it picks up hydrogen ions made during the process. [ citation needed ] Methylene blue is used in aquaculture and by tropical fish hobbyists as a treatment for fungal infections. It can also be effective in treating fish infected with ich although a combination of malachite green and formaldehyde is far more effective against the parasitic protozoa Ichthyophthirius multifiliis . It is usually used to protect newly laid fish eggs from being infected by fungus or bacteria. This is useful when the hobbyist wants to artificially hatch the fish eggs. Methylene blue is also very effective when used as part of a "medicated fish bath" for treatment of ammonia, nitrite, and cyanide poisoning as well as for topical and internal treatment of injured or sick fish as a "first response". Methylene blue is widely used as a redox indicator in analytical chemistry . Solutions of this substance are blue when in an oxidizing environment, but will turn colorless if exposed to a reducing agent. The redox properties can be seen in a classical demonstration of chemical kinetics in general chemistry, the " blue bottle " experiment. Typically, a solution is made of glucose (dextrose), methylene blue, and sodium hydroxide . Upon shaking the bottle, oxygen oxidizes methylene blue, and the solution turns blue. The dextrose will gradually reduce the methylene blue to its colorless, reduced form. Hence, when the dissolved dextrose is entirely consumed, the solution will turn blue again. The redox midpoint potential E 0 ' is +0.01 V. Methylene blue is also a photosensitizer used to create singlet oxygen when exposed to both oxygen and light. It is used in this regard to make organic peroxides by a Diels-Alder reaction which is spin forbidden with normal atmospheric triplet oxygen . [ citation needed ]The formation of methylene blue after the reaction of hydrogen sulfide with dimethyl-p-phenylenediamine and iron(III) at pH 0.4 – 0.7 is used to determine by photometric measurements sulfide concentration in the range 0.020 to 1.50 mg/L (20 ppb to 1.5 ppm). The test is very sensitive and the blue coloration developing upon contact of the reagents with dissolved H 2 S is stable for 60 min. Ready-to-use kits such as the Spectroquant sulfide test facilitate routine analyses. The methylene blue sulfide test is a convenient method often used in soil microbiology to quickly detect in water the metabolic activity of sulfate reducing bacteria (SRB). It must be noted that in this colorimetric test, methylene blue is a product formed by the reaction and not a reagent added to the system. The addition of a strong reducing agent , such as ascorbic acid , to a sulfide-containing solution is sometimes used to prevent sulfide oxidation from atmospheric oxygen. Although it is certainly a sound precaution for the determination of sulfide with an ion selective electrode , it might however hamper the development of the blue color if the freshly formed methylene blue is also reduced, as described here above in the paragraph on redox indicator. Methylene blue is a dye behaving as a redox indicator that is commonly used in the food industry to test the freshness of milk and dairy products. A few drops of methylene blue solution added to a sample of milk should remain blue (oxidized form in the presence of enough dissolved O 2 ), otherwise (discoloration caused by the reduction of methylene blue into its colorless reduced form) the dissolved O 2 concentration in the milk sample is low indicating that the milk is not fresh (already abiotically oxidized by O 2 whose concentration in solution decreases) or could be contaminated by bacteria also consuming the atmospheric O 2 dissolved in the milk. In other words, aerobic conditions should prevail in fresh milk and methylene blue is simply used as an indicator of the dissolved oxygen remaining in the milk. The adsorption of methylene blue serves as an indicator defining the adsorptive capacity of granular activated carbon in water filters. Adsorption of methylene blue is very similar to adsorption of pesticides from water, this quality makes methylene blue serve as a good predictor for filtration qualities of carbon. It is as well a quick method of comparing different batches of activated carbon of the same quality. A color reaction in an acidified, aqueous methylene blue solution containing chloroform can detect anionic surfactants in a water sample. Such a test is known as an MBAS assay (methylene blue active substances assay). The MBAS assay cannot distinguish between specific surfactants, however. Some examples of anionic surfactants are carboxylates , phosphates , sulfates , and sulfonates . [ citation needed ]The methylene blue value is defined as the number of milliliter's standard methylene value solution decolorized 0.1 g of activated carbon (dry basis). Methylene blue value reflects the amount of clay minerals in aggregate samples. In materials science , methylene blue solution is successively added to fine aggregate which is being agitated in water. The presence of free dye solution can be checked with stain test on a filter paper. In biology, methylene blue is used as a dye for a number of different staining procedures, such as Wright's stain and Jenner's stain . Since it is a temporary staining technique, methylene blue can also be used to examine RNA or DNA under the microscope or in a gel: as an example, a solution of methylene blue can be used to stain RNA on hybridization membranes in northern blotting to verify the amount of nucleic acid present. While methylene blue is not as sensitive as ethidium bromide , it is less toxic and it does not intercalate in nucleic acid chains, thus avoiding interference with nucleic acid retention on hybridization membranes or with the hybridization process itself. [ citation needed ] It can also be used as an indicator to determine whether eukaryotic cells such as yeast are alive or dead. The methylene blue is reduced in viable cells, leaving them unstained. However dead cells are unable to reduce the oxidized methylene blue and the cells are stained blue. Methylene blue can interfere with the respiration of the yeast as it picks up hydrogen ions made during the process. [ citation needed ]Methylene blue is used in aquaculture and by tropical fish hobbyists as a treatment for fungal infections. It can also be effective in treating fish infected with ich although a combination of malachite green and formaldehyde is far more effective against the parasitic protozoa Ichthyophthirius multifiliis . It is usually used to protect newly laid fish eggs from being infected by fungus or bacteria. This is useful when the hobbyist wants to artificially hatch the fish eggs. Methylene blue is also very effective when used as part of a "medicated fish bath" for treatment of ammonia, nitrite, and cyanide poisoning as well as for topical and internal treatment of injured or sick fish as a "first response". Methylene blue has been described as "the first fully synthetic drug used in medicine." Methylene blue was first prepared in 1876 by German chemist Heinrich Caro . Its use in the treatment of malaria was pioneered by Paul Guttmann and Paul Ehrlich in 1891. During this period before the first World War, researchers like Ehrlich believed that drugs and dyes worked in the same way, by preferentially staining pathogens and possibly harming them. Changing the cell membrane of pathogens is in fact how various drugs work, so the theory was partially correct although far from complete. Methylene blue continued to be used in the second World War, where it was not well liked by soldiers, who observed, "Even at the loo, we see, we pee, navy blue." Antimalarial use of the drug has recently been revived. It was discovered to be an antidote to carbon monoxide poisoning and cyanide poisoning in 1933 by Matilda Brooks . The blue urine was used to monitor psychiatric patients' compliance with medication regimes. This led to interest - from the 1890s to the present day - in the drug's antidepressant and other psychotropic effects. It became the lead compound in research leading to the discovery of chlorpromazine . The International Nonproprietary Name (INN) of methylene blue is methylthioninium chloride. Methylene blue was identified by Paul Ehrlich about 1891 as a possible treatment for malaria . It disappeared as an anti-malarial during the Pacific War in the tropics, since American and Allied soldiers disliked its two prominent, but reversible side effects: turning the urine blue or green, and the sclera (the whites of the eyes) blue. Interest in its use as an anti-malarial has recently been revived, especially due to its low price. Several clinical trials are in progress, trying to find a suitable drug combination. According to studies on children in Africa, it appears to have efficacy against malaria, but the attempts to combine methylene blue with chloroquine were disappointing. A Phase 3 clinical trial of LMTM (TauRx0237 or LMT-X), a derivative of methylene blue, failed to show any benefit against cognitive or functional decline in people with mild to moderate Alzheimer's disease. Disease progression for both the drug and the placebo were practically identical. Methylene blue has been studied as an adjunctive medication in the treatment of bipolar disorder . It has been studied in AIDS-related Kaposi's sarcoma , West Nile virus , and to inactivate Staphylococcus aureus , and HIV-1. Phenothiazine dyes and light have been known to have virucidal properties for over 70 years. Methylene blue was identified by Paul Ehrlich about 1891 as a possible treatment for malaria . It disappeared as an anti-malarial during the Pacific War in the tropics, since American and Allied soldiers disliked its two prominent, but reversible side effects: turning the urine blue or green, and the sclera (the whites of the eyes) blue. Interest in its use as an anti-malarial has recently been revived, especially due to its low price. Several clinical trials are in progress, trying to find a suitable drug combination. According to studies on children in Africa, it appears to have efficacy against malaria, but the attempts to combine methylene blue with chloroquine were disappointing. A Phase 3 clinical trial of LMTM (TauRx0237 or LMT-X), a derivative of methylene blue, failed to show any benefit against cognitive or functional decline in people with mild to moderate Alzheimer's disease. Disease progression for both the drug and the placebo were practically identical. Methylene blue has been studied as an adjunctive medication in the treatment of bipolar disorder . It has been studied in AIDS-related Kaposi's sarcoma , West Nile virus , and to inactivate Staphylococcus aureus , and HIV-1. Phenothiazine dyes and light have been known to have virucidal properties for over 70 years.

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Yellow fever

Yellow fever is a viral disease of typically short duration . In most cases, symptoms include fever , chills , loss of appetite , nausea , muscle pains—particularly in the back—and headaches . Symptoms typically improve within five days. In about 15% of people, within a day of improving the fever comes back, abdominal pain occurs, and liver damage begins causing yellow skin . If this occurs, the risk of bleeding and kidney problems is increased. The disease is caused by the yellow fever virus and is spread by the bite of an infected mosquito . It infects humans, other primates , and several types of mosquitoes. In cities, it is spread primarily by Aedes aegypti , a type of mosquito found throughout the tropics and subtropics . The virus is an RNA virus of the genus Flavivirus . The disease may be difficult to tell apart from other illnesses, especially in the early stages. To confirm a suspected case, blood-sample testing with a polymerase chain reaction is required. A safe and effective vaccine against yellow fever exists, and some countries require vaccinations for travelers. Other efforts to prevent infection include reducing the population of the transmitting mosquitoes. In areas where yellow fever is common, early diagnosis of cases and immunization of large parts of the population are important to prevent outbreaks . Once a person is infected, management is symptomatic; no specific measures are effective against the virus. Death occurs in up to half of those who get severe disease. In 2013, yellow fever was estimated to have caused 130,000 severe infections and 78,000 deaths in Africa. Approximately 90 percent of an estimated 200,000 cases of yellow fever per year occur in Africa. Nearly a billion people live in an area of the world where the disease is common. It is common in tropical areas of the continents of South America and Africa, but not in Asia. Since the 1980s, the number of cases of yellow fever has been increasing. This is believed to be due to fewer people being immune, more people living in cities, people moving frequently, and changing climate increasing the habitat for mosquitoes. The disease originated in Africa and spread to the Americas starting in the 17th century with the European trafficking of enslaved Africans from sub-Saharan Africa. Since the 17th century, several major outbreaks of the disease have occurred in the Americas, Africa, and Europe. In the 18th and 19th centuries, yellow fever was considered one of the most dangerous infectious diseases ; numerous epidemics swept through major cities of the US and in other parts of the world. In 1927, yellow fever virus became the first human virus to be isolated. Yellow fever begins after an incubation period of three to six days. Most cases cause only mild infection with fever, headache, chills, back pain, fatigue, loss of appetite, muscle pain, nausea, and vomiting. In these cases, the infection lasts only three to six days. But in 15% of cases, people enter a second, toxic phase of the disease characterized by recurring fever, this time accompanied by jaundice due to liver damage , as well as abdominal pain . Bleeding in the mouth, nose, eyes, and the gastrointestinal tract cause vomit containing blood , hence one of the names in Spanish for yellow fever, vómito negro ("black vomit"). There may also be kidney failure, hiccups, and delirium. Among those who develop jaundice, the fatality rate is 20 to 50%, while the overall fatality rate is about 3 to 7.5%. Severe cases may have a mortality rate greater than 50%. Surviving the infection provides lifelong immunity , and normally results in no permanent organ damage. Yellow fever can lead to death for 20% to 50% of those who develop severe disease. Jaundice, fatigue, heart rhythm problems, seizures and internal bleeding may also appear as complications of yellow fever during recovery time. Yellow fever can lead to death for 20% to 50% of those who develop severe disease. Jaundice, fatigue, heart rhythm problems, seizures and internal bleeding may also appear as complications of yellow fever during recovery time. {| class="infobox biota" style="text-align: left; width: 200px; font-size: 100%" |- ! Yellow fever virus |- | |- | Flavivirus structure and genome |- |- |- |- ! Virus classification |- |(unranked): | Virus |- | Realm : | Riboviria |- |Kingdom: | Orthornavirae |- |Phylum: | Kitrinoviricota |- |Class: | Flasuviricetes |- |Order: | Amarillovirales |- |Family: | Flaviviridae |- |Genus: | Flavivirus |- | Species: | |- |- |- |- |- |- |- |- |- |- |- |- |- |- |- |} Yellow fever is caused by Yellow fever virus (YFV), an enveloped RNA virus 40–50 nm in width, the type species and namesake of the family Flaviviridae . It was the first illness shown to be transmissible by filtered human serum and transmitted by mosquitoes, by American doctor Walter Reed around 1900. The positive- sense , single-stranded RNA is around 10,862 nucleotides long and has a single open reading frame encoding a polyprotein . Host proteases cut this polyprotein into three structural (C, prM, E) and seven nonstructural proteins (NS1, NS2A, NS2B, NS3, NS4A, NS4B, NS5); the enumeration corresponds to the arrangement of the protein coding genes in the genome . Minimal YFV 3 ′ UTR region is required for stalling of the host 5 ′ -3 ′ exonuclease XRN1. The UTR contains PKS3 pseudoknot structure, which serves as a molecular signal to stall the exonuclease and is the only viral requirement for subgenomic flavivirus RNA (sfRNA) production. The sfRNAs are a result of incomplete degradation of the viral genome by the exonuclease and are important for viral pathogenicity. Yellow fever belongs to the group of hemorrhagic fevers . The viruses infect, amongst others, monocytes , macrophages , Schwann cells , and dendritic cells . They attach to the cell surfaces via specific receptors and are taken up by an endosomal vesicle . Inside the endosome , the decreased pH induces the fusion of the endosomal membrane with the virus envelope . The capsid enters the cytosol , decays, and releases the genome. Receptor binding, as well as membrane fusion, are catalyzed by the protein E, which changes its conformation at low pH, causing a rearrangement of the 90 homo dimers to 60 homo trimers . After entering the host cell, the viral genome is replicated in the rough endoplasmic reticulum (ER) and in the so-called vesicle packets. At first, an immature form of the virus particle is produced inside the ER, whose M-protein is not yet cleaved to its mature form, so is denoted as precursor M (prM) and forms a complex with protein E. The immature particles are processed in the Golgi apparatus by the host protein furin , which cleaves prM to M. This releases E from the complex, which can now take its place in the mature, infectious virion . Yellow fever virus is mainly transmitted through the bite of the yellow fever mosquito Aedes aegypti , but other mostly Aedes mosquitoes such as the tiger mosquito ( Aedes albopictus ) can also serve as a vector for this virus. Like other arboviruses , which are transmitted by mosquitoes, yellow fever virus is taken up by a female mosquito when it ingests the blood of an infected human or another primate. Viruses reach the stomach of the mosquito, and if the virus concentration is high enough, the virions can infect epithelial cells and replicate there. From there, they reach the haemocoel (the blood system of mosquitoes) and from there the salivary glands . When the mosquito next sucks blood, it injects its saliva into the wound, and the virus reaches the bloodstream of the bitten person. Transovarial transmissionial and transstadial transmission of yellow fever virus within A. aegypti , that is, the transmission from a female mosquito to its eggs and then larvae, are indicated. This infection of vectors without a previous blood meal seems to play a role in single, sudden breakouts of the disease. Three epidemiologically different infectious cycles occur in which the virus is transmitted from mosquitoes to humans or other primates. In the "urban cycle", only the yellow fever mosquito A. aegypti is involved. It is well adapted to urban areas, and can also transmit other diseases, including Zika fever , dengue fever , and chikungunya . The urban cycle is responsible for the major outbreaks of yellow fever that occur in Africa. Except for an outbreak in Bolivia in 1999, this urban cycle no longer exists in South America. Besides the urban cycle, both in Africa and South America, a sylvatic cycle (forest or jungle cycle) is present, where Aedes africanus (in Africa) or mosquitoes of the genus Haemagogus and Sabethes (in South America) serve as vectors. In the jungle, the mosquitoes infect mainly nonhuman primates; the disease is mostly asymptomatic in African primates. In South America, the sylvatic cycle is currently the only way unvaccinated humans can become infected, which explains the low incidence of yellow fever cases on the continent. People who become infected in the jungle can carry the virus to urban areas, where A. aegypti acts as a vector. Because of this sylvatic cycle, yellow fever cannot be eradicated except by eradicating the mosquitoes that serve as vectors. In Africa, a third infectious cycle known as "savannah cycle" or intermediate cycle, occurs between the jungle and urban cycles. Different mosquitoes of the genus Aedes are involved. In recent years, this has been the most common form of transmission of yellow fever in Africa. Concern exists about yellow fever spreading to southeast Asia, where its vector A. aegypti already occurs. Yellow fever virus is mainly transmitted through the bite of the yellow fever mosquito Aedes aegypti , but other mostly Aedes mosquitoes such as the tiger mosquito ( Aedes albopictus ) can also serve as a vector for this virus. Like other arboviruses , which are transmitted by mosquitoes, yellow fever virus is taken up by a female mosquito when it ingests the blood of an infected human or another primate. Viruses reach the stomach of the mosquito, and if the virus concentration is high enough, the virions can infect epithelial cells and replicate there. From there, they reach the haemocoel (the blood system of mosquitoes) and from there the salivary glands . When the mosquito next sucks blood, it injects its saliva into the wound, and the virus reaches the bloodstream of the bitten person. Transovarial transmissionial and transstadial transmission of yellow fever virus within A. aegypti , that is, the transmission from a female mosquito to its eggs and then larvae, are indicated. This infection of vectors without a previous blood meal seems to play a role in single, sudden breakouts of the disease. Three epidemiologically different infectious cycles occur in which the virus is transmitted from mosquitoes to humans or other primates. In the "urban cycle", only the yellow fever mosquito A. aegypti is involved. It is well adapted to urban areas, and can also transmit other diseases, including Zika fever , dengue fever , and chikungunya . The urban cycle is responsible for the major outbreaks of yellow fever that occur in Africa. Except for an outbreak in Bolivia in 1999, this urban cycle no longer exists in South America. Besides the urban cycle, both in Africa and South America, a sylvatic cycle (forest or jungle cycle) is present, where Aedes africanus (in Africa) or mosquitoes of the genus Haemagogus and Sabethes (in South America) serve as vectors. In the jungle, the mosquitoes infect mainly nonhuman primates; the disease is mostly asymptomatic in African primates. In South America, the sylvatic cycle is currently the only way unvaccinated humans can become infected, which explains the low incidence of yellow fever cases on the continent. People who become infected in the jungle can carry the virus to urban areas, where A. aegypti acts as a vector. Because of this sylvatic cycle, yellow fever cannot be eradicated except by eradicating the mosquitoes that serve as vectors. In Africa, a third infectious cycle known as "savannah cycle" or intermediate cycle, occurs between the jungle and urban cycles. Different mosquitoes of the genus Aedes are involved. In recent years, this has been the most common form of transmission of yellow fever in Africa. Concern exists about yellow fever spreading to southeast Asia, where its vector A. aegypti already occurs. After transmission from a mosquito, the viruses replicate in the lymph nodes and infect dendritic cells in particular. From there, they reach the liver and infect hepatocytes (probably indirectly via Kupffer cells ), which leads to eosinophilic degradation of these cells and to the release of cytokines . Apoptotic masses known as Councilman bodies appear in the cytoplasm of hepatocytes. Fatality may occur when cytokine storm , shock , and multiple organ failure follow. Yellow fever is most frequently a clinical diagnosis , based on symptomatology and travel history. Mild cases of the disease can only be confirmed virologically. Since mild cases of yellow fever can also contribute significantly to regional outbreaks, every suspected case of yellow fever (involving symptoms of fever, pain, nausea, and vomiting 6–10 days after leaving the affected area) is treated seriously. If yellow fever is suspected, the virus cannot be confirmed until 6–10 days following the illness. A direct confirmation can be obtained by reverse transcription polymerase chain reaction , where the genome of the virus is amplified. Another direct approach is the isolation of the virus and its growth in cell culture using blood plasma ; this can take 1–4 weeks. Serologically, an enzyme-linked immunosorbent assay during the acute phase of the disease using specific IgM against yellow fever or an increase in specific IgG titer (compared to an earlier sample) can confirm yellow fever. Together with clinical symptoms, the detection of IgM or a four-fold increase in IgG titer is considered sufficient indication for yellow fever. As these tests can cross-react with other flaviviruses, such as dengue virus , these indirect methods cannot conclusively prove yellow fever infection. Liver biopsy can verify inflammation and necrosis of hepatocytes and detect viral antigens . Because of the bleeding tendency of yellow fever patients, a biopsy is only advisable post mortem to confirm the cause of death. In a differential diagnosis , infections with yellow fever must be distinguished from other feverish illnesses such as malaria . Other viral hemorrhagic fevers , such as Ebola virus , Lassa virus , Marburg virus , and Junin virus , must be excluded as the cause. Personal prevention of yellow fever includes vaccination and avoidance of mosquito bites in areas where yellow fever is endemic. Institutional measures for prevention of yellow fever include vaccination programmes and measures to control mosquitoes. Programmes for distribution of mosquito nets for use in homes produce reductions in cases of both malaria and yellow fever. Use of EPA-registered insect repellent is recommended when outdoors. Exposure for even a short time is enough for a potential mosquito bite. Long-sleeved clothing, long pants, and socks are useful for prevention. The application of larvicides to water-storage containers can help eliminate potential mosquito breeding sites. EPA-registered insecticide spray decreases the transmission of yellow fever. Vaccination is recommended for those traveling to affected areas, because non-native people tend to develop more severe illness when infected. Protection begins by the 10th day after vaccine administration in 95% of people, and had been reported to last for at least 10 years. The World Health Organization (WHO) now states that a single dose of vaccine is sufficient to confer lifelong immunity against yellow fever disease. The attenuated live vaccine stem 17D was developed in 1937 by Max Theiler . The WHO recommends routine vaccination for people living in affected areas between the 9th and 12th month after birth. Up to one in four people experience fever, aches, and local soreness and redness at the site of injection. In rare cases (less than one in 200,000 to 300,000), the vaccination can cause yellow fever vaccine-associated viscerotropic disease, which is fatal in 60% of cases. It is probably due to the genetic morphology of the immune system. Another possible side effect is an infection of the nervous system, which occurs in one in 200,000 to 300,000 cases, causing yellow fever vaccine-associated neurotropic disease, which can lead to meningoencephalitis and is fatal in less than 5% of cases. The Yellow Fever Initiative, launched by the WHO in 2006, vaccinated more than 105 million people in 14 countries in West Africa. No outbreaks were reported during 2015. The campaign was supported by the GAVI alliance and governmental organizations in Europe and Africa. According to the WHO, mass vaccination cannot eliminate yellow fever because of the vast number of infected mosquitoes in urban areas of the target countries, but it will significantly reduce the number of people infected. Demand for yellow fever vaccine has continued to increase due to the growing number of countries implementing yellow fever vaccination as part of their routine immunization programmes. Recent upsurges in yellow fever outbreaks in Angola (2015), the Democratic Republic of Congo (2016), Uganda (2016), and more recently in Nigeria and Brazil in 2017 have further increased demand, while straining global vaccine supply. Therefore, to vaccinate susceptible populations in preventive mass immunization campaigns during outbreaks, fractional dosing of the vaccine is being considered as a dose-sparing strategy to maximize limited vaccine supplies. Fractional dose yellow fever vaccination refers to administration of a reduced volume of vaccine dose, which has been reconstituted as per manufacturer recommendations. The first practical use of fractional dose yellow fever vaccination was in response to a large yellow fever outbreak in the Democratic Republic of the Congo in mid-2016. Available evidence shows that fractional dose yellow fever vaccination induces a level of immune response similar to that of the standard full dose. In March 2017, the WHO launched a vaccination campaign in Brazil with 3.5 million doses from an emergency stockpile. In March 2017 the WHO recommended vaccination for travellers to certain parts of Brazil. In March 2018, Brazil shifted its policy and announced it planned to vaccinate all 77.5 million currently unvaccinated citizens by April 2019. Some countries in Asia are considered to be potentially in danger of yellow fever epidemics, as both mosquitoes with the capability to transmit yellow fever as well as susceptible monkeys are present. The disease does not yet occur in Asia. To prevent introduction of the virus, some countries demand previous vaccination of foreign visitors who have passed through yellow fever areas. Vaccination has to be proved by a vaccination certificate, which is valid 10 days after the vaccination and lasts for 10 years. Although the WHO on 17 May 2013 advised that subsequent booster vaccinations are unnecessary, an older (than 10 years) certificate may not be acceptable at all border posts in all affected countries. A list of the countries that require yellow fever vaccination is published by the WHO. If the vaccination cannot be given for some reason, dispensation may be possible. In this case, an exemption certificate issued by a WHO-approved vaccination center is required. Although 32 of 44 countries where yellow fever occurs endemically do have vaccination programmes, in many of these countries, less than 50% of their population is vaccinated. Control of the yellow fever mosquito A. aegypti is of major importance, especially because the same mosquito can also transmit dengue fever and chikungunya disease. A. aegypti breeds preferentially in water, for example, in installations by inhabitants of areas with precarious drinking water supplies, or in domestic refuse, especially tires, cans, and plastic bottles. These conditions are common in urban areas in developing countries. Two main strategies are employed to reduce A. aegypti populations. One approach is to kill the developing larvae. Measures are taken to reduce the water accumulations in which the larvae develop. Larvicides are used, along with larvae-eating fish and copepods , which reduce the number of larvae. For many years, copepods of the genus Mesocyclops have been used in Vietnam for preventing dengue fever. This eradicated the mosquito vector in several areas. Similar efforts may prove effective against yellow fever. Pyriproxyfen is recommended as a chemical larvicide, mainly because it is safe for humans and effective in small doses. The second strategy is to reduce populations of the adult yellow fever mosquito. Lethal ovitraps can reduce Aedes populations, using lesser amounts of pesticide because it targets the pest directly. Curtains and lids of water tanks can be sprayed with insecticides, but application inside houses is not recommended by the WHO. Insecticide-treated mosquito nets are effective, just as they are against the Anopheles mosquito that carries malaria. Vaccination is recommended for those traveling to affected areas, because non-native people tend to develop more severe illness when infected. Protection begins by the 10th day after vaccine administration in 95% of people, and had been reported to last for at least 10 years. The World Health Organization (WHO) now states that a single dose of vaccine is sufficient to confer lifelong immunity against yellow fever disease. The attenuated live vaccine stem 17D was developed in 1937 by Max Theiler . The WHO recommends routine vaccination for people living in affected areas between the 9th and 12th month after birth. Up to one in four people experience fever, aches, and local soreness and redness at the site of injection. In rare cases (less than one in 200,000 to 300,000), the vaccination can cause yellow fever vaccine-associated viscerotropic disease, which is fatal in 60% of cases. It is probably due to the genetic morphology of the immune system. Another possible side effect is an infection of the nervous system, which occurs in one in 200,000 to 300,000 cases, causing yellow fever vaccine-associated neurotropic disease, which can lead to meningoencephalitis and is fatal in less than 5% of cases. The Yellow Fever Initiative, launched by the WHO in 2006, vaccinated more than 105 million people in 14 countries in West Africa. No outbreaks were reported during 2015. The campaign was supported by the GAVI alliance and governmental organizations in Europe and Africa. According to the WHO, mass vaccination cannot eliminate yellow fever because of the vast number of infected mosquitoes in urban areas of the target countries, but it will significantly reduce the number of people infected. Demand for yellow fever vaccine has continued to increase due to the growing number of countries implementing yellow fever vaccination as part of their routine immunization programmes. Recent upsurges in yellow fever outbreaks in Angola (2015), the Democratic Republic of Congo (2016), Uganda (2016), and more recently in Nigeria and Brazil in 2017 have further increased demand, while straining global vaccine supply. Therefore, to vaccinate susceptible populations in preventive mass immunization campaigns during outbreaks, fractional dosing of the vaccine is being considered as a dose-sparing strategy to maximize limited vaccine supplies. Fractional dose yellow fever vaccination refers to administration of a reduced volume of vaccine dose, which has been reconstituted as per manufacturer recommendations. The first practical use of fractional dose yellow fever vaccination was in response to a large yellow fever outbreak in the Democratic Republic of the Congo in mid-2016. Available evidence shows that fractional dose yellow fever vaccination induces a level of immune response similar to that of the standard full dose. In March 2017, the WHO launched a vaccination campaign in Brazil with 3.5 million doses from an emergency stockpile. In March 2017 the WHO recommended vaccination for travellers to certain parts of Brazil. In March 2018, Brazil shifted its policy and announced it planned to vaccinate all 77.5 million currently unvaccinated citizens by April 2019. Some countries in Asia are considered to be potentially in danger of yellow fever epidemics, as both mosquitoes with the capability to transmit yellow fever as well as susceptible monkeys are present. The disease does not yet occur in Asia. To prevent introduction of the virus, some countries demand previous vaccination of foreign visitors who have passed through yellow fever areas. Vaccination has to be proved by a vaccination certificate, which is valid 10 days after the vaccination and lasts for 10 years. Although the WHO on 17 May 2013 advised that subsequent booster vaccinations are unnecessary, an older (than 10 years) certificate may not be acceptable at all border posts in all affected countries. A list of the countries that require yellow fever vaccination is published by the WHO. If the vaccination cannot be given for some reason, dispensation may be possible. In this case, an exemption certificate issued by a WHO-approved vaccination center is required. Although 32 of 44 countries where yellow fever occurs endemically do have vaccination programmes, in many of these countries, less than 50% of their population is vaccinated. Some countries in Asia are considered to be potentially in danger of yellow fever epidemics, as both mosquitoes with the capability to transmit yellow fever as well as susceptible monkeys are present. The disease does not yet occur in Asia. To prevent introduction of the virus, some countries demand previous vaccination of foreign visitors who have passed through yellow fever areas. Vaccination has to be proved by a vaccination certificate, which is valid 10 days after the vaccination and lasts for 10 years. Although the WHO on 17 May 2013 advised that subsequent booster vaccinations are unnecessary, an older (than 10 years) certificate may not be acceptable at all border posts in all affected countries. A list of the countries that require yellow fever vaccination is published by the WHO. If the vaccination cannot be given for some reason, dispensation may be possible. In this case, an exemption certificate issued by a WHO-approved vaccination center is required. Although 32 of 44 countries where yellow fever occurs endemically do have vaccination programmes, in many of these countries, less than 50% of their population is vaccinated. Control of the yellow fever mosquito A. aegypti is of major importance, especially because the same mosquito can also transmit dengue fever and chikungunya disease. A. aegypti breeds preferentially in water, for example, in installations by inhabitants of areas with precarious drinking water supplies, or in domestic refuse, especially tires, cans, and plastic bottles. These conditions are common in urban areas in developing countries. Two main strategies are employed to reduce A. aegypti populations. One approach is to kill the developing larvae. Measures are taken to reduce the water accumulations in which the larvae develop. Larvicides are used, along with larvae-eating fish and copepods , which reduce the number of larvae. For many years, copepods of the genus Mesocyclops have been used in Vietnam for preventing dengue fever. This eradicated the mosquito vector in several areas. Similar efforts may prove effective against yellow fever. Pyriproxyfen is recommended as a chemical larvicide, mainly because it is safe for humans and effective in small doses. The second strategy is to reduce populations of the adult yellow fever mosquito. Lethal ovitraps can reduce Aedes populations, using lesser amounts of pesticide because it targets the pest directly. Curtains and lids of water tanks can be sprayed with insecticides, but application inside houses is not recommended by the WHO. Insecticide-treated mosquito nets are effective, just as they are against the Anopheles mosquito that carries malaria. As with other Flavivirus infections, no cure is known for yellow fever. Hospitalization is advisable and intensive care may be necessary because of rapid deterioration in some cases. Certain acute treatment methods lack efficacy: passive immunization after the emergence of symptoms is probably without effect; ribavirin and other antiviral drugs , as well as treatment with interferons , are ineffective in yellow fever patients. Symptomatic treatment includes rehydration and pain relief with drugs such as paracetamol (acetaminophen). However, aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) are often avoided because of an increased risk of gastrointestinal bleeding due to their anticoagulant effects. Yellow fever is common in tropical and subtropical areas of South America and Africa. Worldwide, about 600 million people live in endemic areas. The WHO estimates 200,000 cases of yellow fever worldwide each year. About 15% of people infected with yellow fever progress to a severe form of the illness, and up to half of those will die, as there is no cure for yellow fever. An estimated 90% of yellow fever infections occur on the African continent. In 2016, a large outbreak originated in Angola and spread to neighboring countries before being contained by a massive vaccination campaign. In March and April 2016, 11 imported cases of the Angola genotype in unvaccinated Chinese nationals were reported in China, the first appearance of the disease in Asia in recorded history. Phylogenetic analysis has identified seven genotypes of yellow fever viruses, and they are assumed to be differently adapted to humans and to the vector A. aegypti . Five genotypes (Angola, Central/East Africa, East Africa, West Africa I, and West Africa II) occur only in Africa. West Africa genotype I is found in Nigeria and the surrounding region. West Africa genotype I appears to be especially infectious, as it is often associated with major outbreaks. The three genotypes found outside of Nigeria and Angola occur in areas where outbreaks are rare. Two outbreaks, in Kenya (1992–1993) and Sudan (2003 and 2005), involved the East African genotype, which had remained undetected in the previous 40 years. In South America, two genotypes have been identified (South American genotypes I and II). Based on phylogenetic analysis these two genotypes appear to have originated in West Africa and were first introduced into Brazil. The date of introduction of the predecessor African genotype which gave rise to the South American genotypes appears to be 1822 (95% confidence interval 1701 to 1911). The historical record shows an outbreak of yellow fever occurred in Recife, Brazil, between 1685 and 1690. The disease seems to have disappeared, with the next outbreak occurring in 1849. It was likely introduced with the trafficking of slaves through the slave trade from Africa. Genotype I has been divided into five subclades, A through E. In late 2016, a large outbreak began in Minas Gerais state of Brazil that was characterized as a sylvatic or jungle epizootic . Real-time phylogenetic investigations at the epicentre of the outbreak revealed that the outbreak was caused by the introduction of a virus lineage from the Amazon region into the southeast region around July 2016, spreading rapidly across several neotropical monkey species, including brown howler monkeys, which serve as a sentinel species for yellow fever. No cases had been transmitted between humans by the A. aegypti mosquito, which can sustain urban outbreaks that can spread rapidly. In April 2017, the sylvatic outbreak continued moving toward the Brazilian coast, where most people were unvaccinated. By the end of May the outbreak appeared to be declining after more than 3,000 suspected cases, 758 confirmed and 264 deaths confirmed to be yellow fever. The Health Ministry launched a vaccination campaign and was concerned about spread during the Carnival season in February and March. The CDC issued a Level 2 alert (practice enhanced precautions.) A Bayesian analysis of genotypes I and II has shown that genotype I accounts for virtually all the current infections in Brazil , Colombia , Venezuela , and Trinidad and Tobago , while genotype II accounted for all cases in Peru . Genotype I originated in the northern Brazilian region around 1908 (95% highest posterior density interval [HPD]: 1870–1936). Genotype II originated in Peru in 1920 (95% HPD: 1867–1958). The estimated rate of mutation for both genotypes was about 5 × 10 −4 substitutions/site/year, similar to that of other RNA viruses. The main vector ( A. aegypti ) also occurs in tropical and subtropical regions of Asia, the Pacific, and Australia, but yellow fever had never occurred there until jet travel introduced 11 cases from the 2016 Angola and DR Congo yellow fever outbreak in Africa. Proposed explanations include: But none is considered satisfactory. Another proposal is the absence of a slave trade to Asia on the scale of that to the Americas. The trans-Atlantic slave trade probably introduced yellow fever into the Western Hemisphere from Africa. An estimated 90% of yellow fever infections occur on the African continent. In 2016, a large outbreak originated in Angola and spread to neighboring countries before being contained by a massive vaccination campaign. In March and April 2016, 11 imported cases of the Angola genotype in unvaccinated Chinese nationals were reported in China, the first appearance of the disease in Asia in recorded history. Phylogenetic analysis has identified seven genotypes of yellow fever viruses, and they are assumed to be differently adapted to humans and to the vector A. aegypti . Five genotypes (Angola, Central/East Africa, East Africa, West Africa I, and West Africa II) occur only in Africa. West Africa genotype I is found in Nigeria and the surrounding region. West Africa genotype I appears to be especially infectious, as it is often associated with major outbreaks. The three genotypes found outside of Nigeria and Angola occur in areas where outbreaks are rare. Two outbreaks, in Kenya (1992–1993) and Sudan (2003 and 2005), involved the East African genotype, which had remained undetected in the previous 40 years. In South America, two genotypes have been identified (South American genotypes I and II). Based on phylogenetic analysis these two genotypes appear to have originated in West Africa and were first introduced into Brazil. The date of introduction of the predecessor African genotype which gave rise to the South American genotypes appears to be 1822 (95% confidence interval 1701 to 1911). The historical record shows an outbreak of yellow fever occurred in Recife, Brazil, between 1685 and 1690. The disease seems to have disappeared, with the next outbreak occurring in 1849. It was likely introduced with the trafficking of slaves through the slave trade from Africa. Genotype I has been divided into five subclades, A through E. In late 2016, a large outbreak began in Minas Gerais state of Brazil that was characterized as a sylvatic or jungle epizootic . Real-time phylogenetic investigations at the epicentre of the outbreak revealed that the outbreak was caused by the introduction of a virus lineage from the Amazon region into the southeast region around July 2016, spreading rapidly across several neotropical monkey species, including brown howler monkeys, which serve as a sentinel species for yellow fever. No cases had been transmitted between humans by the A. aegypti mosquito, which can sustain urban outbreaks that can spread rapidly. In April 2017, the sylvatic outbreak continued moving toward the Brazilian coast, where most people were unvaccinated. By the end of May the outbreak appeared to be declining after more than 3,000 suspected cases, 758 confirmed and 264 deaths confirmed to be yellow fever. The Health Ministry launched a vaccination campaign and was concerned about spread during the Carnival season in February and March. The CDC issued a Level 2 alert (practice enhanced precautions.) A Bayesian analysis of genotypes I and II has shown that genotype I accounts for virtually all the current infections in Brazil , Colombia , Venezuela , and Trinidad and Tobago , while genotype II accounted for all cases in Peru . Genotype I originated in the northern Brazilian region around 1908 (95% highest posterior density interval [HPD]: 1870–1936). Genotype II originated in Peru in 1920 (95% HPD: 1867–1958). The estimated rate of mutation for both genotypes was about 5 × 10 −4 substitutions/site/year, similar to that of other RNA viruses. The main vector ( A. aegypti ) also occurs in tropical and subtropical regions of Asia, the Pacific, and Australia, but yellow fever had never occurred there until jet travel introduced 11 cases from the 2016 Angola and DR Congo yellow fever outbreak in Africa. Proposed explanations include: But none is considered satisfactory. Another proposal is the absence of a slave trade to Asia on the scale of that to the Americas. The trans-Atlantic slave trade probably introduced yellow fever into the Western Hemisphere from Africa. The evolutionary origins of yellow fever most likely lie in Africa, with transmission of the disease from nonhuman primates to humans. The virus is thought to have originated in East or Central Africa and spread from there to West Africa. As it was endemic in Africa, local populations had developed some immunity to it. When an outbreak of yellow fever would occur in an African community where colonists resided, most Europeans died, while the indigenous Africans usually developed nonlethal symptoms resembling influenza . This phenomenon, in which certain populations develop immunity to yellow fever due to prolonged exposure in their childhood, is known as acquired immunity . The virus, as well as the vector A. aegypti, were probably transferred to North and South America with the trafficking of slaves from Africa, part of the Columbian exchange following European exploration and colonization. However, some researchers have argued that yellow fever might have existed in the Americas during the pre-Columbian period as mosquitoes of the genus Haemagogus , which is indigenous to the Americas, have been known to carry the disease. The first definitive outbreak of yellow fever in the New World was in 1647 on the island of Barbados . An outbreak was recorded by Spanish colonists in 1648 in the Yucatán Peninsula , where the indigenous Mayan people called the illness xekik ("blood vomit"). In 1685, Brazil suffered its first epidemic in Recife . The first mention of the disease by the name "yellow fever" occurred in 1744. However, Dr. Mitchell misdiagnosed the disease that he observed and treated, and the disease was probably Weil's disease or hepatitis. McNeill argues that the environmental and ecological disruption caused by the introduction of sugar plantations created the conditions for mosquito and viral reproduction, and subsequent outbreaks of yellow fever. Deforestation reduced populations of insectivorous birds and other creatures that fed on mosquitoes and their eggs. In Colonial times and during the Napoleonic Wars , the West Indies were known as a particularly dangerous posting for soldiers due to yellow fever being endemic in the area. The mortality rate in British garrisons in Jamaica was seven times that of garrisons in Canada, mostly because of yellow fever and other tropical diseases. Both English and French forces posted there were seriously affected by the "yellow jack" . Wanting to regain control of the lucrative sugar trade in Saint-Domingue (Hispaniola), and with an eye on regaining France's New World empire, Napoleon sent an army under the command of his brother-in-law General Charles Leclerc to Saint-Domingue to seize control after a slave revolt. The historian J. R. McNeill asserts that yellow fever accounted for about 35,000 to 45,000 casualties of these forces during the fighting. Only one third of the French troops survived for withdrawal and return to France. Napoleon gave up on the island and his plans for North America, selling the Louisiana Purchase to the US in 1803. In 1804, Haiti proclaimed its independence as the second republic in the Western Hemisphere. Considerable debate exists over whether the number of deaths caused by disease in the Haitian Revolution was exaggerated. Although yellow fever is most prevalent in tropical-like climates, the northern United States were not exempted from the fever. The first outbreak in English-speaking North America occurred in New York City in 1668. English colonists in Philadelphia and the French in the Mississippi River Valley recorded major outbreaks in 1669, as well as additional yellow fever epidemics in Philadelphia, Baltimore , and New York City in the 18th and 19th centuries. The disease traveled along steamboat routes from New Orleans, causing some 100,000–150,000 deaths in total. The yellow fever epidemic of 1793 in Philadelphia, which was then the capital of the United States, resulted in the deaths of several thousand people, more than 9% of the population. One of these deaths was James Hutchinson , a physician helping to treat the population of the city. The national government fled the city to Trenton, New Jersey, including President George Washington . The southern city of New Orleans was plagued with major epidemics during the 19th century, most notably in 1833 and 1853. A major epidemic occurred in both New Orleans and Shreveport, Louisiana in 1873. Its residents called the disease "yellow jack". Urban epidemics continued in the United States until 1905, with the last outbreak affecting New Orleans. At least 25 major outbreaks took place in the Americas during the 18th and 19th centuries, including particularly serious ones in Cartagena, Chile , in 1741; Cuba in 1762 and 1900; Santo Domingo in 1803; and Memphis, Tennessee , in 1878. In the early 19th century, the prevalence of yellow fever in the Caribbean "led to serious health problems" and alarmed the United States Navy as numerous deaths and sickness curtailed naval operations and destroyed morale. One episode began in April 1822 when the frigate USS Macedonian left Boston and became part of Commodore James Biddle's West India Squadron. Unbeknownst to all, they were about to embark on a cruise to disaster and their assignment "would prove a cruise through hell". Secretary of the Navy Smith Thompson had assigned the squadron to guard United States merchant shipping and suppress piracy. During their time on deployment from 26 May to 3 August 1822, 76 of the Macedonian's officers and men died, including John Cadle, surgeon USN. Seventy-four of these deaths were attributed to yellow fever. Biddle reported that another 52 of his crew were on sick-list. In their report to the secretary of the Navy, Biddle and Surgeon's Mate Charles Chase stated the cause as "fever". As a consequence of this loss, Biddle noted that his squadron was forced to return to Norfolk Navy Yard early. Upon arrival, the Macedonian's crew were provided medical care and quarantined at Craney Island, Virginia. In 1853, Cloutierville, Louisiana , had a late-summer outbreak of yellow fever that quickly killed 68 of the 91 inhabitants. A local doctor concluded that some unspecified infectious agent had arrived in a package from New Orleans. In 1854, 650 residents of Savannah, Georgia , died from yellow fever. In 1858, St. Matthew's German Evangelical Lutheran Church in Charleston, South Carolina , had 308 yellow fever deaths, reducing the congregation by half. A ship carrying persons infected with the virus arrived in Hampton Roads in southeastern Virginia in June 1855. The disease spread quickly through the community, eventually killing over 3,000 people, mostly residents of Norfolk and Portsmouth . In 1873, Shreveport, Louisiana , lost 759 citizens in an 80-day period to a yellow fever epidemic, with over 400 additional victims eventually succumbing. The total death toll from August through November was approximately 1,200. In 1878, about 20,000 people died in a widespread epidemic in the Mississippi River Valley. That year, Memphis had an unusually large amount of rain, which led to an increase in the mosquito population. The result was a huge epidemic of yellow fever. The steamship John D. Porter took people fleeing Memphis northward in hopes of escaping the disease, but passengers were not allowed to disembark due to concerns of spreading yellow fever. The ship roamed the Mississippi River for the next two months before unloading her passengers. Major outbreaks have also occurred in southern Europe. Gibraltar lost many lives to outbreaks in 1804, 1814, and 1828. Barcelona suffered the loss of several thousand citizens during an outbreak in 1821. The Duke de Richelieu deployed 30,000 French troops to the border between France and Spain in the Pyrenees Mountains , to establish a cordon sanitaire in order to prevent the epidemic from spreading from Spain into France. Ezekiel Stone Wiggins , known as the Ottawa Prophet, proposed that the cause of a yellow fever epidemic in Jacksonville, Florida , in 1888, was astrological. The planets were in the same line as the sun and earth and this produced, besides Cyclones, Earthquakes, etc., a denser atmosphere holding more carbon and creating microbes. Mars had an uncommonly dense atmosphere, but its inhabitants were probably protected from the fever by their newly discovered canals , which were perhaps made to absorb carbon and prevent the disease. In 1848, Josiah C. Nott suggested that yellow fever was spread by insects such as moths or mosquitoes, basing his ideas on the pattern of transmission of the disease. Carlos Finlay , a Cuban-Spanish doctor and scientist, proposed in 1881 that yellow fever might be transmitted by previously infected mosquitoes rather than by direct contact from person to person, as had long been believed. Since the losses from yellow fever in the Spanish–American War in the 1890s were extremely high, U.S. Army doctors began research experiments with a team led by Walter Reed , and composed of doctors James Carroll , Aristides Agramonte , and Jesse William Lazear . They successfully proved Finlay's "mosquito hypothesis". Yellow fever was the first virus shown to be transmitted by mosquitoes. The physician William Gorgas applied these insights and eradicated yellow fever from Havana . He also campaigned against yellow fever during the construction of the Panama Canal . A previous effort of canal building by the French had failed in part due to mortality from the high incidence of yellow fever and malaria, which killed many workers. Although Reed has received much of the credit in United States history books for "beating" yellow fever, he had fully credited Finlay with the discovery of the yellow fever vector, and how it might be controlled. Reed often cited Finlay's papers in his own articles, and also credited him for the discovery in his personal correspondence. The acceptance of Finlay's work was one of the most important and far-reaching effects of the U.S. Army Yellow Fever Commission of 1900. Applying methods first suggested by Finlay, the United States government and Army eradicated yellow fever in Cuba and later in Panama, allowing completion of the Panama Canal. While Reed built on the research of Finlay, historian François Delaporte notes that yellow fever research was a contentious issue. Scientists, including Finlay and Reed, became successful by building on the work of less prominent scientists, without always giving them the credit they were due. Reed's research was essential in the fight against yellow fever. He is also credited for using the first type of medical consent form during his experiments in Cuba, an attempt to ensure that participants knew they were taking a risk by being part of testing. Like Cuba and Panama, Brazil also led a highly successful sanitation campaign against mosquitoes and yellow fever. Beginning in 1903, the campaign led by Oswaldo Cruz , then director general of public health, resulted not only in eradicating the disease but also in reshaping the physical landscape of Brazilian cities such as Rio de Janeiro. During rainy seasons, Rio de Janeiro had regularly suffered floods, as water from the bay surrounding the city overflowed into Rio's narrow streets. Coupled with the poor drainage systems found throughout Rio, this created swampy conditions in the city's neighborhoods. Pools of stagnant water stood year-long in city streets and proved to be a fertile ground for disease-carrying mosquitoes. Thus, under Cruz's direction, public health units known as "mosquito inspectors" fiercely worked to combat yellow fever throughout Rio by spraying, exterminating rats, improving drainage, and destroying unsanitary housing. Ultimately, the city's sanitation and renovation campaigns reshaped Rio de Janeiro's neighborhoods. Its poor residents were pushed from city centers to Rio's suburbs, or to towns found in the outskirts of the city. In later years, Rio's most impoverished inhabitants would come to reside in favelas . During 1920–1923, the Rockefeller Foundation 's International Health Board undertook an expensive and successful yellow fever eradication campaign in Mexico. The IHB gained the respect of Mexico's federal government because of the success. The eradication of yellow fever strengthened the relationship between the US and Mexico, which had not been very good in the years prior. The eradication of yellow fever was also a major step toward better global health. In 1927, scientists isolated the yellow fever virus in West Africa. Following this, two vaccines were developed in the 1930s. Max Theiler led the completion of the 17D yellow fever vaccine in 1937, for which he was subsequently awarded the Nobel Prize in Physiology or Medicine . That vaccine, 17D, is still in use, although newer vaccines, based on vero cells , are in development (as of 2018). Using vector control and strict vaccination programs, the urban cycle of yellow fever was nearly eradicated from South America. Since 1943, only a single urban outbreak in Santa Cruz de la Sierra , Bolivia, has occurred. Since the 1980s, however, the number of yellow fever cases has been increasing again, and A. aegypti has returned to the urban centers of South America. This is partly due to limitations on available insecticides, as well as habitat dislocations caused by climate change. It is also because the vector control program was abandoned. Although no new urban cycle has yet been established, scientists believe this could happen again at any point. An outbreak in Paraguay in 2008 was thought to be urban in nature, but this ultimately proved not to be the case. In Africa, virus eradication programs have mostly relied upon vaccination. These programs have largely been unsuccessful because they were unable to break the sylvatic cycle involving wild primates. With few countries establishing regular vaccination programs, measures to fight yellow fever have been neglected, making the future spread of the virus more likely. The evolutionary origins of yellow fever most likely lie in Africa, with transmission of the disease from nonhuman primates to humans. The virus is thought to have originated in East or Central Africa and spread from there to West Africa. As it was endemic in Africa, local populations had developed some immunity to it. When an outbreak of yellow fever would occur in an African community where colonists resided, most Europeans died, while the indigenous Africans usually developed nonlethal symptoms resembling influenza . This phenomenon, in which certain populations develop immunity to yellow fever due to prolonged exposure in their childhood, is known as acquired immunity . The virus, as well as the vector A. aegypti, were probably transferred to North and South America with the trafficking of slaves from Africa, part of the Columbian exchange following European exploration and colonization. However, some researchers have argued that yellow fever might have existed in the Americas during the pre-Columbian period as mosquitoes of the genus Haemagogus , which is indigenous to the Americas, have been known to carry the disease. The first definitive outbreak of yellow fever in the New World was in 1647 on the island of Barbados . An outbreak was recorded by Spanish colonists in 1648 in the Yucatán Peninsula , where the indigenous Mayan people called the illness xekik ("blood vomit"). In 1685, Brazil suffered its first epidemic in Recife . The first mention of the disease by the name "yellow fever" occurred in 1744. However, Dr. Mitchell misdiagnosed the disease that he observed and treated, and the disease was probably Weil's disease or hepatitis. McNeill argues that the environmental and ecological disruption caused by the introduction of sugar plantations created the conditions for mosquito and viral reproduction, and subsequent outbreaks of yellow fever. Deforestation reduced populations of insectivorous birds and other creatures that fed on mosquitoes and their eggs. In Colonial times and during the Napoleonic Wars , the West Indies were known as a particularly dangerous posting for soldiers due to yellow fever being endemic in the area. The mortality rate in British garrisons in Jamaica was seven times that of garrisons in Canada, mostly because of yellow fever and other tropical diseases. Both English and French forces posted there were seriously affected by the "yellow jack" . Wanting to regain control of the lucrative sugar trade in Saint-Domingue (Hispaniola), and with an eye on regaining France's New World empire, Napoleon sent an army under the command of his brother-in-law General Charles Leclerc to Saint-Domingue to seize control after a slave revolt. The historian J. R. McNeill asserts that yellow fever accounted for about 35,000 to 45,000 casualties of these forces during the fighting. Only one third of the French troops survived for withdrawal and return to France. Napoleon gave up on the island and his plans for North America, selling the Louisiana Purchase to the US in 1803. In 1804, Haiti proclaimed its independence as the second republic in the Western Hemisphere. Considerable debate exists over whether the number of deaths caused by disease in the Haitian Revolution was exaggerated. Although yellow fever is most prevalent in tropical-like climates, the northern United States were not exempted from the fever. The first outbreak in English-speaking North America occurred in New York City in 1668. English colonists in Philadelphia and the French in the Mississippi River Valley recorded major outbreaks in 1669, as well as additional yellow fever epidemics in Philadelphia, Baltimore , and New York City in the 18th and 19th centuries. The disease traveled along steamboat routes from New Orleans, causing some 100,000–150,000 deaths in total. The yellow fever epidemic of 1793 in Philadelphia, which was then the capital of the United States, resulted in the deaths of several thousand people, more than 9% of the population. One of these deaths was James Hutchinson , a physician helping to treat the population of the city. The national government fled the city to Trenton, New Jersey, including President George Washington . The southern city of New Orleans was plagued with major epidemics during the 19th century, most notably in 1833 and 1853. A major epidemic occurred in both New Orleans and Shreveport, Louisiana in 1873. Its residents called the disease "yellow jack". Urban epidemics continued in the United States until 1905, with the last outbreak affecting New Orleans. At least 25 major outbreaks took place in the Americas during the 18th and 19th centuries, including particularly serious ones in Cartagena, Chile , in 1741; Cuba in 1762 and 1900; Santo Domingo in 1803; and Memphis, Tennessee , in 1878. In the early 19th century, the prevalence of yellow fever in the Caribbean "led to serious health problems" and alarmed the United States Navy as numerous deaths and sickness curtailed naval operations and destroyed morale. One episode began in April 1822 when the frigate USS Macedonian left Boston and became part of Commodore James Biddle's West India Squadron. Unbeknownst to all, they were about to embark on a cruise to disaster and their assignment "would prove a cruise through hell". Secretary of the Navy Smith Thompson had assigned the squadron to guard United States merchant shipping and suppress piracy. During their time on deployment from 26 May to 3 August 1822, 76 of the Macedonian's officers and men died, including John Cadle, surgeon USN. Seventy-four of these deaths were attributed to yellow fever. Biddle reported that another 52 of his crew were on sick-list. In their report to the secretary of the Navy, Biddle and Surgeon's Mate Charles Chase stated the cause as "fever". As a consequence of this loss, Biddle noted that his squadron was forced to return to Norfolk Navy Yard early. Upon arrival, the Macedonian's crew were provided medical care and quarantined at Craney Island, Virginia. In 1853, Cloutierville, Louisiana , had a late-summer outbreak of yellow fever that quickly killed 68 of the 91 inhabitants. A local doctor concluded that some unspecified infectious agent had arrived in a package from New Orleans. In 1854, 650 residents of Savannah, Georgia , died from yellow fever. In 1858, St. Matthew's German Evangelical Lutheran Church in Charleston, South Carolina , had 308 yellow fever deaths, reducing the congregation by half. A ship carrying persons infected with the virus arrived in Hampton Roads in southeastern Virginia in June 1855. The disease spread quickly through the community, eventually killing over 3,000 people, mostly residents of Norfolk and Portsmouth . In 1873, Shreveport, Louisiana , lost 759 citizens in an 80-day period to a yellow fever epidemic, with over 400 additional victims eventually succumbing. The total death toll from August through November was approximately 1,200. In 1878, about 20,000 people died in a widespread epidemic in the Mississippi River Valley. That year, Memphis had an unusually large amount of rain, which led to an increase in the mosquito population. The result was a huge epidemic of yellow fever. The steamship John D. Porter took people fleeing Memphis northward in hopes of escaping the disease, but passengers were not allowed to disembark due to concerns of spreading yellow fever. The ship roamed the Mississippi River for the next two months before unloading her passengers. Major outbreaks have also occurred in southern Europe. Gibraltar lost many lives to outbreaks in 1804, 1814, and 1828. Barcelona suffered the loss of several thousand citizens during an outbreak in 1821. The Duke de Richelieu deployed 30,000 French troops to the border between France and Spain in the Pyrenees Mountains , to establish a cordon sanitaire in order to prevent the epidemic from spreading from Spain into France. Ezekiel Stone Wiggins , known as the Ottawa Prophet, proposed that the cause of a yellow fever epidemic in Jacksonville, Florida , in 1888, was astrological. The planets were in the same line as the sun and earth and this produced, besides Cyclones, Earthquakes, etc., a denser atmosphere holding more carbon and creating microbes. Mars had an uncommonly dense atmosphere, but its inhabitants were probably protected from the fever by their newly discovered canals , which were perhaps made to absorb carbon and prevent the disease. In 1848, Josiah C. Nott suggested that yellow fever was spread by insects such as moths or mosquitoes, basing his ideas on the pattern of transmission of the disease. Carlos Finlay , a Cuban-Spanish doctor and scientist, proposed in 1881 that yellow fever might be transmitted by previously infected mosquitoes rather than by direct contact from person to person, as had long been believed. Since the losses from yellow fever in the Spanish–American War in the 1890s were extremely high, U.S. Army doctors began research experiments with a team led by Walter Reed , and composed of doctors James Carroll , Aristides Agramonte , and Jesse William Lazear . They successfully proved Finlay's "mosquito hypothesis". Yellow fever was the first virus shown to be transmitted by mosquitoes. The physician William Gorgas applied these insights and eradicated yellow fever from Havana . He also campaigned against yellow fever during the construction of the Panama Canal . A previous effort of canal building by the French had failed in part due to mortality from the high incidence of yellow fever and malaria, which killed many workers. Although Reed has received much of the credit in United States history books for "beating" yellow fever, he had fully credited Finlay with the discovery of the yellow fever vector, and how it might be controlled. Reed often cited Finlay's papers in his own articles, and also credited him for the discovery in his personal correspondence. The acceptance of Finlay's work was one of the most important and far-reaching effects of the U.S. Army Yellow Fever Commission of 1900. Applying methods first suggested by Finlay, the United States government and Army eradicated yellow fever in Cuba and later in Panama, allowing completion of the Panama Canal. While Reed built on the research of Finlay, historian François Delaporte notes that yellow fever research was a contentious issue. Scientists, including Finlay and Reed, became successful by building on the work of less prominent scientists, without always giving them the credit they were due. Reed's research was essential in the fight against yellow fever. He is also credited for using the first type of medical consent form during his experiments in Cuba, an attempt to ensure that participants knew they were taking a risk by being part of testing. Like Cuba and Panama, Brazil also led a highly successful sanitation campaign against mosquitoes and yellow fever. Beginning in 1903, the campaign led by Oswaldo Cruz , then director general of public health, resulted not only in eradicating the disease but also in reshaping the physical landscape of Brazilian cities such as Rio de Janeiro. During rainy seasons, Rio de Janeiro had regularly suffered floods, as water from the bay surrounding the city overflowed into Rio's narrow streets. Coupled with the poor drainage systems found throughout Rio, this created swampy conditions in the city's neighborhoods. Pools of stagnant water stood year-long in city streets and proved to be a fertile ground for disease-carrying mosquitoes. Thus, under Cruz's direction, public health units known as "mosquito inspectors" fiercely worked to combat yellow fever throughout Rio by spraying, exterminating rats, improving drainage, and destroying unsanitary housing. Ultimately, the city's sanitation and renovation campaigns reshaped Rio de Janeiro's neighborhoods. Its poor residents were pushed from city centers to Rio's suburbs, or to towns found in the outskirts of the city. In later years, Rio's most impoverished inhabitants would come to reside in favelas . During 1920–1923, the Rockefeller Foundation 's International Health Board undertook an expensive and successful yellow fever eradication campaign in Mexico. The IHB gained the respect of Mexico's federal government because of the success. The eradication of yellow fever strengthened the relationship between the US and Mexico, which had not been very good in the years prior. The eradication of yellow fever was also a major step toward better global health. In 1927, scientists isolated the yellow fever virus in West Africa. Following this, two vaccines were developed in the 1930s. Max Theiler led the completion of the 17D yellow fever vaccine in 1937, for which he was subsequently awarded the Nobel Prize in Physiology or Medicine . That vaccine, 17D, is still in use, although newer vaccines, based on vero cells , are in development (as of 2018). Using vector control and strict vaccination programs, the urban cycle of yellow fever was nearly eradicated from South America. Since 1943, only a single urban outbreak in Santa Cruz de la Sierra , Bolivia, has occurred. Since the 1980s, however, the number of yellow fever cases has been increasing again, and A. aegypti has returned to the urban centers of South America. This is partly due to limitations on available insecticides, as well as habitat dislocations caused by climate change. It is also because the vector control program was abandoned. Although no new urban cycle has yet been established, scientists believe this could happen again at any point. An outbreak in Paraguay in 2008 was thought to be urban in nature, but this ultimately proved not to be the case. In Africa, virus eradication programs have mostly relied upon vaccination. These programs have largely been unsuccessful because they were unable to break the sylvatic cycle involving wild primates. With few countries establishing regular vaccination programs, measures to fight yellow fever have been neglected, making the future spread of the virus more likely. In the hamster model of yellow fever, early administration of the antiviral ribavirin is an effective treatment of many pathological features of the disease. Ribavirin treatment during the first five days after virus infection improved survival rates, reduced tissue damage in the liver and spleen , prevented hepatocellular steatosis , and normalised levels of alanine aminotransferase, a liver damage marker. The mechanism of action of ribavirin in reducing liver pathology in yellow fever virus infection may be similar to its activity in treatment of hepatitis C , a related virus. Because ribavirin had failed to improve survival in a virulent rhesus model of yellow fever infection, it had been previously discounted as a possible therapy. Infection was reduced in mosquitoes with the wMel strain of Wolbachia . Yellow fever has been researched by several countries as a potential biological weapon .

Wiki

West Nile

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Cataracts of the Nile

The Cataracts of the Nile are shallow lengths (or whitewater rapids ) of the Nile river, between Khartoum and Aswan , where the surface of the water is broken by many small boulders and stones jutting out of the river bed, as well as many rocky islets . In some places, these stretches are punctuated by whitewater, while at others the water flow is smoother but still shallow.Counted going upstream (from north to south): In Egypt : In Sudan :Geologists indicate that the region of northern Sudan is tectonically active and this activity has caused the river to take on "youthful" characteristics. The Nubian Swell has diverted the river's course to the west, while keeping its depth shallow and causing the formation of the cataracts. Even as the river bed is worn down by erosion , the landmass is lifted, keeping parts of the river bed exposed. These distinctive features of the river between Aswan and Khartoum have led to the stretch being often referred to as the Cataract Nile , while the downstream portion is occasionally referred to as the "Egyptian" Nile. The geological distinction between these two portions of the river is considerable. North of Aswan, the river bed is not rocky, but is instead composed of sediment, and far from being a shallow river. It is believed that the bedrock was previously eroded to be several thousand feet deep. This created a vast canyon that is now filled with sediment. Despite these characteristics, some of the cataracts which are normally impassable by boat because of the shallow water have become navigable during the flood season.The word "cataract" comes from the Greek word καταρρέω ("to flow down"), although the original Greek term was the plural-only ÎšÎ±Ï„Î¬Î´Î¿Ï Ï€Î¿Î¹ . However, contrary to this, none of the Nile 's six primary cataracts could be accurately described as waterfalls, and given a broader definition, this is the same with many of the minor cataracts. In ancient times, Upper Egypt extended from south of the Nile Delta to the first cataract, while further upstream, the land was controlled by the ancient Kingdom of Kush that would later take over Egypt from 760 to 656 BC. Besides the Kushite invasion, for most of Egyptian history, the Nile's cataracts, particularly the First Cataract, primarily served as a natural border to prevent most crossings from the south, as those in said region would rely on river travel to venture north and south. This allowed Egypt's southern border to be relatively protected from invasions, and besides brief Kushite rule, it remained a natural border for most of Egyptian history. Eratosthenes gave a precise description of the Cataract-Nile: It has a similar shape to a backwards letter N. It flows northward from Meroë about 2700 stadia, then turns back to the south and the winter sunset for about 3700 stadia, and it almost reaches the same parallel as the Meroë region and makes its way far into Libya. Then it makes another turn, and flows northward 5300 stadia to the great cataract, curving slightly to the east; then 1200 stadia to the smaller cataract at Syene (i.e. Aswan ), and then 5300 more to the sea. The six cataracts of the Nile are depicted extensively by European visitors, notably by Winston Churchill in The River War (1899), where he recounts the exploits of the British trying to return to the Sudan between 1896 and 1898 , after they were forced to leave in 1885 . Today, Lake Nasser has filled most of the area between the first and second cataracts (known as Lower Nubia ), and its monuments moved as part of the International Campaign to Save the Monuments of Nubia .

Wiki

West Nile

https://api.wikimedia.org/core/v1/wikipedia/en/page/Yusuf_Gowon/html

Yusuf Gowon

Yusuf Gowon [lower-alpha 1] (born Yusuf Mogi ; 1936 – 2 February 2024) was a Ugandan military officer who served as chief of staff for the Uganda Army during the dictatorship of Idi Amin . Originally a farmer, Gowon quickly rose in the ranks of the military due to a combination of happenstance and his skills in politics. Compared with other high-ranking officials of Amin's regime, he was regarded as humane; nevertheless, he was probably involved in some political murders. His appointment as chief of staff was mostly owed to the fact that he was regarded by President Amin as loyal, not ambitious, and of no threat to his own rule. Gowon's lack of talent for tactics and strategy came to the fore when the Uganda–Tanzania War broke out in 1978, and his leadership of the Uganda Army during this conflict was extensively criticised. Many of his comrades and subordinates even blamed him for Uganda's defeat in the conflict with Tanzania. When Amin's regime began collapsing in 1979 and his own soldiers intended to murder him, Gowon fled Uganda. Gowon subsequently settled in Zaire where he worked as businessman. Unlike many of his former comrades, Gowon did not join any insurgent group during his exile. When the new Ugandan government of Yoweri Museveni offered him to return to his home country in 1994, he accepted and founded a nonprofit organization to help ex-combatants to find civilian jobs. He also became head of a veterans association. In 2001, Gowon was arrested and tried for the suspected involvement in the murder of Eliphaz Laki during Amin's rule. The trial generated much publicity and was controversial, as some regarded it as important chance to finally address the crimes of Amin's dictatorship, while others claimed that it was politically motivated. Gowon denied any involvement in Laki's murder, and was acquitted due to lack of evidence in 2003.Gowon was born as Yusuf Mogi in Ladonga, a village in the West Nile Province of the British Uganda Protectorate in 1936. His father Ibrahim was born a Catholic Christian and an ethnic Kakwa , but converted to Islam and adopted a Nubian identity ; as a result, Gowon's cheeks were cut with three marks after his birth, signalling him belonging to the Nubians. [lower-alpha 2] Though his family was not wealthy, his father was a clan chieftain and owned some farmland. In his youth, Yusuf would help out on his family's farm by looking after its fields, goats and cows. Occasionally, he went hunting with bows and arrows. Ibrahim could only afford to send one of his children to an Islamic primary school in the provincial capital of Arua ; he chose Yusuf. To pay for his son's education, he sold some of his cattle to the disapproval of other clan elders who reminded Ibrahim that the West Nile region was too poor to offer any employment for educated men. Sending Yusuf to school was regarded as wasted money. Yusuf wanted to go to school, however, and convinced his father to pay a few years of tuition. In Arua, Yusuf stayed at the house of a family friend, working on the fields and helping in the household to earn his keep. Arua served as center for the British colonial troops, the King's African Rifles , and many of Yusuf's classmates adored the military. He was an exception in this regard, and showed no interest in military matters at all. His classmates regarded him as sociable prankster who would entertain others with jokes and songs. Yusuf was known for dressing fashionably, thereby earning the nickname "Goan". This was a reference to the city of Goa in India , as the region's best tailors were Indians. Having taken a great liking for the nickname, he eventually adopted it with slight changes as his official last name. The West Nile Province was a poor region, and offered few occupation opportunities for young men. As a result, most of Gowon's friends joined the King's African Rifles when they finished primary school. In contrast, he opted to attend the junior high school, and subsequently an agricultural college. There, Gowon learned how to drive a tractor, and used his new skills to set up his own farm. This endeavor yielded little monetary gains, so Gowon decided to switch to working on a prison farm producing cotton in 1964. He enjoyed the work, and a British overseer taught him to repair the farm's machinery. Gowon later described this time as the happiest of his life. Gowon left the prisons service in 1968, and enlisted in the military. This decision partially stemmed from the changed political situation in Uganda. The country had become independent in 1962, and the Ugandan King's African Rifles units had been transformed into the Uganda Army . At the same time, politicians began to conspire and struggle for power, backed by the country's numerous tribal groups. By the late 1960s, the main opposing factions were led by Army chief of staff Idi Amin (mainly supported by the West Nile tribes) and President Milton Obote (mainly backed by the Acholi and Langi ). In order to secure the power over the Uganda Army, both launched extensive recruitment drives to enlist as many members of their own respective tribal groups as possible. As a result, military service offered great social and financial rewards which appealed to Gowon despite his disinterest in warfare. At first, Gowon was sent to a boot camp north of Kampala , Uganda's capital, where Amin was training a new elite unit. Obote considered this new unit a potential threat, however, and ordered its disbandment. As result, Gowon was reassigned to the military police, and later to the paratroopers trained by Israeli experts. At some point after 1969, he was among those sent to Greece for a course in commando tactics. In 1971, Amin launched a coup d'état and installed himself as President, though Obote found refuge in Tanzania . Amin's military dictatorship promptly purged the army of all those who were believed loyal to Obote, including most Acholi and Langi. The vacant leadership positions were then filled with soldiers who were loyal to Amin and usually from the West Nile Province. Gowon returned to Uganda after the coup's conclusion, and was promoted to major and appointed second-in-command of the Simba Battalion, stationed at Mbarara . Another Ugandan ex-officer later commented that Gowon was not prepared for such a promotion, and was just appointed because he belonged to Amin's own tribal group and religion. With the President as his personal patron, Gowon held great power over the Simba Battalion, probably more than the official commanding officer, Colonel Ali Fadhul . "Some men will themselves to power. Gowon, it seemed, had just happened into it." —Researcher Andrew Rice about Gowon's rise in the ranks of the Uganda Army Despite his inexperience, Gowon won some respect as second-in-command of the Simba Battalion, and was regarded as more polite and humane than other military officers who abused their power. While he was stationed at Mbarara, the Simba Battalion carried out numerous massacres of Acholi and Langi; Gowon later claimed that he knew nothing of any mass murders. On 17 September 1972, rebels loyal to Obote launched an invasion of Uganda from Tanzania. As Colonel Fadhul went missing amid the attack's early stages, Gowon was left in command of the Simba Battalion, and organized a counter-attack against a rebel column of 350 fighters. This counter-attack completely overwhelmed the rebels, most of whom were killed or captured. After Obote's invasion had been repelled, Amin ordered a purge of any possible rebel supporters throughout Uganda. One of Gowon's subordinates, Nasur Gille, later testified under disputed circumstances [lower-alpha 3] that Gowon ordered and organized the political murders in Mbarara. It is known that the commander had good connections to at least some members of the State Research Bureau , Amin's secret police organisation, and some victims of the purges as well as their families believe that Gowon ordered their deaths. Despite this, several residents of Mbarara argued that Gowon actually saved many lives during the mass killings. They later recalled that people had been marked for execution, but been freed on Gowon's orders. When questioned about his involvement in some political murders, the commander later told that "Any commanding officer who defended them [i.e. the victims]... When you defend, you become a collaborator", meaning one would in turn be marked for death. Gowon's reputation improved due to his role in defeating Obote's invasion, and he consequently rose in the ranks. When Amin ordered the expulsion of Asians from Uganda , Gowon was one of those responsible for redistributing the properties of about 40,000 deported Indian businessmen. This job was not just profitable and made him quite wealthy, but helped him to forge political connections. He proved extremely adapt at politics, and gradually gained a reputation as "ruthless infighter" in the Uganda Army who would manipulate others to get his way. Nevertheless, Gowon almost fell from power after the Arube uprising , a coup attempt against Amin in 1974. An unidentified person told the President that Gowon was secretly a Christian which was enough to warrant suspicions about him being a supporter of the coup attempt. [lower-alpha 4] He was placed under house arrest, but Army Chief of Staff Mustafa Adrisi intervened on his behalf, allowing Gowon to be flown to Libya for medical treatment of a stomach ailment. In this way, he avoided the worst purges, and upon returning was even promoted to commander of a unit in eastern Uganda. Over the following years, Gowon rose to lieutenant colonel, colonel, and brigadier general. By 1976, he commanded the Eastern Brigade. "Amin, I must leave my work. I may die like Gowon is going to die. These Nubians are deceiving you." — Mustafa Adrisi begging for President Idi Amin to spare Gowon's life Around 1976, Gowon was again accused of treason as result of political conspiracies among Amin's inner circles. A rival alleged that he was in contact with anti-Amin rebels in Tanzania. He was arrested by the State Research Bureau, and, alongside his protector Adrisi, brought into the President's bureau. There, Amin told them that more evidence had surfaced about Gowon's support for the 1974 coup attempt, and had him ordered out of sight. Gowon believed that he was going to be executed. Adrisi fell on his knees and begged the President to reconsider, claiming that the entire affair was engineered by a clique of Nubians. Amin finally relented, and ordered Gowon back into the room. He then got everyone a cup of tea and told Gowon that he was spared. Regardless, the President also threatened that if the general was accused one more time of involvement in the 1974 coup, he would be executed. Despite this incident, Gowon remained one of Amin's most trusted followers. The general would spy for the President on other officers, while trying to remove his own rivals. His military rivals referred to him as "snake" as a commentary on his apparent deft political abilities which facilitated his rise in the ranks. His political skills did not endear him to his subordinates who held little respect for him. They regarded Gowon as an "uneducated rube", and promoted far above his station. He was even derogatorily nicknamed "the tractor driver" by soldiers due to his past as a farmer. Some officers also disliked Gowon due to his tendency to circumvent them and deal with the lower ranks directly. In contrast, he was popular among the people of his birthplace, Ladonga, because he paid school tuition for local children, and built a primary school and a medical clinic. In early 1978, Adrisi was almost killed in a car accident that was suspected by some to be an assassination attempt. Amin consequently purged several of Adrisi's followers from the government, including Uganda Army Chief of Staff Isaac Lumago . Gowon was made acting Army Chief of Staff, and promoted to major general on 8 May 1978. He was formally appointed as Lumago's successor in June. By this point, the repeated purges had reduced Amin's inner circle to a small number of officers. Gowon's appointment was mostly owed to the fact that he was regarded as loyal to Amin, and lacked a power base in the military to threaten the President. After becoming chief of staff, one reporter described him as the "second-most powerful man in the country". As chief of staff, Gowon was tasked by Amin to carry out another purge in the Uganda Army's upper ranks. He disempowered the heads of two intelligence services, and also moved against his long-time rival General Moses Ali . Ali was removed from his posts in April 1978, and almost killed by hitmen when he went into self-imposed exile in his home town in West Nile. He consequently blamed Gowon for these events. Although Gowon had thus risen to one of Amin's closest allies and proven to be competent in politics, he was not qualified as head of the military, and lacked training in basic strategy. In September 1978 Amin, in response to international criticisms of his regime, announced the creation of a human rights committee "charged with the duty of explaining Uganda's position abroad". Gowon was made a member of the body, though subsequent events prevented it from performing any work. In late 1978, tensions between Uganda and Tanzania culminated in open warfare. The exact circumstances of the conflict's outbreak remain unclear, but President Amin ordered an invasion of northwestern Tanzania on 30 October 1978. Gowon was put in charge of about 3,000 soldiers to carry out the operation which initially went well. The Tanzanian border guards were overwhelmed and the Kagera salient occupied, whereupon the Ugandan troops launched a spree of plundering, rape, and murder. Gowon joined the looting, and reportedly demoted an Ugandan captain when the latter refused to hand over a stolen tractor to him. [lower-alpha 5] After the Uganda Army blew up a bridge across the Kagera river, Gowon believed that he had made a Tanzanian counter-offensive impossible and thereby won the war. This turned out to be a catastrophic miscalculation, as the Tanzania People's Defence Force (TPDF) counter-attacked using a pontoon bridge , routing the Ugandans. Thereafter, Tanzania began preparing a counter-invasion of Uganda, but Gowon and other high-ranking commanders ignored warnings by subordinate officers about an impending Tanzanian offensive. Colonel Bernard Rwehururu in particular accused Gowon of gross incompetence, recalling an occasion when he showed the Chief of Staff a map with possible Tanzanian invasion routes. Gowon was allegedly unimpressed, and replied "What's wrong with you? You are always thinking of maps. Do you fight with maps?" Another officer stated that the Chief of Staff lied to the President about the military situation, and ignored messages by frontline commanders. Other unidentified officers alleged that Gowon and other Ugandan high-ranking commanders focused more on "their petty feuds" than on the war. One of the greatest problems for the Uganda Army was its lack of artillery, while the Tanzanians had ample access to Katyusha rocket launchers . Gowon put off this issue until another Ugandan general urged him to finally do something about it. Gowon asked Amin to buy artillery abroad, but the man who was entrusted this task simply pocketed the money. The TPDF invaded on 21 January 1979, and defeated the Uganda Army in a series of battles. Amin consequently dispatched Gowon to the frontlines which was "widely interpreted as a punishment". Eventually, Amin's Libyan ally Muammar Gaddafi intervened by sending an expeditionary force, whereupon a combined Ugandan-Libyan counter-offensive was launched against Lukaya on 10 March 1979. The battle turned against the Ugandans on 11 March, as the TPDF launched a successful counter-attack. In an attempt to strengthen morale, Gowon and General Isaac Maliyamungu joined their troops on the front line at Lukaya. For unknown reasons, the positions the two men took were frequently subject to sudden, intense rocket fire. Ugandan junior officers tried to convince their men that the Tanzanians were probably aware of the generals' presence and were targeting them with precise bombardments. The Ugandan troops nonetheless felt that Maliyamungu and Gowon were harbingers of misfortune and nicknamed them bisirani , or "bad omen". The leading Ugandan commander at Lukaya, Godwin Sule , realised the generals were not having a positive effect and asked them to leave the front. According to an unidentified "high Ugandan official" who was in exile in Nairobi at the time, Gowon and other officers unsuccessfully urged Amin to step down as President after the Battle of Lukaya. Soon after, a Libyan officer visited Gowon's headquarters, and relayed that Amin had fired him. The Libyan then mounted a tank and addressed the Ugandan soldiers present, telling them that Gowon had betrayed them to the Tanzanians. The soldiers were enraged, and wanted to murder their former Chief of Staff, but Gowon claimed that he intended to muster reinforcements. Using this excuse, he fled to Kampala and from there to Wile Nile on a motorcycle. His troops believed that he had deserted, prompting one of them to comment in an interview with the Drum magazine that "Our recent chief of staff, Major General Gowon, has disappeared. Only hell knows where he is." He was succeeded as Chief of Staff by Ali Fadhul. When Gowon arrived in Arua, West Nile, he initially laid low and planned his possible exile. However, he eventually chanced upon a detachment of Ugandan soldiers who knew him. These troopers arrested him as traitor, and confiscated his wealth. [lower-alpha 6] By chance, Gowon's old ally Mustafa Adrisi visited Arua shortly after his arrest, and ordered his release. Adrisi told Gowon that he should flee Uganda as soon as possible, and the former Chief of Staff followed this recommendation. He was unsure whether to go into exile in Zaire or Sudan, but chose the former because most Amin loyalists – who intended to kill him – were fleeing to Sudan. Gowon initially found refuge with Catholic missionaries. Meanwhile, Amin's regime collapsed as the Tanzanians and their Ugandan rebel allies occupied Kampala , prompting most Uganda Army loyalists to flee into Sudan and Zaire. [lower-alpha 7] Zairean dictator Mobutu Sese Seko allowed the Ugandan exiles, including Gowon, to stay in his country. As many believed that Gowon had actually been bribed by the Tanzanians and lost the war on purpose, he became a persona non grata among the Ugandan exiles and thus excluded from plans by Amin loyalists to launch a rebellion to regain power. Gowon was actually pleased about this, as he had no interest in resuming fighting. Instead, Gowon focused on building a new life in Zaire, taking up residency in Kisangani . By befriending a Zairean customs officer, he had transported some trucks out of Uganda and would subsequently rent them out. He was also involved in smuggling, and eventually made enough money to buy a house in Bunia where he was joined by two of his wives. At the same time, Uganda descended into civil war which resulted in Yoweri Museveni 's rise to presidency in 1986. Museveni's government focused on national reconstruction, and offered reconciliation to Amin's former followers. Gowon took up this offer in 1994. He returned to Uganda with 25 other ex-officers, hundreds of dependants, and over ten thousand civilian refugees. Museveni personally welcomed Gowon back to Uganda, and the two even laughingly reminisced about the 1972 invasion during which they had fought each other (Museveni had been part of Obote's rebel alliance at the time). Mbarara threw a "huge party" in Gowon's honor. The Ugandan government rented him a house in Ntinda , and granted him a stipend. Grateful for this treatment, Gowon subsequently supported Museveni, and made speeches in his favor during the 1996 Ugandan presidential election . The former Chief of Staff also founded "Good Hope" and "Alternatives to Violence", nonprofit organizations to help ex-combatants to find civilian jobs. The Ugandan government promised Gowon funds to set up companies in which the ex-rebels could be employed, but the money never materialised. Over the next years, his stipend was paid ever less regularly, and Gowon was no longer able to pay his rent. He was evicted from his Ntinda residence, and had to relocate to live in a bicycle shop run by one of his sons. Broke and without a job, he spent most his time in the Slow Boat Pub . At some point, Gowon became the leader of a Uganda Army veterans association. Gowon lived in retirement until 2001, when he was arrested by the Ugandan police for the murder of county chief Eliphaz Laki. According to the testimony of two former subordinates of Gowon, Laki had been murdered on his orders during the purges following the 1972 invasion. The former Chief of Staff disputed any knowledge of or involvement in Laki's death, but was placed in the Luzira Maximum Security Prison and put on trial. Gowon faced the death sentence if convicted of the murder. His trial generated much publicity in Uganda, as most crimes during Amin's regime remained unresolved due to lack of evidence and lack of interest in prosecuting them on the side of the Ugandan government which wants to maintain communal peace. The prosecutors, the families of victims, and reporters saw Gowon's trial as the last chance to finally address the injustices of Amin's regime which had killed between 100,000 and 300,000 people, as the majority of the perpetrators were already quite old. Lead prosecutor Simon Byabakama Mugenyi stated that "It's like our Nuremberg Trial ." Others, mostly people from West Nile, saw Gowon as victim of political conspiracies. Gowon believed that his old rival, Moses Ali, was behind his trial. By then, Ali had risen to minister of internal affairs in Museveni's government and was quite influential. At some point, the minister allegedly visited Luzira Prison just to enjoy seeing Gowon imprisoned; Ali denied all of this, once stating that he "did not even know [that Gowon] was arrested" until reading of it in the newspapers. In general, prison life was difficult for Gowon and he lost more than thirty pounds while incarcerated. However, he had few problems with most other prisoners at Luzira and even developed a friendship with one of his former enemies who also served a prison term. However, he had a tense relationship with those prisoners who had formerly served alongside him in the Uganda Army. The hostility between him and his ex-superior Ali Fadhul was so intense that prison authorities had to keep the two separate. The former Chief of Staff maintained his innocence during the entire trial, stating on one occasion that "These people were civilians. They could not have been killed. This is what I know." Gowon's former subordinates had confessed before the trial that they had murdered Laki on Gowon's direct order, but the reliability of their confessions was questioned during the trial. They had told the police about Gowon's order because they had already been arrested on charges of murder, hoping to be treated leniently by indicting Gowon. When this did not come to pass, the purported witnesses recanted their confessions. As the prosecutors attempted to gather more and firmer evidence for Gowon's guilt, the trial dragged on for almost a year. The trial resulted in tensions among Gowon's family. When well-wishers donated money for his defense, one of his sons absconded with it. The former Chief of Staff then tried to hire an attorney, Caleb Alaka, by promising him a house, but Gowon's wife promptly sued him. She argued that the house in question was rightfully hers. In the end, Alaka still took the case out of respect and pity for the former Chief of Staff. Early in the trial, one person offered Gowon's family and the defense attorney to speak out in favor of the former Chief of Staff in return for a bribe; the family had to refuse, as they were still broke. [lower-alpha 8] Though Laki's son had managed to gather evidence which suggested that Gowon was guilty, it was regarded as inadmissible by the judge. The defense attempted to discredit other evidence which had been found by a private investigator who died while the trial was still ongoing, arguing that the latter had died of a mental disorder although he had in fact died of HIV/AIDS . In the middle of the trial, defense attorney Caleb Alaka simply disappeared; he later resurfaced in Western Nile, where he had taken a job representing a rebel group which had signed a peace deal with the Ugandan government. Five months later he rejoined Gowon's trial, only to disappear again in February 2003, this time for good. For lack of firm evidence, the judge acquitted Gowon and the two other defendants on 25 September 2003. His release was celebrated by his family and sympathizers, mostly from West Nile, while Laki's family and sympathizers, mostly from southern Uganda, decried it as injustice. Some even spread conspiracy theories according to which the government had installed the judge, a Muslim, because he would support Gowon and his co-defendants. The former Chief of Staff regarded the verdict as vindication of his innocence. Following his release, Gowon resumed his work in the veterans association, and consequently advocated for a greater unity among ex-combatants of West Nile origin. However, he struggled to pay the legal bills of the trial. By 2005, he was spending most of his time at Arua where he still possessed a house, and had joined a class action lawsuit against several banks that had frozen assets of Amin-era officials worth 50 million dollars. Gowon died of heart failure at a hospital in Arua on 2 February 2024, at the age of 85. He was buried the following day in the Arua Muslim Cemetery. After his death, he was praised by President Museveni and Swaib Toko , Resident District Commissioner of Madi-Okollo . Gowon was born as Yusuf Mogi in Ladonga, a village in the West Nile Province of the British Uganda Protectorate in 1936. His father Ibrahim was born a Catholic Christian and an ethnic Kakwa , but converted to Islam and adopted a Nubian identity ; as a result, Gowon's cheeks were cut with three marks after his birth, signalling him belonging to the Nubians. [lower-alpha 2] Though his family was not wealthy, his father was a clan chieftain and owned some farmland. In his youth, Yusuf would help out on his family's farm by looking after its fields, goats and cows. Occasionally, he went hunting with bows and arrows. Ibrahim could only afford to send one of his children to an Islamic primary school in the provincial capital of Arua ; he chose Yusuf. To pay for his son's education, he sold some of his cattle to the disapproval of other clan elders who reminded Ibrahim that the West Nile region was too poor to offer any employment for educated men. Sending Yusuf to school was regarded as wasted money. Yusuf wanted to go to school, however, and convinced his father to pay a few years of tuition. In Arua, Yusuf stayed at the house of a family friend, working on the fields and helping in the household to earn his keep. Arua served as center for the British colonial troops, the King's African Rifles , and many of Yusuf's classmates adored the military. He was an exception in this regard, and showed no interest in military matters at all. His classmates regarded him as sociable prankster who would entertain others with jokes and songs. Yusuf was known for dressing fashionably, thereby earning the nickname "Goan". This was a reference to the city of Goa in India , as the region's best tailors were Indians. Having taken a great liking for the nickname, he eventually adopted it with slight changes as his official last name. The West Nile Province was a poor region, and offered few occupation opportunities for young men. As a result, most of Gowon's friends joined the King's African Rifles when they finished primary school. In contrast, he opted to attend the junior high school, and subsequently an agricultural college. There, Gowon learned how to drive a tractor, and used his new skills to set up his own farm. This endeavor yielded little monetary gains, so Gowon decided to switch to working on a prison farm producing cotton in 1964. He enjoyed the work, and a British overseer taught him to repair the farm's machinery. Gowon later described this time as the happiest of his life. Gowon left the prisons service in 1968, and enlisted in the military. This decision partially stemmed from the changed political situation in Uganda. The country had become independent in 1962, and the Ugandan King's African Rifles units had been transformed into the Uganda Army . At the same time, politicians began to conspire and struggle for power, backed by the country's numerous tribal groups. By the late 1960s, the main opposing factions were led by Army chief of staff Idi Amin (mainly supported by the West Nile tribes) and President Milton Obote (mainly backed by the Acholi and Langi ). In order to secure the power over the Uganda Army, both launched extensive recruitment drives to enlist as many members of their own respective tribal groups as possible. As a result, military service offered great social and financial rewards which appealed to Gowon despite his disinterest in warfare. At first, Gowon was sent to a boot camp north of Kampala , Uganda's capital, where Amin was training a new elite unit. Obote considered this new unit a potential threat, however, and ordered its disbandment. As result, Gowon was reassigned to the military police, and later to the paratroopers trained by Israeli experts. At some point after 1969, he was among those sent to Greece for a course in commando tactics. In 1971, Amin launched a coup d'état and installed himself as President, though Obote found refuge in Tanzania . Amin's military dictatorship promptly purged the army of all those who were believed loyal to Obote, including most Acholi and Langi. The vacant leadership positions were then filled with soldiers who were loyal to Amin and usually from the West Nile Province. Gowon returned to Uganda after the coup's conclusion, and was promoted to major and appointed second-in-command of the Simba Battalion, stationed at Mbarara . Another Ugandan ex-officer later commented that Gowon was not prepared for such a promotion, and was just appointed because he belonged to Amin's own tribal group and religion. With the President as his personal patron, Gowon held great power over the Simba Battalion, probably more than the official commanding officer, Colonel Ali Fadhul . "Some men will themselves to power. Gowon, it seemed, had just happened into it." —Researcher Andrew Rice about Gowon's rise in the ranks of the Uganda Army Despite his inexperience, Gowon won some respect as second-in-command of the Simba Battalion, and was regarded as more polite and humane than other military officers who abused their power. While he was stationed at Mbarara, the Simba Battalion carried out numerous massacres of Acholi and Langi; Gowon later claimed that he knew nothing of any mass murders. On 17 September 1972, rebels loyal to Obote launched an invasion of Uganda from Tanzania. As Colonel Fadhul went missing amid the attack's early stages, Gowon was left in command of the Simba Battalion, and organized a counter-attack against a rebel column of 350 fighters. This counter-attack completely overwhelmed the rebels, most of whom were killed or captured. After Obote's invasion had been repelled, Amin ordered a purge of any possible rebel supporters throughout Uganda. One of Gowon's subordinates, Nasur Gille, later testified under disputed circumstances [lower-alpha 3] that Gowon ordered and organized the political murders in Mbarara. It is known that the commander had good connections to at least some members of the State Research Bureau , Amin's secret police organisation, and some victims of the purges as well as their families believe that Gowon ordered their deaths. Despite this, several residents of Mbarara argued that Gowon actually saved many lives during the mass killings. They later recalled that people had been marked for execution, but been freed on Gowon's orders. When questioned about his involvement in some political murders, the commander later told that "Any commanding officer who defended them [i.e. the victims]... When you defend, you become a collaborator", meaning one would in turn be marked for death. Gowon's reputation improved due to his role in defeating Obote's invasion, and he consequently rose in the ranks. When Amin ordered the expulsion of Asians from Uganda , Gowon was one of those responsible for redistributing the properties of about 40,000 deported Indian businessmen. This job was not just profitable and made him quite wealthy, but helped him to forge political connections. He proved extremely adapt at politics, and gradually gained a reputation as "ruthless infighter" in the Uganda Army who would manipulate others to get his way. Nevertheless, Gowon almost fell from power after the Arube uprising , a coup attempt against Amin in 1974. An unidentified person told the President that Gowon was secretly a Christian which was enough to warrant suspicions about him being a supporter of the coup attempt. [lower-alpha 4] He was placed under house arrest, but Army Chief of Staff Mustafa Adrisi intervened on his behalf, allowing Gowon to be flown to Libya for medical treatment of a stomach ailment. In this way, he avoided the worst purges, and upon returning was even promoted to commander of a unit in eastern Uganda. Over the following years, Gowon rose to lieutenant colonel, colonel, and brigadier general. By 1976, he commanded the Eastern Brigade. "Amin, I must leave my work. I may die like Gowon is going to die. These Nubians are deceiving you." — Mustafa Adrisi begging for President Idi Amin to spare Gowon's life Around 1976, Gowon was again accused of treason as result of political conspiracies among Amin's inner circles. A rival alleged that he was in contact with anti-Amin rebels in Tanzania. He was arrested by the State Research Bureau, and, alongside his protector Adrisi, brought into the President's bureau. There, Amin told them that more evidence had surfaced about Gowon's support for the 1974 coup attempt, and had him ordered out of sight. Gowon believed that he was going to be executed. Adrisi fell on his knees and begged the President to reconsider, claiming that the entire affair was engineered by a clique of Nubians. Amin finally relented, and ordered Gowon back into the room. He then got everyone a cup of tea and told Gowon that he was spared. Regardless, the President also threatened that if the general was accused one more time of involvement in the 1974 coup, he would be executed. Despite this incident, Gowon remained one of Amin's most trusted followers. The general would spy for the President on other officers, while trying to remove his own rivals. His military rivals referred to him as "snake" as a commentary on his apparent deft political abilities which facilitated his rise in the ranks. His political skills did not endear him to his subordinates who held little respect for him. They regarded Gowon as an "uneducated rube", and promoted far above his station. He was even derogatorily nicknamed "the tractor driver" by soldiers due to his past as a farmer. Some officers also disliked Gowon due to his tendency to circumvent them and deal with the lower ranks directly. In contrast, he was popular among the people of his birthplace, Ladonga, because he paid school tuition for local children, and built a primary school and a medical clinic. In early 1978, Adrisi was almost killed in a car accident that was suspected by some to be an assassination attempt. Amin consequently purged several of Adrisi's followers from the government, including Uganda Army Chief of Staff Isaac Lumago . Gowon was made acting Army Chief of Staff, and promoted to major general on 8 May 1978. He was formally appointed as Lumago's successor in June. By this point, the repeated purges had reduced Amin's inner circle to a small number of officers. Gowon's appointment was mostly owed to the fact that he was regarded as loyal to Amin, and lacked a power base in the military to threaten the President. After becoming chief of staff, one reporter described him as the "second-most powerful man in the country". As chief of staff, Gowon was tasked by Amin to carry out another purge in the Uganda Army's upper ranks. He disempowered the heads of two intelligence services, and also moved against his long-time rival General Moses Ali . Ali was removed from his posts in April 1978, and almost killed by hitmen when he went into self-imposed exile in his home town in West Nile. He consequently blamed Gowon for these events. Although Gowon had thus risen to one of Amin's closest allies and proven to be competent in politics, he was not qualified as head of the military, and lacked training in basic strategy. In September 1978 Amin, in response to international criticisms of his regime, announced the creation of a human rights committee "charged with the duty of explaining Uganda's position abroad". Gowon was made a member of the body, though subsequent events prevented it from performing any work. In late 1978, tensions between Uganda and Tanzania culminated in open warfare. The exact circumstances of the conflict's outbreak remain unclear, but President Amin ordered an invasion of northwestern Tanzania on 30 October 1978. Gowon was put in charge of about 3,000 soldiers to carry out the operation which initially went well. The Tanzanian border guards were overwhelmed and the Kagera salient occupied, whereupon the Ugandan troops launched a spree of plundering, rape, and murder. Gowon joined the looting, and reportedly demoted an Ugandan captain when the latter refused to hand over a stolen tractor to him. [lower-alpha 5] After the Uganda Army blew up a bridge across the Kagera river, Gowon believed that he had made a Tanzanian counter-offensive impossible and thereby won the war. This turned out to be a catastrophic miscalculation, as the Tanzania People's Defence Force (TPDF) counter-attacked using a pontoon bridge , routing the Ugandans. Thereafter, Tanzania began preparing a counter-invasion of Uganda, but Gowon and other high-ranking commanders ignored warnings by subordinate officers about an impending Tanzanian offensive. Colonel Bernard Rwehururu in particular accused Gowon of gross incompetence, recalling an occasion when he showed the Chief of Staff a map with possible Tanzanian invasion routes. Gowon was allegedly unimpressed, and replied "What's wrong with you? You are always thinking of maps. Do you fight with maps?" Another officer stated that the Chief of Staff lied to the President about the military situation, and ignored messages by frontline commanders. Other unidentified officers alleged that Gowon and other Ugandan high-ranking commanders focused more on "their petty feuds" than on the war. One of the greatest problems for the Uganda Army was its lack of artillery, while the Tanzanians had ample access to Katyusha rocket launchers . Gowon put off this issue until another Ugandan general urged him to finally do something about it. Gowon asked Amin to buy artillery abroad, but the man who was entrusted this task simply pocketed the money. The TPDF invaded on 21 January 1979, and defeated the Uganda Army in a series of battles. Amin consequently dispatched Gowon to the frontlines which was "widely interpreted as a punishment". Eventually, Amin's Libyan ally Muammar Gaddafi intervened by sending an expeditionary force, whereupon a combined Ugandan-Libyan counter-offensive was launched against Lukaya on 10 March 1979. The battle turned against the Ugandans on 11 March, as the TPDF launched a successful counter-attack. In an attempt to strengthen morale, Gowon and General Isaac Maliyamungu joined their troops on the front line at Lukaya. For unknown reasons, the positions the two men took were frequently subject to sudden, intense rocket fire. Ugandan junior officers tried to convince their men that the Tanzanians were probably aware of the generals' presence and were targeting them with precise bombardments. The Ugandan troops nonetheless felt that Maliyamungu and Gowon were harbingers of misfortune and nicknamed them bisirani , or "bad omen". The leading Ugandan commander at Lukaya, Godwin Sule , realised the generals were not having a positive effect and asked them to leave the front. According to an unidentified "high Ugandan official" who was in exile in Nairobi at the time, Gowon and other officers unsuccessfully urged Amin to step down as President after the Battle of Lukaya. Soon after, a Libyan officer visited Gowon's headquarters, and relayed that Amin had fired him. The Libyan then mounted a tank and addressed the Ugandan soldiers present, telling them that Gowon had betrayed them to the Tanzanians. The soldiers were enraged, and wanted to murder their former Chief of Staff, but Gowon claimed that he intended to muster reinforcements. Using this excuse, he fled to Kampala and from there to Wile Nile on a motorcycle. His troops believed that he had deserted, prompting one of them to comment in an interview with the Drum magazine that "Our recent chief of staff, Major General Gowon, has disappeared. Only hell knows where he is." He was succeeded as Chief of Staff by Ali Fadhul. Gowon left the prisons service in 1968, and enlisted in the military. This decision partially stemmed from the changed political situation in Uganda. The country had become independent in 1962, and the Ugandan King's African Rifles units had been transformed into the Uganda Army . At the same time, politicians began to conspire and struggle for power, backed by the country's numerous tribal groups. By the late 1960s, the main opposing factions were led by Army chief of staff Idi Amin (mainly supported by the West Nile tribes) and President Milton Obote (mainly backed by the Acholi and Langi ). In order to secure the power over the Uganda Army, both launched extensive recruitment drives to enlist as many members of their own respective tribal groups as possible. As a result, military service offered great social and financial rewards which appealed to Gowon despite his disinterest in warfare. At first, Gowon was sent to a boot camp north of Kampala , Uganda's capital, where Amin was training a new elite unit. Obote considered this new unit a potential threat, however, and ordered its disbandment. As result, Gowon was reassigned to the military police, and later to the paratroopers trained by Israeli experts. At some point after 1969, he was among those sent to Greece for a course in commando tactics. In 1971, Amin launched a coup d'état and installed himself as President, though Obote found refuge in Tanzania . Amin's military dictatorship promptly purged the army of all those who were believed loyal to Obote, including most Acholi and Langi. The vacant leadership positions were then filled with soldiers who were loyal to Amin and usually from the West Nile Province. Gowon returned to Uganda after the coup's conclusion, and was promoted to major and appointed second-in-command of the Simba Battalion, stationed at Mbarara . Another Ugandan ex-officer later commented that Gowon was not prepared for such a promotion, and was just appointed because he belonged to Amin's own tribal group and religion. With the President as his personal patron, Gowon held great power over the Simba Battalion, probably more than the official commanding officer, Colonel Ali Fadhul . "Some men will themselves to power. Gowon, it seemed, had just happened into it." —Researcher Andrew Rice about Gowon's rise in the ranks of the Uganda Army Despite his inexperience, Gowon won some respect as second-in-command of the Simba Battalion, and was regarded as more polite and humane than other military officers who abused their power. While he was stationed at Mbarara, the Simba Battalion carried out numerous massacres of Acholi and Langi; Gowon later claimed that he knew nothing of any mass murders. On 17 September 1972, rebels loyal to Obote launched an invasion of Uganda from Tanzania. As Colonel Fadhul went missing amid the attack's early stages, Gowon was left in command of the Simba Battalion, and organized a counter-attack against a rebel column of 350 fighters. This counter-attack completely overwhelmed the rebels, most of whom were killed or captured. After Obote's invasion had been repelled, Amin ordered a purge of any possible rebel supporters throughout Uganda. One of Gowon's subordinates, Nasur Gille, later testified under disputed circumstances [lower-alpha 3] that Gowon ordered and organized the political murders in Mbarara. It is known that the commander had good connections to at least some members of the State Research Bureau , Amin's secret police organisation, and some victims of the purges as well as their families believe that Gowon ordered their deaths. Despite this, several residents of Mbarara argued that Gowon actually saved many lives during the mass killings. They later recalled that people had been marked for execution, but been freed on Gowon's orders. When questioned about his involvement in some political murders, the commander later told that "Any commanding officer who defended them [i.e. the victims]... When you defend, you become a collaborator", meaning one would in turn be marked for death. Gowon's reputation improved due to his role in defeating Obote's invasion, and he consequently rose in the ranks. When Amin ordered the expulsion of Asians from Uganda , Gowon was one of those responsible for redistributing the properties of about 40,000 deported Indian businessmen. This job was not just profitable and made him quite wealthy, but helped him to forge political connections. He proved extremely adapt at politics, and gradually gained a reputation as "ruthless infighter" in the Uganda Army who would manipulate others to get his way. Nevertheless, Gowon almost fell from power after the Arube uprising , a coup attempt against Amin in 1974. An unidentified person told the President that Gowon was secretly a Christian which was enough to warrant suspicions about him being a supporter of the coup attempt. [lower-alpha 4] He was placed under house arrest, but Army Chief of Staff Mustafa Adrisi intervened on his behalf, allowing Gowon to be flown to Libya for medical treatment of a stomach ailment. In this way, he avoided the worst purges, and upon returning was even promoted to commander of a unit in eastern Uganda. Over the following years, Gowon rose to lieutenant colonel, colonel, and brigadier general. By 1976, he commanded the Eastern Brigade. "Amin, I must leave my work. I may die like Gowon is going to die. These Nubians are deceiving you." — Mustafa Adrisi begging for President Idi Amin to spare Gowon's life Around 1976, Gowon was again accused of treason as result of political conspiracies among Amin's inner circles. A rival alleged that he was in contact with anti-Amin rebels in Tanzania. He was arrested by the State Research Bureau, and, alongside his protector Adrisi, brought into the President's bureau. There, Amin told them that more evidence had surfaced about Gowon's support for the 1974 coup attempt, and had him ordered out of sight. Gowon believed that he was going to be executed. Adrisi fell on his knees and begged the President to reconsider, claiming that the entire affair was engineered by a clique of Nubians. Amin finally relented, and ordered Gowon back into the room. He then got everyone a cup of tea and told Gowon that he was spared. Regardless, the President also threatened that if the general was accused one more time of involvement in the 1974 coup, he would be executed. Despite this incident, Gowon remained one of Amin's most trusted followers. The general would spy for the President on other officers, while trying to remove his own rivals. His military rivals referred to him as "snake" as a commentary on his apparent deft political abilities which facilitated his rise in the ranks. His political skills did not endear him to his subordinates who held little respect for him. They regarded Gowon as an "uneducated rube", and promoted far above his station. He was even derogatorily nicknamed "the tractor driver" by soldiers due to his past as a farmer. Some officers also disliked Gowon due to his tendency to circumvent them and deal with the lower ranks directly. In contrast, he was popular among the people of his birthplace, Ladonga, because he paid school tuition for local children, and built a primary school and a medical clinic. In early 1978, Adrisi was almost killed in a car accident that was suspected by some to be an assassination attempt. Amin consequently purged several of Adrisi's followers from the government, including Uganda Army Chief of Staff Isaac Lumago . Gowon was made acting Army Chief of Staff, and promoted to major general on 8 May 1978. He was formally appointed as Lumago's successor in June. By this point, the repeated purges had reduced Amin's inner circle to a small number of officers. Gowon's appointment was mostly owed to the fact that he was regarded as loyal to Amin, and lacked a power base in the military to threaten the President. After becoming chief of staff, one reporter described him as the "second-most powerful man in the country". As chief of staff, Gowon was tasked by Amin to carry out another purge in the Uganda Army's upper ranks. He disempowered the heads of two intelligence services, and also moved against his long-time rival General Moses Ali . Ali was removed from his posts in April 1978, and almost killed by hitmen when he went into self-imposed exile in his home town in West Nile. He consequently blamed Gowon for these events. Although Gowon had thus risen to one of Amin's closest allies and proven to be competent in politics, he was not qualified as head of the military, and lacked training in basic strategy. In September 1978 Amin, in response to international criticisms of his regime, announced the creation of a human rights committee "charged with the duty of explaining Uganda's position abroad". Gowon was made a member of the body, though subsequent events prevented it from performing any work. In late 1978, tensions between Uganda and Tanzania culminated in open warfare. The exact circumstances of the conflict's outbreak remain unclear, but President Amin ordered an invasion of northwestern Tanzania on 30 October 1978. Gowon was put in charge of about 3,000 soldiers to carry out the operation which initially went well. The Tanzanian border guards were overwhelmed and the Kagera salient occupied, whereupon the Ugandan troops launched a spree of plundering, rape, and murder. Gowon joined the looting, and reportedly demoted an Ugandan captain when the latter refused to hand over a stolen tractor to him. [lower-alpha 5] After the Uganda Army blew up a bridge across the Kagera river, Gowon believed that he had made a Tanzanian counter-offensive impossible and thereby won the war. This turned out to be a catastrophic miscalculation, as the Tanzania People's Defence Force (TPDF) counter-attacked using a pontoon bridge , routing the Ugandans. Thereafter, Tanzania began preparing a counter-invasion of Uganda, but Gowon and other high-ranking commanders ignored warnings by subordinate officers about an impending Tanzanian offensive. Colonel Bernard Rwehururu in particular accused Gowon of gross incompetence, recalling an occasion when he showed the Chief of Staff a map with possible Tanzanian invasion routes. Gowon was allegedly unimpressed, and replied "What's wrong with you? You are always thinking of maps. Do you fight with maps?" Another officer stated that the Chief of Staff lied to the President about the military situation, and ignored messages by frontline commanders. Other unidentified officers alleged that Gowon and other Ugandan high-ranking commanders focused more on "their petty feuds" than on the war. One of the greatest problems for the Uganda Army was its lack of artillery, while the Tanzanians had ample access to Katyusha rocket launchers . Gowon put off this issue until another Ugandan general urged him to finally do something about it. Gowon asked Amin to buy artillery abroad, but the man who was entrusted this task simply pocketed the money. The TPDF invaded on 21 January 1979, and defeated the Uganda Army in a series of battles. Amin consequently dispatched Gowon to the frontlines which was "widely interpreted as a punishment". Eventually, Amin's Libyan ally Muammar Gaddafi intervened by sending an expeditionary force, whereupon a combined Ugandan-Libyan counter-offensive was launched against Lukaya on 10 March 1979. The battle turned against the Ugandans on 11 March, as the TPDF launched a successful counter-attack. In an attempt to strengthen morale, Gowon and General Isaac Maliyamungu joined their troops on the front line at Lukaya. For unknown reasons, the positions the two men took were frequently subject to sudden, intense rocket fire. Ugandan junior officers tried to convince their men that the Tanzanians were probably aware of the generals' presence and were targeting them with precise bombardments. The Ugandan troops nonetheless felt that Maliyamungu and Gowon were harbingers of misfortune and nicknamed them bisirani , or "bad omen". The leading Ugandan commander at Lukaya, Godwin Sule , realised the generals were not having a positive effect and asked them to leave the front. According to an unidentified "high Ugandan official" who was in exile in Nairobi at the time, Gowon and other officers unsuccessfully urged Amin to step down as President after the Battle of Lukaya. Soon after, a Libyan officer visited Gowon's headquarters, and relayed that Amin had fired him. The Libyan then mounted a tank and addressed the Ugandan soldiers present, telling them that Gowon had betrayed them to the Tanzanians. The soldiers were enraged, and wanted to murder their former Chief of Staff, but Gowon claimed that he intended to muster reinforcements. Using this excuse, he fled to Kampala and from there to Wile Nile on a motorcycle. His troops believed that he had deserted, prompting one of them to comment in an interview with the Drum magazine that "Our recent chief of staff, Major General Gowon, has disappeared. Only hell knows where he is." He was succeeded as Chief of Staff by Ali Fadhul. When Gowon arrived in Arua, West Nile, he initially laid low and planned his possible exile. However, he eventually chanced upon a detachment of Ugandan soldiers who knew him. These troopers arrested him as traitor, and confiscated his wealth. [lower-alpha 6] By chance, Gowon's old ally Mustafa Adrisi visited Arua shortly after his arrest, and ordered his release. Adrisi told Gowon that he should flee Uganda as soon as possible, and the former Chief of Staff followed this recommendation. He was unsure whether to go into exile in Zaire or Sudan, but chose the former because most Amin loyalists – who intended to kill him – were fleeing to Sudan. Gowon initially found refuge with Catholic missionaries. Meanwhile, Amin's regime collapsed as the Tanzanians and their Ugandan rebel allies occupied Kampala , prompting most Uganda Army loyalists to flee into Sudan and Zaire. [lower-alpha 7] Zairean dictator Mobutu Sese Seko allowed the Ugandan exiles, including Gowon, to stay in his country. As many believed that Gowon had actually been bribed by the Tanzanians and lost the war on purpose, he became a persona non grata among the Ugandan exiles and thus excluded from plans by Amin loyalists to launch a rebellion to regain power. Gowon was actually pleased about this, as he had no interest in resuming fighting. Instead, Gowon focused on building a new life in Zaire, taking up residency in Kisangani . By befriending a Zairean customs officer, he had transported some trucks out of Uganda and would subsequently rent them out. He was also involved in smuggling, and eventually made enough money to buy a house in Bunia where he was joined by two of his wives. At the same time, Uganda descended into civil war which resulted in Yoweri Museveni 's rise to presidency in 1986. Museveni's government focused on national reconstruction, and offered reconciliation to Amin's former followers. Gowon took up this offer in 1994. He returned to Uganda with 25 other ex-officers, hundreds of dependants, and over ten thousand civilian refugees. Museveni personally welcomed Gowon back to Uganda, and the two even laughingly reminisced about the 1972 invasion during which they had fought each other (Museveni had been part of Obote's rebel alliance at the time). Mbarara threw a "huge party" in Gowon's honor. The Ugandan government rented him a house in Ntinda , and granted him a stipend. Grateful for this treatment, Gowon subsequently supported Museveni, and made speeches in his favor during the 1996 Ugandan presidential election . The former Chief of Staff also founded "Good Hope" and "Alternatives to Violence", nonprofit organizations to help ex-combatants to find civilian jobs. The Ugandan government promised Gowon funds to set up companies in which the ex-rebels could be employed, but the money never materialised. Over the next years, his stipend was paid ever less regularly, and Gowon was no longer able to pay his rent. He was evicted from his Ntinda residence, and had to relocate to live in a bicycle shop run by one of his sons. Broke and without a job, he spent most his time in the Slow Boat Pub . At some point, Gowon became the leader of a Uganda Army veterans association. Gowon lived in retirement until 2001, when he was arrested by the Ugandan police for the murder of county chief Eliphaz Laki. According to the testimony of two former subordinates of Gowon, Laki had been murdered on his orders during the purges following the 1972 invasion. The former Chief of Staff disputed any knowledge of or involvement in Laki's death, but was placed in the Luzira Maximum Security Prison and put on trial. Gowon faced the death sentence if convicted of the murder. His trial generated much publicity in Uganda, as most crimes during Amin's regime remained unresolved due to lack of evidence and lack of interest in prosecuting them on the side of the Ugandan government which wants to maintain communal peace. The prosecutors, the families of victims, and reporters saw Gowon's trial as the last chance to finally address the injustices of Amin's regime which had killed between 100,000 and 300,000 people, as the majority of the perpetrators were already quite old. Lead prosecutor Simon Byabakama Mugenyi stated that "It's like our Nuremberg Trial ." Others, mostly people from West Nile, saw Gowon as victim of political conspiracies. Gowon believed that his old rival, Moses Ali, was behind his trial. By then, Ali had risen to minister of internal affairs in Museveni's government and was quite influential. At some point, the minister allegedly visited Luzira Prison just to enjoy seeing Gowon imprisoned; Ali denied all of this, once stating that he "did not even know [that Gowon] was arrested" until reading of it in the newspapers. In general, prison life was difficult for Gowon and he lost more than thirty pounds while incarcerated. However, he had few problems with most other prisoners at Luzira and even developed a friendship with one of his former enemies who also served a prison term. However, he had a tense relationship with those prisoners who had formerly served alongside him in the Uganda Army. The hostility between him and his ex-superior Ali Fadhul was so intense that prison authorities had to keep the two separate. The former Chief of Staff maintained his innocence during the entire trial, stating on one occasion that "These people were civilians. They could not have been killed. This is what I know." Gowon's former subordinates had confessed before the trial that they had murdered Laki on Gowon's direct order, but the reliability of their confessions was questioned during the trial. They had told the police about Gowon's order because they had already been arrested on charges of murder, hoping to be treated leniently by indicting Gowon. When this did not come to pass, the purported witnesses recanted their confessions. As the prosecutors attempted to gather more and firmer evidence for Gowon's guilt, the trial dragged on for almost a year. The trial resulted in tensions among Gowon's family. When well-wishers donated money for his defense, one of his sons absconded with it. The former Chief of Staff then tried to hire an attorney, Caleb Alaka, by promising him a house, but Gowon's wife promptly sued him. She argued that the house in question was rightfully hers. In the end, Alaka still took the case out of respect and pity for the former Chief of Staff. Early in the trial, one person offered Gowon's family and the defense attorney to speak out in favor of the former Chief of Staff in return for a bribe; the family had to refuse, as they were still broke. [lower-alpha 8] Though Laki's son had managed to gather evidence which suggested that Gowon was guilty, it was regarded as inadmissible by the judge. The defense attempted to discredit other evidence which had been found by a private investigator who died while the trial was still ongoing, arguing that the latter had died of a mental disorder although he had in fact died of HIV/AIDS . In the middle of the trial, defense attorney Caleb Alaka simply disappeared; he later resurfaced in Western Nile, where he had taken a job representing a rebel group which had signed a peace deal with the Ugandan government. Five months later he rejoined Gowon's trial, only to disappear again in February 2003, this time for good. For lack of firm evidence, the judge acquitted Gowon and the two other defendants on 25 September 2003. His release was celebrated by his family and sympathizers, mostly from West Nile, while Laki's family and sympathizers, mostly from southern Uganda, decried it as injustice. Some even spread conspiracy theories according to which the government had installed the judge, a Muslim, because he would support Gowon and his co-defendants. The former Chief of Staff regarded the verdict as vindication of his innocence. Following his release, Gowon resumed his work in the veterans association, and consequently advocated for a greater unity among ex-combatants of West Nile origin. However, he struggled to pay the legal bills of the trial. By 2005, he was spending most of his time at Arua where he still possessed a house, and had joined a class action lawsuit against several banks that had frozen assets of Amin-era officials worth 50 million dollars. Gowon died of heart failure at a hospital in Arua on 2 February 2024, at the age of 85. He was buried the following day in the Arua Muslim Cemetery. After his death, he was praised by President Museveni and Swaib Toko , Resident District Commissioner of Madi-Okollo . Academic Andrew Rice described Gowon as a "simple man" who was "cheerful by disposition", and easily made friends. This view was shared by journalist Clement Aluma. He had 28 children by four different wives, and 22 grandchildren. Gowon was fluent in Swahili , and he understood a little English . He was a Muslim . In his later years, Gowon often entertained visitors at his home to tell them of his experiences in the military.

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West Nile

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Corvus

Many, see List of Corvus species Corvus is a widely distributed genus of passerine birds ranging from medium-sized to large-sized in the family Corvidae . It includes species commonly known as crows , ravens , and rooks. The species commonly encountered in Europe are the carrion crow , hooded crow , common raven , and rook ; those discovered later were named "crow" or "raven" chiefly on the basis of their size, crows generally being smaller. The genus name is Latin for "raven". The 46 or so members of this genus occur on all temperate continents except South America , and several islands. The Corvus genus makes up a third of the species in the family Corvidae. The members appear to have evolved in Asia from the corvid stock, which had evolved in Australia . The collective name for a group of crows is a "flock" or a "murder". Recent research has found some crow species capable of not only tool use , but also tool construction. Crows are now considered to be among the world's most intelligent animals with an encephalization quotient equal to that of many non-human primates. Medium-large species are ascribed to the genus, ranging from 34 cm (13 in) of some small Mexican species to 60–70 cm (24–28 in) of the large common raven and thick-billed raven , which together with the lyrebird represent the larger passerines. These are birds with a robust and slender appearance, equipped with a small, rounded head with a strong, conical beak, elongated and pointed, with a slightly curved end towards the bottom; the legs are strong and the tail is short and wedge-shaped. The coloration of the livery is dominated by shades of black, with some species having plumage with metallic iridescence and others that have white or gray areas on the neck or torso. Australian species have light eyes, while generally the irises of other species are dark. Sexual dimorphism is limited.The members of the genus Corvus are believed to have evolved in Central Asia and radiated out from there into North America , Africa , Europe , and Australia. The center of diversity of Corvus is within Melanesia , Wallacea , and the island of New Guinea and surrounding islands, with numerous species endemic to islands in the area; other areas with a large number of crow species include South and Southeast Asia , East Africa , and Australia. A high density of endemics is also present in Mexico and the Caribbean . The diversification of Corvus corresponded with a quick geographic expansion. The radiation of the genus resulted in rapid expansion of morphological diversity and fast speciation rates, especially around the beginning of the genus' radiation around 10 million years ago. The genus was originally described by Carl Linnaeus in his 1758 10th edition of Systema Naturae . The name is derived from the Latin corvus meaning "raven". The type species is the common raven ( Corvus corax ); others named by Linnaeus in the same work include the carrion crow ( C. corone ), hooded crow ( C. cornix ), rook ( C. frugilegus ), and two species which have since been moved to other genera, the western jackdaw (now Coloeus monedula ) and the Eurasian magpie (now Pica pica ). At least 42 extant species are now considered to be members of Corvus , and at least 14 extinct species have been described. The fossil record of crows is rather dense in Europe, but the relationships among most prehistoric species are not clear. Corvids are found in major cities across the world, and a major increase in the number of crows in urban settings has occurred since the 1900s. Historical records suggest that the population of American crows found in North America has been growing steadily since the introduction of European colonization, and spread east to west with the opening of the frontier. Crows were uncommon in the Pacific Northwest in the 1900s, except in riparian habitats . Populations in the west increased substantially from the late 1800s to the mid-1900s. Crows and ravens spread along with agriculture and urbanization into the western part of North America. Crows gather in large communal roosts numbering between 200 and tens of thousands of individuals during nonbreeding months, particularly in the winter. These gatherings tend to happen near large food sources such as garbage dumps and shopping centers. Countless incidents are recorded of corvids at play. Many behaviourists see play as an essential quality in intelligent animals. Crows and the other members of the genus make a wide variety of calls or vocalizations. Crows have also been observed to respond to calls of other species; presumably, this behavior is learned because it varies regionally. Crows' vocalizations are complex and poorly understood. Some of the many vocalizations that crows make are a "koww", usually echoed back and forth between birds, a series of "kowws" in discrete units, a long caw followed by a series of short caws (usually made when a bird takes off from a perch), an echo-like "eh-aw" sound, and more. These vocalizations vary by species, and within each species they vary regionally. In many species, the pattern and number of the numerous vocalizations have been observed to change in response to events in the surroundings (e.g. arrival or departure of crows). Along with other birds, ravens have been known to associate with other animals such as coyotes and wolves . These associations are linked to feeding and hunting. Ravens use their calls to notify these animals when an injured prey is near. This interaction is most noticeable in winter where ravens are associated with wolf packs nearly 100% of the time. As a result of this connection, studies have been conducted on the reaction of prey animals to the call of the raven. In areas where ravens associate with predators, prey animals are more likely to avoid predation by leaving after hearing the call. Crows are also capable of distinguishing between coyotes and wolves and have shown a preference for wolves. This may be due to the fact that wolves kill larger prey. When hunting, ravens can locate injured animals, like elk, and can call out to wolves to kill them. At times, ravens associate with wolves even when there is no carcass and can even be seen forming relationships with them. This includes playing with cubs by using sticks, picking at their tails, or flying around them. Ravens have been mostly seen among travelling wolf packs rather than resting wolves, possibly due to the increased likelihood of food. They are also known to trust wolves in the pack they follow; when encountering a carcass killed by animals other than wolves, they are more apprehensive to eat from it. This symbiotic relationship between ravens and wolves is shown to be mutualistic ; ravens help wolves find prey and when the wolves kill them the ravens can eat too. However, this relationship is not without its faults. Ravens may sometimes eat more of the prey than the wolf does. This problem has also been linked to wolf pack size, with some researchers suggesting that one of the reasons wolves hunt in larger packs is so that ravens (and other scavengers) get less of the food. Along with contention in wolves, ravens can also bother each other. By feeding off of the same carcass it is possible that some ravens will steal from their conspecifics. This behaviour is related to the ravens' ability to make quick decisions about eating the food then or storing it for later, and to their dominance and fighting ability. As a group, crows show remarkable examples of intelligence. Natural history books from the 18th century recount an often-repeated, but unproven anecdote of "counting crows"—specifically a crow whose ability to count to five (or four in some versions) is established through a logic trap set by a farmer. Crows and ravens often score very highly on intelligence tests. Certain species top the avian IQ scale. Wild hooded crows in Israel have learned to use bread crumbs for bait-fishing. [ unreliable source? ] Crows engage in a kind of midair jousting , or air " chicken " to establish pecking order. They have been found to engage in activities such as sports, tool use, the ability to hide and store food across seasons, episodic-like memory , and the ability to use individual experience in predicting the behavior of proximal conspecifics. One species, the New Caledonian crow , has also been intensively studied recently because of its ability to manufacture and use tools in the day-to-day search for food. On 5 October 2007, researchers from the University of Oxford presented data acquired by mounting tiny video cameras on the tails of New Caledonian crows. They pluck, smooth, and bend twigs and grass stems to procure a variety of foodstuffs. Crows in Queensland have learned how to eat the toxic cane toad by flipping the cane toad on its back and stabbing the throat where the skin is thinner, allowing the crow to access the nontoxic innards; their long beaks ensure that all of the innards can be removed. The western jackdaw and the Eurasian magpie have been found to have a nidopallium about the same relative size as the functionally equivalent neocortex in chimpanzees and humans, and significantly larger than is found in the gibbons . Crows have demonstrated the ability to distinguish individual humans by recognizing facial features. Evidence also suggests they are one of the few nonhuman animals, along with insects like bees or ants, capable of displacement (communication about things that are not immediately present, spatially or temporally). In the Gumyoji Park of Yokohama , Japan , crows have shown the ability to both activate public drinking fountains and adjust the water flow to appropriate levels for either bathing or drinking. Many studies have been conducted to research the ways in which ravens and corvids learn. Some have concluded that the brains of ravens and crows compare in relative size to great apes. The encephalization quotient (EQ) helps to expose the similarities between a great ape brain and a crow/raven brain. This includes cognitive ability. Though the brains differ significantly between mammals and birds, larger forebrains are seen in corvids compared to other birds (except some parrots), especially in areas associated with social learning, planning, decision making in humans and complex cognition in apes. Along with tool use, ravens can recognize themselves in a mirror. This complex cognition can also be extended to socio-cognitive abilities. Studies have been conducted regarding the development and evolution of social abilities in ravens. These results help to show how ravens prefer to form stable relationships with siblings and close social partners as opposed to strangers. The development in social abilities is essential for raven survival, including identifying whether something poses a threat and how ravens alert others nearby of an incoming threat. Crows gather in large communal roosts numbering between 200 and tens of thousands of individuals during nonbreeding months, particularly in the winter. These gatherings tend to happen near large food sources such as garbage dumps and shopping centers. Countless incidents are recorded of corvids at play. Many behaviourists see play as an essential quality in intelligent animals. Crows and the other members of the genus make a wide variety of calls or vocalizations. Crows have also been observed to respond to calls of other species; presumably, this behavior is learned because it varies regionally. Crows' vocalizations are complex and poorly understood. Some of the many vocalizations that crows make are a "koww", usually echoed back and forth between birds, a series of "kowws" in discrete units, a long caw followed by a series of short caws (usually made when a bird takes off from a perch), an echo-like "eh-aw" sound, and more. These vocalizations vary by species, and within each species they vary regionally. In many species, the pattern and number of the numerous vocalizations have been observed to change in response to events in the surroundings (e.g. arrival or departure of crows). Along with other birds, ravens have been known to associate with other animals such as coyotes and wolves . These associations are linked to feeding and hunting. Ravens use their calls to notify these animals when an injured prey is near. This interaction is most noticeable in winter where ravens are associated with wolf packs nearly 100% of the time. As a result of this connection, studies have been conducted on the reaction of prey animals to the call of the raven. In areas where ravens associate with predators, prey animals are more likely to avoid predation by leaving after hearing the call. Crows are also capable of distinguishing between coyotes and wolves and have shown a preference for wolves. This may be due to the fact that wolves kill larger prey. When hunting, ravens can locate injured animals, like elk, and can call out to wolves to kill them. At times, ravens associate with wolves even when there is no carcass and can even be seen forming relationships with them. This includes playing with cubs by using sticks, picking at their tails, or flying around them. Ravens have been mostly seen among travelling wolf packs rather than resting wolves, possibly due to the increased likelihood of food. They are also known to trust wolves in the pack they follow; when encountering a carcass killed by animals other than wolves, they are more apprehensive to eat from it. This symbiotic relationship between ravens and wolves is shown to be mutualistic ; ravens help wolves find prey and when the wolves kill them the ravens can eat too. However, this relationship is not without its faults. Ravens may sometimes eat more of the prey than the wolf does. This problem has also been linked to wolf pack size, with some researchers suggesting that one of the reasons wolves hunt in larger packs is so that ravens (and other scavengers) get less of the food. Along with contention in wolves, ravens can also bother each other. By feeding off of the same carcass it is possible that some ravens will steal from their conspecifics. This behaviour is related to the ravens' ability to make quick decisions about eating the food then or storing it for later, and to their dominance and fighting ability. As a group, crows show remarkable examples of intelligence. Natural history books from the 18th century recount an often-repeated, but unproven anecdote of "counting crows"—specifically a crow whose ability to count to five (or four in some versions) is established through a logic trap set by a farmer. Crows and ravens often score very highly on intelligence tests. Certain species top the avian IQ scale. Wild hooded crows in Israel have learned to use bread crumbs for bait-fishing. [ unreliable source? ] Crows engage in a kind of midair jousting , or air " chicken " to establish pecking order. They have been found to engage in activities such as sports, tool use, the ability to hide and store food across seasons, episodic-like memory , and the ability to use individual experience in predicting the behavior of proximal conspecifics. One species, the New Caledonian crow , has also been intensively studied recently because of its ability to manufacture and use tools in the day-to-day search for food. On 5 October 2007, researchers from the University of Oxford presented data acquired by mounting tiny video cameras on the tails of New Caledonian crows. They pluck, smooth, and bend twigs and grass stems to procure a variety of foodstuffs. Crows in Queensland have learned how to eat the toxic cane toad by flipping the cane toad on its back and stabbing the throat where the skin is thinner, allowing the crow to access the nontoxic innards; their long beaks ensure that all of the innards can be removed. The western jackdaw and the Eurasian magpie have been found to have a nidopallium about the same relative size as the functionally equivalent neocortex in chimpanzees and humans, and significantly larger than is found in the gibbons . Crows have demonstrated the ability to distinguish individual humans by recognizing facial features. Evidence also suggests they are one of the few nonhuman animals, along with insects like bees or ants, capable of displacement (communication about things that are not immediately present, spatially or temporally). In the Gumyoji Park of Yokohama , Japan , crows have shown the ability to both activate public drinking fountains and adjust the water flow to appropriate levels for either bathing or drinking. Many studies have been conducted to research the ways in which ravens and corvids learn. Some have concluded that the brains of ravens and crows compare in relative size to great apes. The encephalization quotient (EQ) helps to expose the similarities between a great ape brain and a crow/raven brain. This includes cognitive ability. Though the brains differ significantly between mammals and birds, larger forebrains are seen in corvids compared to other birds (except some parrots), especially in areas associated with social learning, planning, decision making in humans and complex cognition in apes. Along with tool use, ravens can recognize themselves in a mirror. This complex cognition can also be extended to socio-cognitive abilities. Studies have been conducted regarding the development and evolution of social abilities in ravens. These results help to show how ravens prefer to form stable relationships with siblings and close social partners as opposed to strangers. The development in social abilities is essential for raven survival, including identifying whether something poses a threat and how ravens alert others nearby of an incoming threat. Crows are omnivorous, and their diets are very diverse. They eat almost any food, including other birds, fruits, nuts, mollusks, earthworms, seeds, frogs, eggs, nestlings, mice, and carrion. The origin of placing scarecrows in grain fields resulted from the crow's incessant damaging and scavenging, although crows assist farmers by eating insects otherwise attracted to their crops. Crows reach sexual maturity around the age of three years for females and five years for males. Clutch size is around three to nine eggs, and the nesting period lasts between 20 and 40 days. While crows typically mate for life, extra-pair copulation is not unusual, and young from previous years often help nesting pairs protect a nest and feed nestlings. Crow nestlings in urban areas face threats such as nest entanglement from anthropogenic nesting materials and stunted growth due to poor nutrition. Some crows may live to the age of 20, and the oldest known American crow in the wild was almost 30 years old. The oldest documented captive crow died at age 59. The American crow is highly susceptible to the recently introduced North American strain of West Nile virus . American crows typically die within one week of acquiring the disease and very few survive exposure.Two species of crows have been listed as endangered by the U.S. Fish and Wildlife Service - the Hawaiian crow and the Mariana crow . The American crow, despite having its population reduced by 45% since 1999 by the West Nile virus, is considered a species of least concern .Intelligence and social structures make most crow species adaptable and opportunistic. Crows frequently cause damage to crops and property, strew trash, and transfer disease. In densely populated areas around the world, corvids are generally regarded as nuisance animals. Crows are protected in the U.S. under the federal Migratory Bird Treaty Act of 1918, but because of their perceived destructive nature, control of the species is allowed in certain areas. Because of their intelligence, control is often difficult or expensive. Methods for control include hunting, chemical immobilization, harassment and scare tactics, and trapping. Before any measure is used to confine, trap, kill, poison, immobilize, or alter the habits of any wild bird species, a person must check local, state, and federal regulations pertaining to such actions. In the United States, hunting is allowed under state and federal regulation. Crow hunting is considered a sport in rural areas of the U.S. because the birds are not considered a traditional edible game species. Some cultures do treat various corvid species as a food source. Liability and possible danger to persons and property limit the use of hunting or shooting as control methods in urban areas. Crows' wariness and cunning make harvesting crows in sufficient numbers difficult. Scare tactics have been the most widely used aversion tactic for crows in areas frequented by humans and domestic animal species. This safe method does not require constant maintenance or manpower to operate or monitor. However, corvids quickly become habituated to most tactics such as blast cannons, predator decoys, and traditional scarecrows. Greater success has been achieved by adding sound and motion to predator decoys to mimic a distressed crow being caught by a predator such as an owl or hawk. Work is currently being done which uses multiple aversion techniques in one area. The theory is that multiple techniques used together will confuse the crows, thereby lessening the probability of habituation to stimuli. Trapping is a rarely used technique in the U.S., but is being used with success in parts of Europe and Australia. The ladder-style trap (e.g., Australian Crow Trap or Modified Australian Crow Trap) seems to be the most effective in crow-trapping techniques. Ladder traps are constructed in such a way that unintentional catch of nontarget species is avoided. If a nontarget species is caught, it can be easily released without harm to the bird. The traps are cost-efficient because they are inexpensive and simple to construct, and require little manpower to monitor. The bait used in the traps can also be specific to corvids. Carrion, grains, unshelled raw peanuts, and shiny objects in the trap are effective baits. [ citation needed ] When removing crows from a ladder trap, one living crow is left as an effective decoy for other crows. Trapping is considered [ by whom? ] the most humane method for crow removal because the crows can be relocated without harm or stress. However, most wild birds in general have a knack for returning to their home ranges. Other methods have been used with little or limited success. Lasers have been used successfully to remove large flocks of birds from roost structures in urban areas, but success in keeping crows off roosts has been short-lived. Homeowners can reduce the presence of crows by keeping trash stored in containers, feeding pets indoors, and hanging tin pie-pans or reflective gazing globes around garden areas.In the United States, hunting is allowed under state and federal regulation. Crow hunting is considered a sport in rural areas of the U.S. because the birds are not considered a traditional edible game species. Some cultures do treat various corvid species as a food source. Liability and possible danger to persons and property limit the use of hunting or shooting as control methods in urban areas. Crows' wariness and cunning make harvesting crows in sufficient numbers difficult.Scare tactics have been the most widely used aversion tactic for crows in areas frequented by humans and domestic animal species. This safe method does not require constant maintenance or manpower to operate or monitor. However, corvids quickly become habituated to most tactics such as blast cannons, predator decoys, and traditional scarecrows. Greater success has been achieved by adding sound and motion to predator decoys to mimic a distressed crow being caught by a predator such as an owl or hawk. Work is currently being done which uses multiple aversion techniques in one area. The theory is that multiple techniques used together will confuse the crows, thereby lessening the probability of habituation to stimuli.Trapping is a rarely used technique in the U.S., but is being used with success in parts of Europe and Australia. The ladder-style trap (e.g., Australian Crow Trap or Modified Australian Crow Trap) seems to be the most effective in crow-trapping techniques. Ladder traps are constructed in such a way that unintentional catch of nontarget species is avoided. If a nontarget species is caught, it can be easily released without harm to the bird. The traps are cost-efficient because they are inexpensive and simple to construct, and require little manpower to monitor. The bait used in the traps can also be specific to corvids. Carrion, grains, unshelled raw peanuts, and shiny objects in the trap are effective baits. [ citation needed ] When removing crows from a ladder trap, one living crow is left as an effective decoy for other crows. Trapping is considered [ by whom? ] the most humane method for crow removal because the crows can be relocated without harm or stress. However, most wild birds in general have a knack for returning to their home ranges. Other methods have been used with little or limited success. Lasers have been used successfully to remove large flocks of birds from roost structures in urban areas, but success in keeping crows off roosts has been short-lived. Homeowners can reduce the presence of crows by keeping trash stored in containers, feeding pets indoors, and hanging tin pie-pans or reflective gazing globes around garden areas.Crows were hunted for survival by Curonians , a Baltic tribe, when common food was exhausted and the landscape changed so that farming was not as productive during the 18th and 19th centuries. Fishermen supplemented their diet by gathering coastal bird eggs and preserving crow meat by salting and smoking it. It became a traditional food for poor folk and is documented in a poem, " The Seasons " by K. Donelaitis . After the nonhunting policy was lifted by the Prussian government in 1721–1724 and alternative food supplies increased, the practice was forgotten. The tradition re-emerged after World War I; in marketplaces, butchered crows that were sought after and bought by townsfolk were common. The hunted crows were not the local, but the migrating ones; each year during the spring and autumn, crows migrated via the Curonian Spit between Finland and the rest of Europe. In 1943, the government even issued a hunting quota for such activities. Crows were usually caught by attracting them with smoked fish or grains soaked in spirits and then collecting them with nets. It was a job for the elderly or young who were unable to go to sea to fish, and it was common to catch 150 to 200 birds during a hunting day.The common raven and carrion crow have been blamed for killing weak lambs and are often seen eating freshly dead corpses probably killed by other means. The Australian raven has been documented chasing, attacking, and seriously injuring lambs. Rooks have been blamed for eating grain in the UK and brown-necked ravens for raiding date crops in desert countries. Crows have been shown to have the ability to visually recognize individual humans and to transmit information about "bad" humans by squawking. Crows appear to show appreciation to humans by presenting them with gifts. In Ancient Greece and Rome, several myths about crows and jackdaws included: In the Bible account at 1 Kings 17:6, ravens are credited with providing Elijah food. In Australian Aboriginal mythology , Crow is a trickster , culture hero , and ancestral being. Legends relating to Crow have been observed in various Aboriginal language groups and cultures across Australia; these commonly include stories relating to Crow's role in the theft of fire, the origin of death, and the killing of Eagle's son. Crows are mentioned often in Buddhism , especially Tibetan disciplines. The Dharmapala (protector of the Dharma) Mahakala is represented by a crow in one of his physical/earthly forms. [ citation needed ] In the Chaldean myth , the Epic of Gilgamesh , Utnapishtim releases a dove and raven to find land; however, the dove merely circles and returns. Only then does Utnapishtim send forth the raven, which does not return, and Utnapishtim concludes the raven has found land. In Chinese mythology , the world originally had 10 suns either spiritually embodied as 10 crows and/or carried by 10 crows; when all 10 decided to rise at once, the effect was devastating to crops, so the gods sent their greatest archer Houyi , who shot down nine crows and spared only one. In Denmark , the night raven is considered an exorcised spirit. A hole in its left wing denotes where the stake used to exorcise it was driven into the earth. He who looks through the hole will become a night raven himself. In Hinduism , crows are thought of as carriers of information that give omens to people regarding their situations. For example, when a crow crows in front of a person's house, the resident is expected to have special visitors that day. Also, in Hindu literature, crows have great memories which they use to give information. [ citation needed ] Symbolism is associated with the crow in the Hindu faith. On a positive note, crows are often associated with worship of ancestors because they are believed to be embodying the souls of the recently deceased. However, many other associations with crows are seen in Hinduism. Crows are believed to be connected with both the gods and goddesses, particularly the controversial ones such as Sani, the god of the planet Saturn , who uses a crow as his vehicle. In Hindu astrology, it is said that one who has the effect of Sani in their horoscope are angered easily, and may be unable to take control of their futures, but are extremely intelligent at the same time. Thus the presence of a crow, the vehicle of Sani is believed to have similar effects on the homes it lays its eyes on. Whether these effects are positive or negative is a source of debate in Hinduism. Crows are also considered ancestors in Hinduism and during Śrāddha , the practice of offering food or pinda to crows is still in vogue. Crows are associated with Dhumavati the form of mother goddess that invokes quarrel and fear. Crows are also fed during the fifteen day period of Pitru Paksha , which occurs in the autumn season, as an offering and sacrifice to the ancestors. During the time of Pitra Paksha, it is believed that the ancestors descend on earth from pitra-loka, and are able to eat food offered to them by the means of a crow. This can also occur during the time of Kumbha , many Hindus prepare entire vegetarian meals that are eaten solely by the crows and other birds. In Irish mythology , crows are associated with Morrigan , the goddess of war and death. In Islam, the Surat Al-Ma'ida of the Qur'an describes the story of how the crow teaches the son of Adam to cover the dead body of his brother: "Then Allah sent a crow digging a grave in the ground for a dead crow, in order to show him how to bury the corpse of his brother. He cried, 'Alas! Have I even failed to be like this crow and bury the corpse of my brother?' So he became regretful." In Japanese mythology , a three-legged crow called Yatagarasu ( å «å’«çƒ , "eight-hand-crow") is depicted. In Korean mythology , a three-legged crow is known as Samjokgo (hangul: 삼족오; hanja: 三足烏). [ citation needed ] In Norse mythology , Huginn and Muninn are a pair of common ravens that range the entire world, Midgard , bringing the god Odin information. In Sweden , ravens are held to be the ghosts of murdered men. In Welsh mythology , the god Brân the Blessed – whose name means "crow" or "raven"—is associated with corvids and death; tradition holds that Bran's severed head is buried under the Tower of London , facing France—a possible genesis for the practice of keeping ravens in the Tower, said to protect the fortunes of Britain. In Cornish folklore , crows—magpies particularly—are associated with death and the "other world", and must be greeted respectfully. The origin of "counting crows" as augury is British; however, the British version rather is to "count magpies"—their black and white pied colouring alluding to the realms of the living and dead. In some Native American mythologies , especially those in the Pacific Northwest, the raven is seen as both the Creator of the World and, separately, a trickster god. In medieval times, crows were thought to live abnormally long lives. They were also thought to be monogamous throughout their long lives. They were thought to predict the future, anticipate rain and reveal ambushes. Crows were also thought to lead flocks of storks while they crossed the sea to Asia. In Ancient Greece and Rome, several myths about crows and jackdaws included: In the Bible account at 1 Kings 17:6, ravens are credited with providing Elijah food. In Australian Aboriginal mythology , Crow is a trickster , culture hero , and ancestral being. Legends relating to Crow have been observed in various Aboriginal language groups and cultures across Australia; these commonly include stories relating to Crow's role in the theft of fire, the origin of death, and the killing of Eagle's son. Crows are mentioned often in Buddhism , especially Tibetan disciplines. The Dharmapala (protector of the Dharma) Mahakala is represented by a crow in one of his physical/earthly forms. [ citation needed ] In the Chaldean myth , the Epic of Gilgamesh , Utnapishtim releases a dove and raven to find land; however, the dove merely circles and returns. Only then does Utnapishtim send forth the raven, which does not return, and Utnapishtim concludes the raven has found land. In Chinese mythology , the world originally had 10 suns either spiritually embodied as 10 crows and/or carried by 10 crows; when all 10 decided to rise at once, the effect was devastating to crops, so the gods sent their greatest archer Houyi , who shot down nine crows and spared only one. In Denmark , the night raven is considered an exorcised spirit. A hole in its left wing denotes where the stake used to exorcise it was driven into the earth. He who looks through the hole will become a night raven himself. In Hinduism , crows are thought of as carriers of information that give omens to people regarding their situations. For example, when a crow crows in front of a person's house, the resident is expected to have special visitors that day. Also, in Hindu literature, crows have great memories which they use to give information. [ citation needed ] Symbolism is associated with the crow in the Hindu faith. On a positive note, crows are often associated with worship of ancestors because they are believed to be embodying the souls of the recently deceased. However, many other associations with crows are seen in Hinduism. Crows are believed to be connected with both the gods and goddesses, particularly the controversial ones such as Sani, the god of the planet Saturn , who uses a crow as his vehicle. In Hindu astrology, it is said that one who has the effect of Sani in their horoscope are angered easily, and may be unable to take control of their futures, but are extremely intelligent at the same time. Thus the presence of a crow, the vehicle of Sani is believed to have similar effects on the homes it lays its eyes on. Whether these effects are positive or negative is a source of debate in Hinduism. Crows are also considered ancestors in Hinduism and during Śrāddha , the practice of offering food or pinda to crows is still in vogue. Crows are associated with Dhumavati the form of mother goddess that invokes quarrel and fear. Crows are also fed during the fifteen day period of Pitru Paksha , which occurs in the autumn season, as an offering and sacrifice to the ancestors. During the time of Pitra Paksha, it is believed that the ancestors descend on earth from pitra-loka, and are able to eat food offered to them by the means of a crow. This can also occur during the time of Kumbha , many Hindus prepare entire vegetarian meals that are eaten solely by the crows and other birds. In Irish mythology , crows are associated with Morrigan , the goddess of war and death. In Islam, the Surat Al-Ma'ida of the Qur'an describes the story of how the crow teaches the son of Adam to cover the dead body of his brother: "Then Allah sent a crow digging a grave in the ground for a dead crow, in order to show him how to bury the corpse of his brother. He cried, 'Alas! Have I even failed to be like this crow and bury the corpse of my brother?' So he became regretful." In Japanese mythology , a three-legged crow called Yatagarasu ( å «å’«çƒ , "eight-hand-crow") is depicted. In Korean mythology , a three-legged crow is known as Samjokgo (hangul: 삼족오; hanja: 三足烏). [ citation needed ] In Norse mythology , Huginn and Muninn are a pair of common ravens that range the entire world, Midgard , bringing the god Odin information. In Sweden , ravens are held to be the ghosts of murdered men. In Welsh mythology , the god Brân the Blessed – whose name means "crow" or "raven"—is associated with corvids and death; tradition holds that Bran's severed head is buried under the Tower of London , facing France—a possible genesis for the practice of keeping ravens in the Tower, said to protect the fortunes of Britain. In Cornish folklore , crows—magpies particularly—are associated with death and the "other world", and must be greeted respectfully. The origin of "counting crows" as augury is British; however, the British version rather is to "count magpies"—their black and white pied colouring alluding to the realms of the living and dead. In some Native American mythologies , especially those in the Pacific Northwest, the raven is seen as both the Creator of the World and, separately, a trickster god. In medieval times, crows were thought to live abnormally long lives. They were also thought to be monogamous throughout their long lives. They were thought to predict the future, anticipate rain and reveal ambushes. Crows were also thought to lead flocks of storks while they crossed the sea to Asia.

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Common raven

8–11, see Classification The common raven ( Corvus corax ) is a large all-black passerine bird. It is the most widely distributed of all corvids , found across the Northern Hemisphere . It is a raven known by many names at the subspecies level ; there are at least eight subspecies with little variation in appearance, although recent research has demonstrated significant genetic differences among populations from various regions. It is one of the two largest corvids, alongside the thick-billed raven , and is possibly the heaviest passerine bird; at maturity, the common raven averages 63 centimetres (25 inches) in length and 1.47 kilograms (3.2 pounds) in mass. Although their typical lifespan is considerably shorter, common ravens can live more than 23 years in the wild. Young birds may travel in flocks but later mate for life , with each mated pair defending a territory . Common ravens have coexisted with humans for thousands of years and in some areas have been so numerous that people have regarded them as pests . Part of their success as a species is due to their omnivorous diet ; they are extremely versatile and opportunistic in finding sources of nutrition, feeding on carrion , insects, cereal grains, berries, fruit, small animals, nesting birds, and food waste. Some notable feats of problem-solving provide evidence that the common raven is unusually intelligent . Over the centuries, the raven has been the subject of mythology, folklore, art, and literature. In many cultures, including the indigenous cultures of Scandinavia , ancient Ireland and Wales, Bhutan , the northwest coast of North America , and Siberia and northeast Asia, the common raven has been revered as a spiritual figure or godlike creature.The common raven was one of the many species originally described, with its type locality given as Europe, by Carl Linnaeus in his landmark 1758 10th edition of Systema Naturae , and it still bears its original name of Corvus corax . It is the type species of the genus Corvus , derived from the Latin word for 'raven'. The specific epithet corax is the Latinized form of the Greek word κόραξ , meaning 'raven' or 'crow'. The modern English word raven has cognates in many other Germanic languages , including Old Norse (and subsequently modern Icelandic ) hrafn and Old High German (h)raban , all which descend from Proto-Germanic * khrabanas . An old Scottish word corby or corbie , akin to the French corbeau , has been used for both this bird and the carrion crow . Collective nouns for a group of ravens (or at least the common raven) include "unkindness" and "conspiracy". The closest relatives of the common raven are the brown-necked raven ( C. ruficollis ), the pied crow ( C. albus ) of Africa, and the Chihuahuan raven ( C. cryptoleucus ) of the North American Southwest. While some authorities have recognized as many as 11 subspecies , others recognize only eight: The name C. c. laurencei (also spelt lawrencii or laurencii ) is sometimes used instead of C. c. subcorax . It is based on the population from Sindh described by Hume in 1873 and is sometimes preferred, since the type specimen of subcorax collected by Nikolai Severtzov is possibly a brown-necked raven . The population of this subspecies restricted to the Sindh district of Pakistan and the adjoining regions of northwestern India is sometimes known as the Punjab raven. The common raven evolved in the Old World and crossed the Bering land bridge into North America. Recent genetic studies, which examined the DNA of common ravens from across the world, have determined that the birds fall into at least two clades : a California clade, found only in the southwestern United States, and a Holarctic clade, found across the rest of the Northern Hemisphere. Birds from both clades look alike, but the groups are genetically distinct and began to diverge about two million years ago. The findings indicate that based on mitochondrial DNA , common ravens from the rest of the United States are more closely related to those in Europe and Asia than to those in the California clade, and that common ravens in the California clade are more closely related to the Chihuahuan raven ( C. cryptoleucus ) than to those in the Holarctic clade. Ravens in the Holarctic clade are more closely related to the pied crow ( C. albus ) than they are to the California clade. Thus, the common raven species as traditionally delimited is considered to be paraphyletic . One explanation for these genetic findings is that common ravens settled in California at least two million years ago and became separated from their relatives in Europe and Asia during a glacial period . One million years ago, a group from the California clade evolved into a new species, the Chihuahuan raven. Other members of the Holarctic clade arrived later in a separate migration from Asia, perhaps at the same time as humans. A 2011 study suggested that there are no restrictions on gene flow between the Californian and Holarctic common raven groups, and that the lineages can remerge, effectively reversing a potential speciation. A recent study of raven mitochondrial DNA showed that the isolated population from the Canary Islands is distinct from other populations. The study did not include any individuals from the North African population, and its position is therefore unclear, though its morphology is very close to the population of the Canaries (to the extent that the two are often considered part of a single subspecies). The closest relatives of the common raven are the brown-necked raven ( C. ruficollis ), the pied crow ( C. albus ) of Africa, and the Chihuahuan raven ( C. cryptoleucus ) of the North American Southwest. While some authorities have recognized as many as 11 subspecies , others recognize only eight: The name C. c. laurencei (also spelt lawrencii or laurencii ) is sometimes used instead of C. c. subcorax . It is based on the population from Sindh described by Hume in 1873 and is sometimes preferred, since the type specimen of subcorax collected by Nikolai Severtzov is possibly a brown-necked raven . The population of this subspecies restricted to the Sindh district of Pakistan and the adjoining regions of northwestern India is sometimes known as the Punjab raven. The common raven evolved in the Old World and crossed the Bering land bridge into North America. Recent genetic studies, which examined the DNA of common ravens from across the world, have determined that the birds fall into at least two clades : a California clade, found only in the southwestern United States, and a Holarctic clade, found across the rest of the Northern Hemisphere. Birds from both clades look alike, but the groups are genetically distinct and began to diverge about two million years ago. The findings indicate that based on mitochondrial DNA , common ravens from the rest of the United States are more closely related to those in Europe and Asia than to those in the California clade, and that common ravens in the California clade are more closely related to the Chihuahuan raven ( C. cryptoleucus ) than to those in the Holarctic clade. Ravens in the Holarctic clade are more closely related to the pied crow ( C. albus ) than they are to the California clade. Thus, the common raven species as traditionally delimited is considered to be paraphyletic . One explanation for these genetic findings is that common ravens settled in California at least two million years ago and became separated from their relatives in Europe and Asia during a glacial period . One million years ago, a group from the California clade evolved into a new species, the Chihuahuan raven. Other members of the Holarctic clade arrived later in a separate migration from Asia, perhaps at the same time as humans. A 2011 study suggested that there are no restrictions on gene flow between the Californian and Holarctic common raven groups, and that the lineages can remerge, effectively reversing a potential speciation. A recent study of raven mitochondrial DNA showed that the isolated population from the Canary Islands is distinct from other populations. The study did not include any individuals from the North African population, and its position is therefore unclear, though its morphology is very close to the population of the Canaries (to the extent that the two are often considered part of a single subspecies). A mature common raven ranges between 54 and 71 cm (21 and 28 in) and has a wingspan of 116 to 153 cm (46 to 60 in) . Recorded weights range from 0.69 to 2.250 kg (1.52 to 4.96 lb) , thus making the common raven one of the heaviest passerines . Birds from colder regions such as the Himalayas and Greenland are generally larger with slightly larger bills, while those from warmer regions are smaller with proportionally smaller bills. Representative of the size variation in the species, ravens from California weighed an average of 0.784 kg (1.73 lb) , those from Alaska weighed an average of 1.135 kg (2.50 lb) and those from Nova Scotia weighed an average of 1.230 kg (2.71 lb) . The bill is large and slightly curved, with a culmen length of 5.7 to 8.5 cm (2.2 to 3.3 in) , easily one of the largest bills amongst passerines (perhaps only the thick-billed raven has a noticeably larger bill). It has a longish, strongly graduated tail, at 20 to 26.3 cm (7.9 to 10.4 in) , and mostly black iridescent plumage, and a dark brown iris . The throat feathers are elongated and pointed and the bases of the neck feathers are pale brownish-grey. The legs and feet are good-sized, with a tarsus length of 6 to 7.2 cm (2.4 to 2.8 in) . Juvenile plumage is similar but duller with a blue-grey iris. Apart from its greater size, the common raven differs from its cousins, the crows , by having a larger and heavier black beak, shaggy feathers around the throat and above the beak, and a wedge-shaped tail. Flying ravens are distinguished from crows by their tail shape, larger wing area, and more stable soaring style, which generally involves less wing flapping. Despite their bulk, ravens are easily as agile in flight as their smaller cousins. In flight the feathers produce a creaking sound that has been likened to the rustle of silk. The voice of ravens is also quite distinct, its usual call being a deep croak of a much more sonorous quality than a crow's call. In North America, the Chihuahuan raven ( C. cryptoleucus ) is fairly similar to the relatively small common ravens of the American southwest and is best distinguished by the still relatively smaller size of its bill, beard and body and relatively longer tail. All-black carrion crow ( C. corone ) in Europe may suggest a raven due to their largish bill but are still distinctly smaller and have the wing and tail shapes typical of crows. In the Faroe Islands , a now-extinct white-and-black colour morph of this species existed, known as the pied raven ; the ordinary black-coloured common ravens remain widespread in the archipelago. White ravens are occasionally found in the wild. Birds in British Columbia lack the pink eyes of an albino, and are instead leucistic , a condition where an animal lacks any of several different types of pigment, not simply melanin . Common ravens have a wide range of vocalizations which are of interest to ornithologists . Gwinner carried out important studies in the early 1960s, recording and photographing his findings in great detail. Fifteen to 30 categories of vocalization have been recorded for this species, most of which are used for social interaction. Calls recorded include alarm calls, chase calls, and flight calls. The species has a distinctive, deep, resonant prruk-prruk-prruk call, which to experienced listeners is unlike that of any other corvid. Its very wide and complex vocabulary includes a high, knocking toc-toc-toc , a dry, grating kraa , a low guttural rattle and some calls of an almost musical nature. Like other corvids, the common raven can mimic sounds from their environment, including human speech. Non-vocal sounds produced by the common raven include wing whistles and bill snapping. Clapping or clicking has been observed more often in females than in males. If a member of a pair is lost, its mate reproduces the calls of its lost partner to encourage its return. The common raven can thrive in varied climates; it has the largest range of any member of the genus, and one of the largest of any passerine. They range throughout the Holarctic from Arctic and temperate habitats in North America and Eurasia to the deserts of North Africa, and to islands in the Pacific Ocean. In the British Isles, they are more common in Scotland, Wales, northern England and the west of Ireland. In Tibet , they have been recorded at altitudes up to 5,000 m (16,400 ft), and as high as 6,350 m (20,600 ft) on Mount Everest . The population sometimes known as the Punjab raven—described as Corvus corax laurencei (also spelt lawrencii or laurencii ) by Allan Octavian Hume but more often considered synonymous with subcorax —is restricted to the Sindh district of Pakistan and adjoining regions of northwestern India. They are generally resident within their range for the whole year. In his 1950 work, Grønlands Fugle [ Birds of Greenland ], noted ornithologist Finn Salomonsen indicated that common ravens did not overwinter in the Arctic. However, in Arctic Canada and Alaska, they are found year-round. Young birds may disperse locally. In the United Kingdom, the common raven's range is currently increasing. It favours mountainous or coastal terrain, but can also be found in parks with tall trees suitable for use as habitation. Its population is at its most dense in the north and west of the country, though the species is expanding its population southwards. Most common ravens prefer wooded areas with large expanses of open land nearby, or coastal regions for their nesting sites and feeding grounds. In some areas of dense human population, such as California in the United States, they take advantage of a plentiful food supply and have seen a surge in their numbers. On coasts, individuals of this species are often evenly distributed and prefer to build their nest sites along sea cliffs. Common ravens are often located in coastal regions because these areas provide easy access to water and a variety of food sources. Also, coastal regions have stable weather patterns without extreme cold or hot temperatures. In general, common ravens live in a wide array of environments but prefer heavily contoured landscapes. When the environment changes in vast degrees, these birds will respond with a stress response. The hormone known as corticosterone is activated by the hypothalamic–pituitary–adrenal axis . Corticosterone is activated when the bird is exposed to stress, such as migrating great distances.Common ravens usually travel in mated pairs, although young birds may form flocks . Relationships between common ravens are often quarrelsome, yet they demonstrate considerable devotion to their families. Owing to its size, gregariousness and its defensive abilities, the common raven has few natural predators. Predators of its eggs include owls , martens , and sometimes eagles . Ravens are quite vigorous at defending their young and are usually successful at driving off perceived threats. They attack potential predators by flying at them and lunging with their large bills. Humans are occasionally attacked if they get close to a raven nest, though serious injuries are unlikely. There are a few records of predation by large birds of prey. Their attackers in America have reportedly included great horned owls , northern goshawks , bald eagles , golden eagles and red-tailed hawks . It is possible that the two hawk species only attack young ravens; in one instance a peregrine falcon swooped at a newly fledged raven but was chased off by the parent ravens. In Eurasia , their reported predators include, in addition to golden eagles, Eurasian eagle-owls , white-tailed eagles , Steller's sea-eagles , eastern imperial eagles and gyrfalcons . Because they are potentially hazardous prey for raptorial birds, raptors must usually take them by surprise and most attacks are on fledgling ravens. More rarely still, large mammalian predators such as lynxes , coyotes and cougars have also attacked ravens. This principally occurs at a nest site and when other prey for the carnivores are scarce. Ravens are highly wary around novel carrion sites and, in North America, have been recorded waiting for the presence of American crows and blue jays before approaching to eat. Juveniles begin to court at a very early age, but may not bond for another two or three years. Aerial acrobatics, demonstrations of intelligence, and ability to provide food are key behaviours of courting. Once paired, they tend to nest together for life, usually in the same location. Instances of non-monogamy have been observed in common ravens, by males visiting a female's nest when her mate is away. Breeding pairs must have a territory of their own before they begin nest-building and reproduction, and thus they aggressively defend a territory and its food resources. Nesting territories vary in size according to the density of food resources in the area. The nest is a deep bowl made of large sticks and twigs, bound with an inner layer of roots, mud, and bark and lined with a softer material, such as deer fur. The nest is usually placed in a large tree or on a cliff ledge, or less frequently in old buildings or utility poles. Females lay between three and seven pale bluish-green, brown-blotched eggs. Incubation is about 18 to 21 days, by the female only. The male may stand or crouch over the young, sheltering but not actually brooding them. Young fledge at 35 to 42 days, and are fed by both parents. They stay with their parents for another six months after fledging. In most of their range, egg-laying begins in late February, but it can be as late as April in colder climates such as Greenland and Tibet . In Pakistan, egg-laying takes place in December. Eggs and hatchlings are preyed on, rarely, by large hawks and eagles , large owls , martens and canids . The adults, which are very rarely preyed upon, are often successful in defending their young from these predators, due to their numbers, large size and cunning. They have been observed dropping stones on potential predators that venture close to their nests. Common ravens can be very long-lived, especially in captive or protected conditions; individuals at the Tower of London have lived for more than 40 years. Their lifespans in the wild are shorter, typically 10 to 15 years. The longest known lifespan of a banded wild common raven was 23 years, 3 months, which among passerines only is surpassed by a few Australian species such as the satin bowerbird . Common ravens are omnivorous and highly opportunistic : their diet may vary widely with location, season and serendipity . For example, those foraging on tundra on the Arctic North Slope of Alaska obtained about half their energy needs from predation , mainly of microtine rodents , and half by scavenging, mainly of caribou and ptarmigan carcasses. In some places they are mainly scavengers , feeding on carrion as well as the associated maggots and carrion beetles . With large-bodied carrion, which they are not equipped to tear through as well as birds such as hook-billed vultures , they must wait for the prey to be torn open by another predator or flayed by other means. They are also known to eat the afterbirth of ewes and other large mammals. Plant food includes cereal grains, acorns, buds, berries and fruit. They prey on small invertebrates , amphibians, reptiles, small mammals and birds. Ravens may also consume the undigested portions of animal feces, and human food waste. They store surplus food items, especially those containing fat, and will learn to hide such food out of the sight of other common ravens. Ravens also raid the food caches of other species, such as the Arctic fox . They sometimes associate with another canine, the grey wolf , as a kleptoparasite , following to scavenge wolf-kills in winter. Ravens are regular predators at bird nests, brazenly picking off eggs, nestlings and sometimes adult birds when they spot an opportunity. They are considered perhaps the primary natural threat to the nesting success of the critically endangered California condor , since they readily take condor eggs and are very common in the areas where the species is being re-introduced. On the other hand, when they defend their own adjacent nests, they may incidentally benefit condors since they chase golden eagles out of the area that may otherwise prey upon larger nestling and fledging condors. Condors, despite their large size, do not seem to have well developed nest defenses. Common ravens nesting near sources of human garbage included a higher percentage of food waste in their diet, birds nesting near roads consumed more road-killed vertebrates , and those nesting far from these sources of food ate more arthropods and plant material. Fledging success was higher for those using human garbage as a food source. In contrast, a 1984–1986 study of common raven diet in an agricultural region of southwestern Idaho found that cereal grains were the principal constituent of pellets , though small mammals, grasshoppers, cattle carrion and birds were also eaten. One behaviour is recruitment, where juvenile ravens call other ravens to a food bonanza, usually a carcass, with a series of loud yells. In Ravens in Winter , Bernd Heinrich posited that this behaviour evolved to allow the juveniles to outnumber the resident adults, thus allowing them to feed on the carcass without being chased away. A more mundane explanation is that individuals co-operate in sharing information about carcasses of large mammals because they are too big for just a few birds to exploit. Experiments with baits however show that such recruitment behaviour is independent of the size of the bait. Furthermore, there has been research suggesting that the common raven is involved in seed dispersal. In the wild, the common raven chooses the best habitat and disperses seeds in locations best suited for its survival. The brain of the common raven is among the largest of any bird species. Specifically, their hyperpallium is large for a bird. They display ability in problem-solving, as well as other cognitive processes such as imitation and insight . Linguist Derek Bickerton , building on the work of biologist Bernd Heinrich , has argued that ravens are one of only four known animals (the others being bees , ants , and humans) who have demonstrated displacement , the capacity to communicate about objects or events that are distant in space or time. Subadult ravens roost together at night, but usually forage alone during the day. However, when one discovers a large carcass guarded by a pair of adult ravens, the unmated raven will return to the roost and communicate the find. The following day, a flock of unmated ravens will fly to the carcass and chase off the adults. Bickerton argues that the advent of linguistic displacement was perhaps the most important event in the evolution of human language, and that ravens are the only other vertebrate to share this with humans. One experiment designed to evaluate insight and problem-solving ability involved a piece of meat attached to a string hanging from a perch. To reach the food, the bird needed to stand on the perch, pull the string up a little at a time, and step on the loops to gradually shorten the string. Four of five common ravens eventually succeeded, and "the transition from no success (ignoring the food or merely yanking at the string) to constant reliable access (pulling up the meat) occurred with no demonstrable trial-and-error learning." This supports the hypothesis that common ravens are 'inventors', implying that they can solve problems. Many of the feats of common ravens were formerly argued to be stereotyped innate behaviour, but it now has been established that their aptitudes for solving problems individually and learning from each other reflect a flexible capacity for intelligent insight unusual among non-human animals. Another experiment showed that some common ravens could intentionally deceive their conspecifics. A study published in 2011 found that ravens can recognise when they are given an unfair trade during reciprocal interactions with conspecifics or humans, retaining memory of the interaction for a prolonged period of time. Birds that were given a fair trade by experimenters were found to prefer interacting with these experimenters compared to those that did not. Furthermore, ravens in the wild have also been observed to stop cooperating with other ravens if they observe them cheating during group tasks. Common ravens have been observed calling wolves to the site of dead animals. The wolves open the carcass, leaving the scraps more accessible to the birds. They watch where other common ravens bury their food and remember the locations of each other's food caches, so they can steal from them. This type of theft occurs so regularly that common ravens will fly extra distances from a food source to find better hiding places for food. They have also been observed pretending to make a cache without actually depositing the food, presumably to confuse onlookers. Common ravens are known to steal and cache shiny objects such as pebbles, pieces of metal, and golf balls. One theory is that they hoard shiny objects to impress other ravens. Other research indicates that juveniles are deeply curious about all new things, and that common ravens retain an attraction to bright, round objects based on their similarity to bird eggs. Mature birds lose their intense interest in the unusual, and become highly neophobic . The first large-scale assessment of ravens' cognitive abilities suggests that, by four months of age, ravens do about as well as adult chimps and orangutans on tests of causal reasoning , social learning , theory of mind , etc. There has been increasing recognition of the extent to which birds engage in play . Juvenile common ravens are among the most playful of bird species. They have been observed to slide down snowbanks, apparently purely for fun. They even engage in games with other species, such as playing catch-me-if-you-can with wolves, otters and dogs. Common ravens are known for spectacular aerobatic displays, such as flying in loops or interlocking talons with each other in flight. They are also one of only a few wild animals who make their own toys. They have been observed breaking off twigs to play with socially. Owing to its size, gregariousness and its defensive abilities, the common raven has few natural predators. Predators of its eggs include owls , martens , and sometimes eagles . Ravens are quite vigorous at defending their young and are usually successful at driving off perceived threats. They attack potential predators by flying at them and lunging with their large bills. Humans are occasionally attacked if they get close to a raven nest, though serious injuries are unlikely. There are a few records of predation by large birds of prey. Their attackers in America have reportedly included great horned owls , northern goshawks , bald eagles , golden eagles and red-tailed hawks . It is possible that the two hawk species only attack young ravens; in one instance a peregrine falcon swooped at a newly fledged raven but was chased off by the parent ravens. In Eurasia , their reported predators include, in addition to golden eagles, Eurasian eagle-owls , white-tailed eagles , Steller's sea-eagles , eastern imperial eagles and gyrfalcons . Because they are potentially hazardous prey for raptorial birds, raptors must usually take them by surprise and most attacks are on fledgling ravens. More rarely still, large mammalian predators such as lynxes , coyotes and cougars have also attacked ravens. This principally occurs at a nest site and when other prey for the carnivores are scarce. Ravens are highly wary around novel carrion sites and, in North America, have been recorded waiting for the presence of American crows and blue jays before approaching to eat. Juveniles begin to court at a very early age, but may not bond for another two or three years. Aerial acrobatics, demonstrations of intelligence, and ability to provide food are key behaviours of courting. Once paired, they tend to nest together for life, usually in the same location. Instances of non-monogamy have been observed in common ravens, by males visiting a female's nest when her mate is away. Breeding pairs must have a territory of their own before they begin nest-building and reproduction, and thus they aggressively defend a territory and its food resources. Nesting territories vary in size according to the density of food resources in the area. The nest is a deep bowl made of large sticks and twigs, bound with an inner layer of roots, mud, and bark and lined with a softer material, such as deer fur. The nest is usually placed in a large tree or on a cliff ledge, or less frequently in old buildings or utility poles. Females lay between three and seven pale bluish-green, brown-blotched eggs. Incubation is about 18 to 21 days, by the female only. The male may stand or crouch over the young, sheltering but not actually brooding them. Young fledge at 35 to 42 days, and are fed by both parents. They stay with their parents for another six months after fledging. In most of their range, egg-laying begins in late February, but it can be as late as April in colder climates such as Greenland and Tibet . In Pakistan, egg-laying takes place in December. Eggs and hatchlings are preyed on, rarely, by large hawks and eagles , large owls , martens and canids . The adults, which are very rarely preyed upon, are often successful in defending their young from these predators, due to their numbers, large size and cunning. They have been observed dropping stones on potential predators that venture close to their nests. Common ravens can be very long-lived, especially in captive or protected conditions; individuals at the Tower of London have lived for more than 40 years. Their lifespans in the wild are shorter, typically 10 to 15 years. The longest known lifespan of a banded wild common raven was 23 years, 3 months, which among passerines only is surpassed by a few Australian species such as the satin bowerbird . Common ravens are omnivorous and highly opportunistic : their diet may vary widely with location, season and serendipity . For example, those foraging on tundra on the Arctic North Slope of Alaska obtained about half their energy needs from predation , mainly of microtine rodents , and half by scavenging, mainly of caribou and ptarmigan carcasses. In some places they are mainly scavengers , feeding on carrion as well as the associated maggots and carrion beetles . With large-bodied carrion, which they are not equipped to tear through as well as birds such as hook-billed vultures , they must wait for the prey to be torn open by another predator or flayed by other means. They are also known to eat the afterbirth of ewes and other large mammals. Plant food includes cereal grains, acorns, buds, berries and fruit. They prey on small invertebrates , amphibians, reptiles, small mammals and birds. Ravens may also consume the undigested portions of animal feces, and human food waste. They store surplus food items, especially those containing fat, and will learn to hide such food out of the sight of other common ravens. Ravens also raid the food caches of other species, such as the Arctic fox . They sometimes associate with another canine, the grey wolf , as a kleptoparasite , following to scavenge wolf-kills in winter. Ravens are regular predators at bird nests, brazenly picking off eggs, nestlings and sometimes adult birds when they spot an opportunity. They are considered perhaps the primary natural threat to the nesting success of the critically endangered California condor , since they readily take condor eggs and are very common in the areas where the species is being re-introduced. On the other hand, when they defend their own adjacent nests, they may incidentally benefit condors since they chase golden eagles out of the area that may otherwise prey upon larger nestling and fledging condors. Condors, despite their large size, do not seem to have well developed nest defenses. Common ravens nesting near sources of human garbage included a higher percentage of food waste in their diet, birds nesting near roads consumed more road-killed vertebrates , and those nesting far from these sources of food ate more arthropods and plant material. Fledging success was higher for those using human garbage as a food source. In contrast, a 1984–1986 study of common raven diet in an agricultural region of southwestern Idaho found that cereal grains were the principal constituent of pellets , though small mammals, grasshoppers, cattle carrion and birds were also eaten. One behaviour is recruitment, where juvenile ravens call other ravens to a food bonanza, usually a carcass, with a series of loud yells. In Ravens in Winter , Bernd Heinrich posited that this behaviour evolved to allow the juveniles to outnumber the resident adults, thus allowing them to feed on the carcass without being chased away. A more mundane explanation is that individuals co-operate in sharing information about carcasses of large mammals because they are too big for just a few birds to exploit. Experiments with baits however show that such recruitment behaviour is independent of the size of the bait. Furthermore, there has been research suggesting that the common raven is involved in seed dispersal. In the wild, the common raven chooses the best habitat and disperses seeds in locations best suited for its survival. The brain of the common raven is among the largest of any bird species. Specifically, their hyperpallium is large for a bird. They display ability in problem-solving, as well as other cognitive processes such as imitation and insight . Linguist Derek Bickerton , building on the work of biologist Bernd Heinrich , has argued that ravens are one of only four known animals (the others being bees , ants , and humans) who have demonstrated displacement , the capacity to communicate about objects or events that are distant in space or time. Subadult ravens roost together at night, but usually forage alone during the day. However, when one discovers a large carcass guarded by a pair of adult ravens, the unmated raven will return to the roost and communicate the find. The following day, a flock of unmated ravens will fly to the carcass and chase off the adults. Bickerton argues that the advent of linguistic displacement was perhaps the most important event in the evolution of human language, and that ravens are the only other vertebrate to share this with humans. One experiment designed to evaluate insight and problem-solving ability involved a piece of meat attached to a string hanging from a perch. To reach the food, the bird needed to stand on the perch, pull the string up a little at a time, and step on the loops to gradually shorten the string. Four of five common ravens eventually succeeded, and "the transition from no success (ignoring the food or merely yanking at the string) to constant reliable access (pulling up the meat) occurred with no demonstrable trial-and-error learning." This supports the hypothesis that common ravens are 'inventors', implying that they can solve problems. Many of the feats of common ravens were formerly argued to be stereotyped innate behaviour, but it now has been established that their aptitudes for solving problems individually and learning from each other reflect a flexible capacity for intelligent insight unusual among non-human animals. Another experiment showed that some common ravens could intentionally deceive their conspecifics. A study published in 2011 found that ravens can recognise when they are given an unfair trade during reciprocal interactions with conspecifics or humans, retaining memory of the interaction for a prolonged period of time. Birds that were given a fair trade by experimenters were found to prefer interacting with these experimenters compared to those that did not. Furthermore, ravens in the wild have also been observed to stop cooperating with other ravens if they observe them cheating during group tasks. Common ravens have been observed calling wolves to the site of dead animals. The wolves open the carcass, leaving the scraps more accessible to the birds. They watch where other common ravens bury their food and remember the locations of each other's food caches, so they can steal from them. This type of theft occurs so regularly that common ravens will fly extra distances from a food source to find better hiding places for food. They have also been observed pretending to make a cache without actually depositing the food, presumably to confuse onlookers. Common ravens are known to steal and cache shiny objects such as pebbles, pieces of metal, and golf balls. One theory is that they hoard shiny objects to impress other ravens. Other research indicates that juveniles are deeply curious about all new things, and that common ravens retain an attraction to bright, round objects based on their similarity to bird eggs. Mature birds lose their intense interest in the unusual, and become highly neophobic . The first large-scale assessment of ravens' cognitive abilities suggests that, by four months of age, ravens do about as well as adult chimps and orangutans on tests of causal reasoning , social learning , theory of mind , etc. There has been increasing recognition of the extent to which birds engage in play . Juvenile common ravens are among the most playful of bird species. They have been observed to slide down snowbanks, apparently purely for fun. They even engage in games with other species, such as playing catch-me-if-you-can with wolves, otters and dogs. Common ravens are known for spectacular aerobatic displays, such as flying in loops or interlocking talons with each other in flight. They are also one of only a few wild animals who make their own toys. They have been observed breaking off twigs to play with socially. Compared to many smaller Corvus species (such as American crow ), ravens prefer undisturbed mountain or forest habitat or rural areas over urban areas. In other areas, their numbers have increased dramatically and they have become agricultural pests . Common ravens can cause damage to crops, such as nuts and grain, or can harm livestock, particularly by killing young goat kids, lambs and calves. Ravens generally attack the faces of young livestock, but the more common raven behaviour of scavenging may be misidentified as predation by ranchers. In the western Mojave Desert , human settlement and land development have led to an estimated 16-fold increase in the common raven population over 25 years. Towns, landfills, sewage treatment plants and artificial ponds create sources of food and water for scavenging birds. Ravens also find nesting sites in utility poles and ornamental trees, and are attracted to roadkill on highways. The explosion in the common raven population in the Mojave has raised concerns for the desert tortoise , a threatened species . Common ravens prey upon juvenile tortoises, which have soft shells and move slowly. Plans to control the population have included shooting and trapping birds, as well as contacting landfill operators to ask that they reduce the amount of exposed garbage. A hunting bounty as a method of control was historically used in Finland from the mid-18th century until 1923. Culling has taken place to a limited extent in Alaska , where the population increase in common ravens is threatening the vulnerable Steller's eider ( Polysticta stelleri ). Ravens, like other corvids, are definitive hosts of West Nile Virus (WNV). The transmission can be from infected birds to humans, and ravens are susceptible to WNV. However, in a 2010 study, it was shown that the California Common Ravens did not have a high positivity rate of WNV. Across its range in the Northern Hemisphere, and throughout human history, the common raven has been a powerful symbol and a popular subject of mythology and folklore. In some Western traditions , ravens have long been considered to be birds of ill omen, death and evil in general, in part because of the negative symbolism of their all- black plumage and the eating of carrion . In Sweden, ravens are known as the ghosts of murdered people, and in Germany as the souls of the damned. In Danish folklore , valravne that ate a king's heart gained human knowledge, could perform great malicious acts, could lead people astray, had superhuman powers, and were "terrible animals". It continues to be used as a symbol in areas where it once had mythological status: as the national bird of Bhutan ( kings of Bhutan wear the Raven Crown ), official bird of the Yukon territory, and on the coat of arms of the Isle of Man (once a Viking colony). In Persia and Arabia the raven was held as a bird of bad omen but a 14th-century Arabic work reports use of the raven in falconry. The modern unisex given name Raven is derived from the English word "raven". As a masculine name, Raven parallels the Old Norse Hrafn , and Old English *Hræfn , which were both bynames and personal names . In Tlingit and Haida cultures , Raven was both a trickster and creator god . Related beliefs are widespread among the peoples of Siberia and northeastern Asia. The Kamchatka Peninsula , for example, was supposed to have been created by the raven god Kutkh . There are several references to common ravens in the Old Testament of the Bible and it is an aspect of Mahakala in Bhutanese mythology. In Norse mythology , Huginn (from the Old Norse for "thought") and Muninn (from the Old Norse for "memory" or "mind") are a pair of ravens that fly all over the world of humans, Midgard , and bring the god Odin information. Additionally among the Norse, raven banner standards were carried by such figures as the Jarls of Orkney , King Cnut the Great of England, Norway and Denmark, and Harald Hardrada . In the British Isles, ravens also were symbolic to the Celts . In Irish mythology , the goddess Morrígan alighted on the hero Cú Chulainn 's shoulder in the form of a raven after his death. In Welsh mythology they were associated with the Welsh god Brân the Blessed , whose name translates to "crow". According to the Mabinogion , Brân's head was buried in the White Hill of London as a talisman against invasion. A legend developed that England would not fall to a foreign invader as long as there were ravens at the Tower of London ; although this is often thought to be an ancient belief, the official Tower of London historian, Geoff Parnell, believes that this is actually a romantic Victorian invention. In the Jewish , Christian and Islamic traditions, the raven was the first animal to be released from Noah's Ark . "So it came to pass, at the end of forty days, that Noah opened the window of the ark which he had made. Then he sent out a raven, which kept going to and fro until the waters had dried up from the earth. He also sent out from himself a dove, to see if the waters had receded from the face of the ground." The raven is mentioned 12 times in the Bible. In the New Testament Jesus tells a parable using the raven to show how people should rely on God for their needs and not riches ( Luke 12:24 ). The raven is also mentioned in the Quran at the story of Cain and Abel . Adam 's firstborn son Cain kills his brother Abel, but he does not know what to do with the corpse: "Then Allah sent a raven scratching up the ground, to show him how to hide his brother's naked corpse. He said: Woe unto me! Am I not able to be as this raven and so hide my brother's naked corpse? And he became repentant." Compared to many smaller Corvus species (such as American crow ), ravens prefer undisturbed mountain or forest habitat or rural areas over urban areas. In other areas, their numbers have increased dramatically and they have become agricultural pests . Common ravens can cause damage to crops, such as nuts and grain, or can harm livestock, particularly by killing young goat kids, lambs and calves. Ravens generally attack the faces of young livestock, but the more common raven behaviour of scavenging may be misidentified as predation by ranchers. In the western Mojave Desert , human settlement and land development have led to an estimated 16-fold increase in the common raven population over 25 years. Towns, landfills, sewage treatment plants and artificial ponds create sources of food and water for scavenging birds. Ravens also find nesting sites in utility poles and ornamental trees, and are attracted to roadkill on highways. The explosion in the common raven population in the Mojave has raised concerns for the desert tortoise , a threatened species . Common ravens prey upon juvenile tortoises, which have soft shells and move slowly. Plans to control the population have included shooting and trapping birds, as well as contacting landfill operators to ask that they reduce the amount of exposed garbage. A hunting bounty as a method of control was historically used in Finland from the mid-18th century until 1923. Culling has taken place to a limited extent in Alaska , where the population increase in common ravens is threatening the vulnerable Steller's eider ( Polysticta stelleri ). Ravens, like other corvids, are definitive hosts of West Nile Virus (WNV). The transmission can be from infected birds to humans, and ravens are susceptible to WNV. However, in a 2010 study, it was shown that the California Common Ravens did not have a high positivity rate of WNV. Across its range in the Northern Hemisphere, and throughout human history, the common raven has been a powerful symbol and a popular subject of mythology and folklore. In some Western traditions , ravens have long been considered to be birds of ill omen, death and evil in general, in part because of the negative symbolism of their all- black plumage and the eating of carrion . In Sweden, ravens are known as the ghosts of murdered people, and in Germany as the souls of the damned. In Danish folklore , valravne that ate a king's heart gained human knowledge, could perform great malicious acts, could lead people astray, had superhuman powers, and were "terrible animals". It continues to be used as a symbol in areas where it once had mythological status: as the national bird of Bhutan ( kings of Bhutan wear the Raven Crown ), official bird of the Yukon territory, and on the coat of arms of the Isle of Man (once a Viking colony). In Persia and Arabia the raven was held as a bird of bad omen but a 14th-century Arabic work reports use of the raven in falconry. The modern unisex given name Raven is derived from the English word "raven". As a masculine name, Raven parallels the Old Norse Hrafn , and Old English *Hræfn , which were both bynames and personal names . In Tlingit and Haida cultures , Raven was both a trickster and creator god . Related beliefs are widespread among the peoples of Siberia and northeastern Asia. The Kamchatka Peninsula , for example, was supposed to have been created by the raven god Kutkh . There are several references to common ravens in the Old Testament of the Bible and it is an aspect of Mahakala in Bhutanese mythology. In Norse mythology , Huginn (from the Old Norse for "thought") and Muninn (from the Old Norse for "memory" or "mind") are a pair of ravens that fly all over the world of humans, Midgard , and bring the god Odin information. Additionally among the Norse, raven banner standards were carried by such figures as the Jarls of Orkney , King Cnut the Great of England, Norway and Denmark, and Harald Hardrada . In the British Isles, ravens also were symbolic to the Celts . In Irish mythology , the goddess Morrígan alighted on the hero Cú Chulainn 's shoulder in the form of a raven after his death. In Welsh mythology they were associated with the Welsh god Brân the Blessed , whose name translates to "crow". According to the Mabinogion , Brân's head was buried in the White Hill of London as a talisman against invasion. A legend developed that England would not fall to a foreign invader as long as there were ravens at the Tower of London ; although this is often thought to be an ancient belief, the official Tower of London historian, Geoff Parnell, believes that this is actually a romantic Victorian invention. In the Jewish , Christian and Islamic traditions, the raven was the first animal to be released from Noah's Ark . "So it came to pass, at the end of forty days, that Noah opened the window of the ark which he had made. Then he sent out a raven, which kept going to and fro until the waters had dried up from the earth. He also sent out from himself a dove, to see if the waters had receded from the face of the ground." The raven is mentioned 12 times in the Bible. In the New Testament Jesus tells a parable using the raven to show how people should rely on God for their needs and not riches ( Luke 12:24 ). The raven is also mentioned in the Quran at the story of Cain and Abel . Adam 's firstborn son Cain kills his brother Abel, but he does not know what to do with the corpse: "Then Allah sent a raven scratching up the ground, to show him how to hide his brother's naked corpse. He said: Woe unto me! Am I not able to be as this raven and so hide my brother's naked corpse? And he became repentant." In Tlingit and Haida cultures , Raven was both a trickster and creator god . Related beliefs are widespread among the peoples of Siberia and northeastern Asia. The Kamchatka Peninsula , for example, was supposed to have been created by the raven god Kutkh . There are several references to common ravens in the Old Testament of the Bible and it is an aspect of Mahakala in Bhutanese mythology. In Norse mythology , Huginn (from the Old Norse for "thought") and Muninn (from the Old Norse for "memory" or "mind") are a pair of ravens that fly all over the world of humans, Midgard , and bring the god Odin information. Additionally among the Norse, raven banner standards were carried by such figures as the Jarls of Orkney , King Cnut the Great of England, Norway and Denmark, and Harald Hardrada . In the British Isles, ravens also were symbolic to the Celts . In Irish mythology , the goddess Morrígan alighted on the hero Cú Chulainn 's shoulder in the form of a raven after his death. In Welsh mythology they were associated with the Welsh god Brân the Blessed , whose name translates to "crow". According to the Mabinogion , Brân's head was buried in the White Hill of London as a talisman against invasion. A legend developed that England would not fall to a foreign invader as long as there were ravens at the Tower of London ; although this is often thought to be an ancient belief, the official Tower of London historian, Geoff Parnell, believes that this is actually a romantic Victorian invention. In the Jewish , Christian and Islamic traditions, the raven was the first animal to be released from Noah's Ark . "So it came to pass, at the end of forty days, that Noah opened the window of the ark which he had made. Then he sent out a raven, which kept going to and fro until the waters had dried up from the earth. He also sent out from himself a dove, to see if the waters had receded from the face of the ground." The raven is mentioned 12 times in the Bible. In the New Testament Jesus tells a parable using the raven to show how people should rely on God for their needs and not riches ( Luke 12:24 ). The raven is also mentioned in the Quran at the story of Cain and Abel . Adam 's firstborn son Cain kills his brother Abel, but he does not know what to do with the corpse: "Then Allah sent a raven scratching up the ground, to show him how to hide his brother's naked corpse. He said: Woe unto me! Am I not able to be as this raven and so hide my brother's naked corpse? And he became repentant."

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West Nile

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Sandfly

Sandfly or sand fly is a colloquial name for any species or genus of flying, biting, blood-sucking dipteran (fly) encountered in sandy areas. In the United States , sandfly may refer to certain horse flies that are also known as "greenheads" (family Tabanidae ), or to members of the family Ceratopogonidae . The bites usually result in a small, intensely itchy bump or welt, the strength of which intensifies over a period of 5-7 days before dissipating. Moderate relief is achieved with varying success through the application of over the counter products such as Benadryl (ingested) or an analgesic cream such as After Bite (applied topically). Outside the United States, sandfly may refer to members of the subfamily Phlebotominae within the Psychodidae . Biting midges ( Ceratopogonidae ) are sometimes called sandflies or no-see-ums (no-see-em, noseeum). New Zealand sandflies are in the genus of sand fly Austrosimulium , a type of black fly . In the various sorts of sandfly only the female is responsible for biting and sucking the blood of mammals, reptiles and birds; the protein in the blood is necessary for the production of eggs, making the sandfly an anautogenous reproducer. Some sandfly genera of the subfamily Phlebotominae are the primary vectors of leishmaniasis and pappataci fever ; both diseases are confusingly referred to as sandfly fever. In Asia, Africa, and Europe, leishmaniasis is spread by sand flies of the genus Phlebotomus ; in the Americas, the disease is spread by sandflies of the genus Lutzomyia . Belize and Honduras are notorious in the Caribbean for their sandfly populations and travel pages frequently warn tourists to bring bug spray containing high concentrations of DEET .Among the viruses that sandflies can carry is the Chandipura virus , which, as a cousin of rabies , is deadly. There was an outbreak in India in 2010.Leishmaniasis , a disease caused by several species of the genus Leishmania , is transmitted by various sandflies. Leishmania donovani causes spiking fevers, hepatosplenomegaly , and pancytopenia . It can be diagnosed through microscopic review by visualizing amastigotes in containing macrophages , and is treatable with sodium stibogluconate .Bartonella bacilliformis , the causal agent of Carrion's disease , is transmitted by different members of the genus Lutzomyia . This disease is restricted to Andean areas of Peru and Ecuador, with historical reports in Southern Colombia. Over-the-counter repellents with high concentrations of DEET or picaridin are proven to work; however effectiveness seems to differ among individuals with some people reporting better results with one product over another while other people finding neither product effective for them. This may be partially due to various species living in different areas. A particular extract of lemon eucalyptus oil (not the essential oil) has now been shown to be as effective as DEET in various studies. Most information on repellents focuses on mosquitoes, but mosquito repellents are effective for sandflies and midges as well. New Zealand sandflies (which are taxonomically blackflies— Simulidae ) have a native Māori legend wherein "the god Tu-te-raki-whanoa had just finished creating the landscape of Fiordland , it was absolutely stunning... so stunning that it stopped people from working. They just stood around gazing at the beauty instead. The goddess Hine-nui-te-pō became angry at these unproductive people, so she created the sandfly to bite them and get them moving". These sand flies were able, according to another Māori legend, to revive the dead hero Ha-tupatu .

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West Nile

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Uganda National Rescue Front

The Uganda National Rescue Front (UNRF), refers to two former armed rebel groups in Uganda 's West Nile sub-region that first opposed, then became incorporated into the Ugandan armed forces.The first Uganda National Rescue Front, also known as "National Salvation Front", was formed to oppose Milton Obote during his second term (1980–1985) as president of Uganda. The UNRF was composed of former supporters of Idi Amin , and headed by Brigadier Moses Ali , formerly Amin's Minister of Finance. After the fall of Obote in July 1984/5, over 1000 of the UNRF joined Yoweri Museveni 's government. Luwero Moses Ali held a large number and variety of positions in Museveni's government, including Minister of Tourism and Wildlife, and Minister of Youth, Culture and Sport. In April 1990 he was arrested on treason charges, and incarcerated until June 1992, when he was released and acquitted. This did not prevent his appointment as Minister of Internal Affairs, Minister for Disaster Preparedness, and Deputy Prime Minister.The Uganda National Rescue Front II was a group that broke from the West Nile Bank Front in 1996, and included members of the original UNRF that did not make peace with Museveni. It operated mostly in Aringa County, Arua District , out of bases in southern Sudan , and received support from the Sudanese government (the National Islamic Front ), in retaliation for Ugandan government support for the Sudan People's Liberation Army . It was led by Major General Ali Bamuze. On December 24, 2002, the UNRF II signed a formal ceasefire with the government in the town of Yumbe in northwestern Uganda. Terms included a battalion of UNRF II soldiers being incorporated in the Ugandan army, and USh 4.2 billion being distributed to the group. Moses Ali is reported to have participated in the negotiations.

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West Nile

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Shoebill

The shoebill ( Balaeniceps rex ), also known as the whalebill , whale-headed stork , and shoe-billed stork , is a large long-legged wading bird. It derives its name from its enormous shoe-shaped bill . It has a somewhat stork-like overall form and has previously been classified with the storks in the order Ciconiiformes based on this morphology. However, genetic evidence places it with pelicans and herons in the Pelecaniformes . The adult is mainly grey while the juveniles are more brown. It lives in tropical East Africa in large swamps from South Sudan to Zambia.The shoebill may have been known to Ancient Egyptians but was not classified until the 19th century, after skins and eventually live specimens were brought to Europe. John Gould very briefly described it in 1850 from the skin of a specimen collected on the upper White Nile by the English traveller Mansfield Parkyns . Gould provided a more detailed description in the following year. He placed the species in its own genus Balaeniceps and coined the binomial name Balaeniceps rex . The genus name comes from the Latin words balaena "whale", and caput "head", abbreviated to -ceps in compound words. Alternative common names are whalebill, shoe-billed stork and whale-headed stork. Traditionally considered as allied with the storks ( Ciconiiformes ), it was retained there in the Sibley-Ahlquist taxonomy which lumped a massive number of unrelated taxa into their "Ciconiiformes". Based on osteological evidence, the suggestion of a pelecaniform affinity was made in 1957 by Patricia Cottam. Microscopic analysis of eggshell structure by Konstantin Mikhailov in 1995 found that the eggshells of shoebills closely resembled those of other Pelecaniformes in having a covering of thick microglobular material over the crystalline shells. In 2003, the shoebill was again suggested as closer to the pelicans (based on anatomical comparisons) or the herons (based on biochemical evidence). A 2008 DNA study reinforces their membership among the Pelecaniformes. So far, two fossilized relatives of the shoebill have been described: Goliathia from the early Oligocene of Egypt and Paludavis from the Early Miocene of the same country. It has been suggested that the enigmatic African fossil bird Eremopezus was a relative too, but the evidence for that is unconfirmed. All that is known of Eremopezus is that it was a very large, probably flightless bird with a flexible foot, allowing it to handle either vegetation or prey.The shoebill is a tall bird, with a typical height range of 110 to 140 cm (43 to 55 in) and some specimens reaching as much as 152 cm (60 in) . Length from tail to beak can range from 100 to 140 cm (39 to 55 in) and wingspan is 230 to 260 cm (7 ft 7 in to 8 ft 6 in) . Weight has reportedly ranged from 4 to 7 kg (8.8 to 15.4 lb) . A male will weigh on average around 5.6 kg (12 lb) and is larger than a typical female of 4.9 kg (11 lb) . The signature feature of the species is its huge, bulbous bill , which is straw-coloured with erratic greyish markings. The exposed culmen (or the measurement along the top of the upper mandible) is 18.8 to 24 cm (7.4 to 9.4 in) , the third longest bill among extant birds after pelicans and large storks, and can outrival the pelicans in bill circumference, especially if the bill is considered as the hard, bony keratin portion. As in the pelicans, the upper mandible is strongly keeled, ending in a sharp nail. The dark coloured legs are fairly long, with a tarsus length of 21.7 to 25.5 cm (8.5 to 10.0 in) . The shoebill's feet are exceptionally large, with the middle toe reaching 16.8 to 18.5 cm (6.6 to 7.3 in) in length, likely assisting the species in its ability to stand on aquatic vegetation while hunting. The neck is relatively shorter and thicker than other long-legged wading birds such as herons and cranes . The wings are broad, with a wing chord length of 58.8 to 78 cm (23.1 to 30.7 in) , and well-adapted to soaring . The plumage of adult birds is blue-grey with darker slaty -grey flight feathers . The breast presents some elongated feathers, which have dark shafts. The juvenile has a similar plumage colour, but is a darker grey with a brown tinge. When they are first born, shoebills have a more modestly-sized bill, which is initially silvery-grey. The bill becomes more noticeably large when the chicks are 23 days old and becomes well developed by 43 days. The shoebill is normally silent, but they perform bill-clattering displays at the nest. When engaging in these displays, adult birds have also been noted to utter a cow -like moo as well as high-pitched whines. Both nestlings and adults engage in bill-clattering during the nesting season as a means of communication. When young are begging for food, they call out with a sound uncannily like human hiccups. In one case, a flying adult bird was heard uttering hoarse croaks, apparently as a sign of aggression at a nearby marabou stork ( Leptoptilos crumeniferus ). Its wings are held flat while soaring and, as in the pelicans and the storks of the genus Leptoptilos , the shoebill flies with its neck retracted. Its flapping rate, at an estimated 150 flaps per minute, is one of the slowest of any bird, with the exception of the larger stork species. The pattern is alternating flapping and gliding cycles of approximately seven seconds each, putting its gliding distance somewhere between the larger storks and the Andean condor ( Vultur gryphus ). When flushed, shoebills usually try to fly no more than 100 to 500 m (330 to 1,640 ft) . Long flights of the shoebill are rare, and only a few flights beyond its minimum foraging distance of 20 m (66 ft) have been recorded.The shoebill is normally silent, but they perform bill-clattering displays at the nest. When engaging in these displays, adult birds have also been noted to utter a cow -like moo as well as high-pitched whines. Both nestlings and adults engage in bill-clattering during the nesting season as a means of communication. When young are begging for food, they call out with a sound uncannily like human hiccups. In one case, a flying adult bird was heard uttering hoarse croaks, apparently as a sign of aggression at a nearby marabou stork ( Leptoptilos crumeniferus ). Its wings are held flat while soaring and, as in the pelicans and the storks of the genus Leptoptilos , the shoebill flies with its neck retracted. Its flapping rate, at an estimated 150 flaps per minute, is one of the slowest of any bird, with the exception of the larger stork species. The pattern is alternating flapping and gliding cycles of approximately seven seconds each, putting its gliding distance somewhere between the larger storks and the Andean condor ( Vultur gryphus ). When flushed, shoebills usually try to fly no more than 100 to 500 m (330 to 1,640 ft) . Long flights of the shoebill are rare, and only a few flights beyond its minimum foraging distance of 20 m (66 ft) have been recorded.The shoebill is distributed in freshwater swamps of central tropical Africa, from southern Sudan and South Sudan through parts of eastern Congo , Rwanda , Uganda , western Tanzania and northern Zambia . The species is most numerous in the West Nile sub-region and South Sudan (especially the Sudd , a main stronghold for the species); it is also significant in wetlands of Uganda and western Tanzania. More isolated records have been reported of shoebills in Kenya , the Central African Republic , northern Cameroon , south-western Ethiopia , Malawi . Vagrant strays to the Okavango Basin , Botswana and the upper Congo River have also been sighted. The distribution of this species seems to largely coincide with that of papyrus and lungfish . They are often found in areas of flood plain interspersed with undisturbed papyrus and reedbeds. When shoebill storks are in an area with deep water, a bed of floating vegetation is a requirement. They are also found where there is poorly oxygenated water. This causes the fish living in the water to surface for air more often, increasing the likelihood a shoebill stork will successfully capture it. The shoebill is non-migratory with limited seasonal movements due to habitat changes, food availability and disturbance by humans. Petroglyphs from Oued Djerat , eastern Algeria , show that the shoebill occurred during the Early Holocene much more to the north, in the wetlands that covered the present-day Sahara Desert at that time. The shoebill occurs in extensive, dense freshwater marshes . Almost all wetlands that attract the species have undisturbed Cyperus papyrus and reed beds of Phragmites and Typha . Although their distribution largely seems to correspond with the distribution of papyrus in central Africa, the species seems to avoid pure papyrus swamps and is often attracted to areas with mixed vegetation. More rarely, the species has been seen foraging in rice fields and flooded plantations . The shoebill is noted for its slow movements and tendency to stay still for long periods, resulting in descriptions of the species as "statue-like". They are quite sensitive to human disturbance and may abandon their nests if flushed by humans. However, while foraging, if dense vegetation stands between it and humans, this wader can be fairly tame. The shoebill is attracted to poorly oxygenated waters such as swamps, marshes, and bogs where fish frequently surface to breathe. They also seem to exhibit migratory behaviors based upon differences in the surface water level. Immature shoebills abandon nesting sites which increased in the surface water level whereas adult shoebills abandon nesting sites which decreased in surface water level. It is suggested that both adult and immature shoebills prefer nesting sites with similar surface water levels. Exceptionally for a bird this large, the shoebill often stands and perches on floating vegetation, making them appear somewhat like a giant jacana , although the similarly sized and occasionally sympatric Goliath heron ( Ardea goliath ) is also known to stand on aquatic vegetation. Shoebills, being solitary, forage at 20 m (66 ft) or more from one another even where relatively densely populated. This species stalks its prey patiently, in a slow and lurking fashion. While hunting, the shoebill strides very slowly and is frequently motionless. Unlike some other large waders, this species hunts entirely using vision and is not known to engage in tactile hunting. When prey is spotted, it launches a quick violent strike. However, depending on the size of the prey, handling time after the strike can exceed 10 minutes. Around 60% of strikes yield prey. Frequently water and vegetation is snatched up during the strike and is spilled out from the edges of the mandibles. The activity of hippopotamus may inadvertently benefit the shoebill, as submerged hippos occasionally force fish to the surface. The solitary nature of shoebills extends to their breeding habits. Nests typically occur at less than three nests per square kilometre, unlike herons, cormorants , pelicans, and storks, which predominantly nest in colonies. The breeding pair of shoebills vigorously defends a territory of 2 to 4 km 2 (0.77 to 1.54 sq mi) from conspecifics . In the extreme north and south of the species' range, nesting starts right after the rains end. In more central regions of the range, it may nest near the end of the wet season in order for the eggs to hatch around the beginning of the following wet season. Both parents engage in building the nest on a floating platform after clearing out an area of approximately 3 m (9.8 ft) across. The large, flattish nesting platform is often partially submerged in water and can be as much as 3 m (9.8 ft) deep. The nest itself is about 1 to 1.7 m (3.3 to 5.6 ft) wide. Both the nest and platform are made of aquatic vegetation. From one to three white eggs are laid. These eggs measure 80 to 90 mm (3.1 to 3.5 in) high by 56 to 61 mm (2.2 to 2.4 in) and weigh around 164 g (5.8 oz) . Incubation lasts for approximately 30 days. Both parents actively brood, shade, guard and feed the nestling, though the females are perhaps slightly more attentive. Shoebills use their mandibles to cool their eggs with water during days with high temperatures around 30–33 °C (86–91 °F) . They fill their mandible once, swallow the water, and fill another mandible full of water before proceeding back to their nest where they pour out the water and regurgitate the previously swallowed water onto both the nest and eggs. Food items are regurgitated whole from the gullet straight into the bill of the young. Shoebills rarely raise more than one chick but will hatch more. The younger chicks usually die and are intended as "back-ups" in case the eldest chick dies or is weak. Fledging is reached at around 105 days and the young birds can fly well by 112 days. However, they are still fed for possibly a month or more after this. It will take the young shoebills three years before they become fully sexually mature. Shoebills are elusive when nesting, so cameras must be placed to observe them from afar to collect behavioral data. There is an advantage for birds that are early breeders, as the chicks are tended for a longer period. Shoebills are largely piscivorous but are assured predators of a considerable range of wetland vertebrates. Preferred prey species have reportedly included marbled lungfish ( Protopterus aethiopicus ), African lungfish ( Protopterus annectens ), and Senegal bichir ( Polypterus senegalus ), various Tilapia species and catfish , the latter mainly in the genus Clarias . Other prey eaten by this species has included frogs , water snakes , Nile monitors ( Varanus niloticus ) and baby crocodiles . More rarely, small turtles , snails , rodents , small waterfowl and carrion have reportedly been eaten. Given its sharp-edged beak, huge bill, and wide gape, the shoebill can hunt large prey, often targeting prey bigger than is taken by other large wading birds. In the Bangweulu Swamps of Zambia, fish eaten by this species are commonly in the range of 15 to 50 cm (5.9 to 19.7 in) . The main prey items fed to young by the parents were the catfish Clarias gariepinus , ( syn. C. mossambicus ) and 50 to 60 cm (20 to 24 in) long water snakes. In Uganda, lungfish and catfish were mainly fed to the young. Larger lungfish and catfish were taken in Malagarasi wetlands in western Tanzania. During this study, fish around 60 to 80 cm (24 to 31 in) were quite frequently taken and the largest fish caught by the shoebill was 99 cm long. Fish exceeding 60 cm were usually cut into sections and swallowed at intervals. The entire process from scooping to swallowing ranged from 2 to 30 minutes depending on prey size. However, these large prey are relatively hard to handle and often targeted by African fish eagle ( Haliaeetus vocifer ), which frequently steal large wading bird's prey. The solitary nature of shoebills extends to their breeding habits. Nests typically occur at less than three nests per square kilometre, unlike herons, cormorants , pelicans, and storks, which predominantly nest in colonies. The breeding pair of shoebills vigorously defends a territory of 2 to 4 km 2 (0.77 to 1.54 sq mi) from conspecifics . In the extreme north and south of the species' range, nesting starts right after the rains end. In more central regions of the range, it may nest near the end of the wet season in order for the eggs to hatch around the beginning of the following wet season. Both parents engage in building the nest on a floating platform after clearing out an area of approximately 3 m (9.8 ft) across. The large, flattish nesting platform is often partially submerged in water and can be as much as 3 m (9.8 ft) deep. The nest itself is about 1 to 1.7 m (3.3 to 5.6 ft) wide. Both the nest and platform are made of aquatic vegetation. From one to three white eggs are laid. These eggs measure 80 to 90 mm (3.1 to 3.5 in) high by 56 to 61 mm (2.2 to 2.4 in) and weigh around 164 g (5.8 oz) . Incubation lasts for approximately 30 days. Both parents actively brood, shade, guard and feed the nestling, though the females are perhaps slightly more attentive. Shoebills use their mandibles to cool their eggs with water during days with high temperatures around 30–33 °C (86–91 °F) . They fill their mandible once, swallow the water, and fill another mandible full of water before proceeding back to their nest where they pour out the water and regurgitate the previously swallowed water onto both the nest and eggs. Food items are regurgitated whole from the gullet straight into the bill of the young. Shoebills rarely raise more than one chick but will hatch more. The younger chicks usually die and are intended as "back-ups" in case the eldest chick dies or is weak. Fledging is reached at around 105 days and the young birds can fly well by 112 days. However, they are still fed for possibly a month or more after this. It will take the young shoebills three years before they become fully sexually mature. Shoebills are elusive when nesting, so cameras must be placed to observe them from afar to collect behavioral data. There is an advantage for birds that are early breeders, as the chicks are tended for a longer period. Shoebills are largely piscivorous but are assured predators of a considerable range of wetland vertebrates. Preferred prey species have reportedly included marbled lungfish ( Protopterus aethiopicus ), African lungfish ( Protopterus annectens ), and Senegal bichir ( Polypterus senegalus ), various Tilapia species and catfish , the latter mainly in the genus Clarias . Other prey eaten by this species has included frogs , water snakes , Nile monitors ( Varanus niloticus ) and baby crocodiles . More rarely, small turtles , snails , rodents , small waterfowl and carrion have reportedly been eaten. Given its sharp-edged beak, huge bill, and wide gape, the shoebill can hunt large prey, often targeting prey bigger than is taken by other large wading birds. In the Bangweulu Swamps of Zambia, fish eaten by this species are commonly in the range of 15 to 50 cm (5.9 to 19.7 in) . The main prey items fed to young by the parents were the catfish Clarias gariepinus , ( syn. C. mossambicus ) and 50 to 60 cm (20 to 24 in) long water snakes. In Uganda, lungfish and catfish were mainly fed to the young. Larger lungfish and catfish were taken in Malagarasi wetlands in western Tanzania. During this study, fish around 60 to 80 cm (24 to 31 in) were quite frequently taken and the largest fish caught by the shoebill was 99 cm long. Fish exceeding 60 cm were usually cut into sections and swallowed at intervals. The entire process from scooping to swallowing ranged from 2 to 30 minutes depending on prey size. However, these large prey are relatively hard to handle and often targeted by African fish eagle ( Haliaeetus vocifer ), which frequently steal large wading bird's prey. This species is considered to be one of the five most desirable birds in Africa by birdwatchers . They are docile with humans and show no threatening behavior. Researchers were able to observe a bird on its nest at a close distance – within 2 meters (6 ft 7 in) . Shoebills are often kept in zoos, but breeding is rarely reported. Shoebills have bred successfully at Pairi Daiza in Belgium and at Tampa's Lowry Park Zoo in Florida. Beginning in 2014 and with various interspersed surges of attention since then, the shoebill has become the subject of internet memes , in part due to its intimidating demeanor and tendency to stand still for long periods of time. One such example is a video of a shoebill standing in the rain whilst staring into the camera . These memes have since also appeared on the social media platform TikTok , bringing a comparatively unknown species of bird into popular culture . Even before that, the shoebill inspired the design of the fictional Loftwing birds of the 2011 game The Legend of Zelda: Skyward Sword . Beginning in 2014 and with various interspersed surges of attention since then, the shoebill has become the subject of internet memes , in part due to its intimidating demeanor and tendency to stand still for long periods of time. One such example is a video of a shoebill standing in the rain whilst staring into the camera . These memes have since also appeared on the social media platform TikTok , bringing a comparatively unknown species of bird into popular culture . Even before that, the shoebill inspired the design of the fictional Loftwing birds of the 2011 game The Legend of Zelda: Skyward Sword . The population is estimated at between 5,000 and 8,000 individuals, the majority of which live in swamps in South Sudan, Uganda, eastern Democratic Republic of the Congo, and Zambia. There is also a viable population in the Malagarasi wetlands in Tanzania. BirdLife International has classified it as Vulnerable with the main threats being habitat destruction , disturbance and hunting. The bird is listed under Appendix II of the Convention on International Trade in Endangered Species of Wild Fauna and Flora ( CITES ). Habitat destruction and degradation, hunting, disturbance and illegal capture are all contributing factors to the decline of this species. Agriculture cultivation and pasture for cattle have also caused significant habitat loss. Indigenous communities that surround Shoebill habitats capture their eggs and chicks for human consumption and for trade. Frequent fires in southern Sudan and deliberate fires for grazing access contribute to habitat loss. Lastly, swamps in Sudan are being drained for construction of a nearby canal that allows for artificial control of nearby waterways.

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West Nile

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Icaridin

KBR 3023 Hydroxyethyl isobutyl piperidine carboxylate sec -Butyl 2-(2-hydroxyethyl)piperidine-1-carboxylate InChI=1S/C12H23NO3/c1-3-10(2)16-12(15)13-8-5-4-6-11(13)7-9-14/h10-11,14H,3-9H2,1-2H3 Y Key: QLHULAHOXSSASE-UHFFFAOYSA-N Y InChI=1/C12H23NO3/c1-3-10(2)16-12(15)13-8-5-4-6-11(13)7-9-14/h10-11,14H,3-9H2,1-2H3 Key: QLHULAHOXSSASE-UHFFFAOYAQ O=C(OC(C)CC)N1C(CCO)CCCC1 Icaridin , also known as picaridin , is an insect repellent which can be used directly on skin or clothing. It has broad efficacy against various arthropods such as mosquitos, ticks, gnats, flies and fleas, and is almost colorless and odorless. A study performed in 2010 showed that picaridin spray and cream at the 20% concentration provided 12 hours of protection against ticks. Unlike DEET , icaridin does not dissolve plastics, synthetics or sealants, is odorless and non-greasy and presents a lower risk of toxicity when used with sunscreen, as it may reduce skin absorption of both compounds. The name picaridin was proposed as an International Nonproprietary Name (INN) to the World Health Organization (WHO), but the official name that has been approved by the WHO is icaridin . The chemical is part of the piperidine family, along with many pharmaceuticals and alkaloids such as piperine , which gives black pepper its spicy taste. Trade names include Bayrepel and Saltidin among others. The compound was developed by the German chemical company Bayer in the 1980s and was given the name Bayrepel . In 2005, Lanxess AG and its subsidiary Saltigo GmbH were spun off from Bayer and the product was renamed Saltidin in 2008. Having been sold in Europe since 1998, on 23 July 2020, icaridin was approved again by the EU Commission for use in repellent products. The approval entered into force on 1 February 2022 and is valid for ten years. Icaridin and DEET are the most effective insect repellents available. A 2018 systematic review found no consistent performance difference between icaridin and DEET in field studies and concluded that they are equally preferred mosquito repellents, noting that 50% DEET offers longer protection but is not available in some countries. Icaridin has been reported to be as effective as DEET at a 20% concentration without the irritation associated with DEET. According to the WHO, icaridin "demonstrates excellent repellent properties comparable to, and often superior to, those of the standard DEET." Icaridin-based products have been evaluated by Consumer Reports in 2016 as among the most effective insect repellents when used at a 20% concentration. Icaridin was earlier reported to be effective by Consumer Reports (7% solution) and the Australian Army (20% solution). Consumer Reports retests in 2006 gave as result that a 7% solution of icaridin offered little or no protection against Aedes mosquitoes ( vector of dengue fever ) and a protection time of about 2.5 hours against Culex (vector of West Nile virus), while a 15% solution was good for about one hour against Aedes and 4.8 hours against Culex . The United States Centers for Disease Control and Prevention recommends using repellents based on icaridin, DEET , ethyl butylacetylaminopropionate (IR3535), or oil of lemon eucalyptus (containing p -menthane-3,8-diol , PMD) for effective protection against mosquitoes that carry the West Nile virus , eastern equine encephalitis and other illnesses. Icaridin can cause mild to moderate eye irritation on contact and is slightly toxic if ingested. A 2018 study found that a commercial repellent product containing 20% icaridin, in what the authors described as "conservative exposure doses", is highly toxic to larval salamanders, a major predator of mosquito larvae. The study observed high larval salamander mortality occurring delayed after the four days of exposure. Because the widely used LC50 test for assessing a chemical's environmental toxicity is based on mortality within four days, the authors suggested that icaridin would be incorrectly deemed as "safe" under the test protocol. However, icaridin was also non-toxic in a 21-day reproduction test on the water flea Daphnia magna and a 32-day early life-stage test in zebrafish. Since only the icaridin content of the tested repellent product is known, the observed effects cannot be readily attributed to icaridin. Furthermore, the effects of the repellent product showed no dose-response relationship, i.e., there was neither an increase of the magnitude or severity of the observed effects (mortality, tail deformation), nor did the effects occur at earlier time points. The study has been regarded as invalid by the Danish Environmental Protection Agency, which has evaluated icaridin prior to its approval under the EU Biocidal Product Regulation. The reasons for rejection were the testing of a mixture of undisclosed composition, the use of a non-standard test organism, the lack of analytical verification of actual test concentrations, and the fact that the test solution was never renewed with the 25 days of study duration.In 2014, a potential odorant receptor for icaridin (and DEET), CquiOR136•CquiOrco, was suggested for Culex quinquefasciatus mosquito. Recent crystal and solution studies showed that icaridin binds to Anopheles gambiae odorant binding protein 1 (AgamOBP1). The crystal structure of AgamOBP1•icaridin complex (PDB: 5EL2 ) revealed that icaridin binds to the DEET-binding site in two distinct orientations and also to a second binding site (sIC-binding site) located at the C-terminal region of the AgamOBP1. Recent evidence with Anopheles gambiae mosquitoes suggests icaridin does not strongly activate olfactory receptors neurons, but instead functions to reduce the volatility of the odorants to which it is mixed. By reducing odor volatility, icaridin functions to "mask" the ability of volatile odorants on the skin to activate olfactory neurons and attract mosquitoes. Icaridin contains two stereocenters : one where the hydroxyethyl chain attaches to the ring, and one where the sec -butyl attaches to the oxygen of the carbamate . The commercial material contains a mixture of all four stereoisomers.Commercial products containing icaridin include Cutter Advanced, Muskol, Repeltec, Skin So Soft Bug Guard Plus, Off! FamilyCare, Autan, Smidge, PiActive and MOK.O.

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West Nile

https://api.wikimedia.org/core/v1/wikipedia/en/page/Kunjin_virus/html

Kunjin virus

Kunjin virus ( KUNV ) is a zoonotic virus of the family Flaviviridae and the genus Flavivirus . It is a subtype of West Nile virus endemic to Oceania .The virus was first isolated from Culex annulirostris mosquitoes in Australia in 1960. The name of Kunjin virus derives from an Aboriginal clan living on the Mitchell River close to where the virus was first isolated in Kowanyama , northern Queensland . Kunjin virus is a zoonotic virus of the family Flaviviridae and the genus Flavivirus . It is an arbovirus which is transmitted by mosquitoes and is part of the Japanese encephalitis serological complex. It is antigenically and genetically very similar to West Nile virus and in 1999 was reclassified as a subtype of WNV. Its genome is positive- sense single stranded RNA made up of 10,644 nucleotides . Infection with the virus often causes no symptoms, but it can lead to either an encephalitic disease or a non-encephalitic disease. Non-encephalitic Kunjin virus disease can cause symptoms including acute febrile illness, headache , arthralgia , myalgia , fatigue and rash . Kunjin virus encephalitis features acute febrile meningoencephalitis . Both forms of Kunjin virus disease are milder than the diseases caused by West Nile virus and Murray Valley encephalitis virus . Kunjin virus is transmitted by mosquito vectors , especially the Culex annulirostris . They pass the virus to waterbird reservoir hosts ; a major example is the nankeen night heron . It is also passed to horses and humans. The virus has been isolated in mosquitoes in South East Asia but in humans, only in Australia. It has been found all over Australia and is particularly prevalent in areas near wetlands and rivers. The control of Kunjin virus is achieved in the same ways as other mosquito-borne diseases. These include individuals using insect repellent , wearing long-sleeved clothes and avoiding areas where mosquitoes are particularly prevalent. Habitat control by government agencies can take the form of reducing the amount of water available for mosquitoes to breed in, and the use of insecticides . There is no available vaccine against Kunjin virus. In 2005, scientists at the Queensland Institute of Medical Research and the University of Queensland found that modified Kunjin virus particles injected into mice were able to deliver a gene into the immune system targeting cancer cells. This research may lead to vaccines for cancer and HIV .

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West Nile

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List of deadliest animals to humans

This is a list of the deadliest animals to humans worldwide, measured by the number of humans killed per year. Different lists have varying criteria and definitions, so lists from different sources disagree and can be contentious. [ clarification needed ] This article contains a compilation of lists from several reliable sources.per year per year per year

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West Nile

https://api.wikimedia.org/core/v1/wikipedia/en/page/Lugbara_people/html

Lugbara people

The Lugbara are a Central Sudanic ethnic group who live primarily in the West Nile region of Uganda , in the adjoining area of the Democratic Republic of the Congo (DRC) with a few living in South Sudan . They speak the Lugbara language , a Central Sudanic language similar to the language spoken by the Madi , with whom they also share many cultural similarities. Traditionally, the Lugbara are farmers who rear some livestock and poultry, mainly guineafowl locally known as ope ; they are the predominant keepers of guineafowl in Uganda. Lugbara occupy the West Nile region of Uganda (Arua City, Arua, Maracha, Terego, Madi-Okollo, Yumbe and Koboko districts of Uganda to be specific). The Lugbara are divided into many dialects which are easily understandable to each other. These include: Ayivu, Maracha, Terego, Vurra and Aringa. Tribes related to the Lugbara in language include Madi and Keliko in South Sudan. The Lugbara also have a special name-giving ceremony called Cikiri every time a child is born. In the early days, the Lugbara were a mainly chiefdom-based community. They did not have kingdoms and kings presiding over them like other ethnic groups in Uganda. They mainly had chiefs who were their leaders. They formed friendly alliances with neighbouring tribes so as to ensure their security against attacks from other ethnic groups. The earlier Lugbara did not have soldiers or a standing army in their chiefdoms. Every able-bodied man had the duty to protect his village hence all able-bodied men were automatically considered a soldier though this was not a permanent duty. The Lugbara were originally animists as their mythology attests. However, Christianity is now the predominant religion amongst them with Islam another major religion. According to the 2002 Census of Uganda, the majority of Lugbara people at around 48.6% are Roman Catholic , while 21.4% are Anglican and 29.1% are Sunni Muslim . They are settled subsistence farmers . Cassava is now the traditional staple. They also grow millet , sorghum , legumes , pigeon peas, beans and a variety of root crops . Before cassava was introduced to the Lugbara to manage famine when the cereals millet and sorghum failed due to drought in the 1960s; millet and sorghum used to be their staple food. Chicken , pigs , goats , and at higher elevations, cattle are also important. Groundnuts, simsim [sesame], chick peas and sweet potatoes are also grown. Maize is grown for brewing beer , and tobacco is a very important cash crop . Emerging cashcrops are avocado, pineapple, and mangoes. In early days of 1874 the North Eastern side of the Democratic Republic of Congo, a faction of the Lugbara were called "The Naked People", due to their attitude towards clothing. Most women did not wear shirts and many of them did not wear even dresses, but they were covered with grass skirts or leaves. Taller than many Congolese, the Lugbara men are great hunters as well, using powerful bows with long arrows that have fishing hooks type tips. This ethnic group straddles the common border between Uganda and the Democratic Republic of Congo with the majority of their population in the Congo side of the border. Some live in South Sudan. A collection of the proverbs of the Lugbara have been published, and also a description of how their proverbs relate to ethics. The same author has described other parts of traditional Lugbara customs and society. Famous and well known Lugbara include Dorcus Inzikuru , the 3000-metre steeple chase world champion in Helsinki 2005 and Jackson Asiku, the previous Commonwealth boxing light-weight champion. Another important Lugbara is John Munduga, an international boxer plus Idi Amin Dada , former president of Uganda mostly remembered/ known for expelling the Asians. The cultural symbol of the Lugbara is a leopard with 300 spots.

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West Nile

https://api.wikimedia.org/core/v1/wikipedia/en/page/Flaviviridae/html

Flaviviridae

Flaviviridae is a family of enveloped positive-strand RNA viruses which mainly infect mammals and birds . They are primarily spread through arthropod vectors (mainly ticks and mosquitoes ). The family gets its name from the yellow fever virus; flavus is Latin for "yellow", and yellow fever in turn was named because of its propensity to cause jaundice in victims. There are 89 species in the family divided among four genera. Diseases associated with the group include: hepatitis ( hepaciviruses ), hemorrhagic syndromes , fatal mucosal disease ( pestiviruses ), hemorrhagic fever , encephalitis , and the birth defect microcephaly ( flaviviruses ). Virus particles are enveloped and spherical with icosahedral-like geometries that have pseudo T=3 symmetry. They are about 40–60 nm in diameter. Members of the family Flaviviridae have monopartite, linear, single-stranded RNA genomes of positive polarity, and 9.6 to 12.3 kilobase in total length. The 5'-termini of flaviviruses carry a methylated nucleotide cap, while other members of this family are uncapped and encode an internal ribosome entry site. The genome encodes a single polyprotein with multiple transmembrane domains that is cleaved, by both host and viral proteases, into structural and non-structural proteins. Among the non-structural protein products (NS), the locations and sequences of NS3 and NS5, which contain motifs essential for polyprotein processing and RNA replication respectively, are relatively well conserved across the family and may be useful for phylogenetic analysis.Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment of the viral envelope protein E to host receptors, which mediates clathrin -mediated endocytosis. Replication follows the positive-stranded RNA virus replication model. Positive-stranded RNA virus transcription is the method of transcription. Translation takes place by viral initiation. The virus exits the host cell by budding. Humans and mammals serve as the natural hosts. The virus is transmitted via vectors (ticks and mosquitoes). The family has four genera: Other Orthoflaviviruses are known that have yet to be classified. These include Wenling shark virus. Jingmenvirus is a group of unclassified viruses in the family which includes Alongshan virus , Guaico Culex virus, Jingmen tick virus and Mogiana tick virus. These viruses have a segmented genome of 4 or 5 pieces. Two of these segments are derived from flaviviruses. A number of viruses may be related to the flaviviruses, but have features that are atypical of the flaviviruses. These include citrus Jingmen-like virus, soybean cyst nematode virus 5, Toxocara canis larva agent, Wuhan cricket virus, and possibly Gentian Kobu-sho-associated virus.Major diseases caused by members of the family Flaviviridae include:

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West Nile

https://api.wikimedia.org/core/v1/wikipedia/en/page/The_Jewel_of_the_Nile/html

The Jewel of the Nile

Peter Boita Michael Ellis December 11, 1985 ( 1985-12-11 ) The Jewel of the Nile is a 1985 American action-adventure romantic comedy film directed by Lewis Teague and produced by Michael Douglas , who also starred in the lead role, reuniting with co-stars Kathleen Turner and Danny DeVito , reprising their roles from the 1984 action-adventure film Romancing the Stone . Like Romancing the Stone , the opening scene takes place in one of Joan's novels. This time, instead of Jesse and Angelina in Joan's wild-west scenario, Joan and Jack are about to be married when pirates attack their ship. The Jewel of the Nile sends its characters off on a new adventure in a fictional African desert, in an effort to find the fabled "Jewel of the Nile ". The song performed by Billy Ocean , " When the Going Gets Tough, the Tough Get Going ", became a major international hit, reaching #1 in the UK and #2 in the US. Six months after the original events in Romancing the Stone , Joan Wilder's ( Kathleen Turner ) and Jack Colton's ( Michael Douglas ) romance has grown stale. While moored at a port in the South of France , Joan, suffering writer's block , wants to return to New York, while Jack prefers aimlessly sailing the world on his boat, the Angelina . At a book signing engagement, Joan meets Omar Khalifa ( Spiros Focás ), a charming Arab ruler who wants Joan to write his biography. Joan accepts and leaves with Omar over Jack's protests. Jack later runs into Ralph ( Danny DeVito ), the swindler from Jack and Joan's previous adventure in Colombia , who demands Jack turn over the stone Jack and Joan found. Shortly after, an Arab, Tarak (Paul David Magid), informs Jack about Omar's true intentions and claims that Omar has the "Jewel of the Nile"; just as Tarak finishes his explanations, the Angelina explodes from a bomb set by one of Omar's men. Ralph and Jack team up to find Joan and the fabled jewel. Joan soon discovers that Omar is a brutal dictator rather than the enlightened ruler which he claimed will unite the Arab world. In the palace jail, Joan encounters Al-Julhara ( Avner Eisenberg ), a holy man who is, in fact, the "Jewel of the Nile" and whom Omar fears. [Note 1] Al-Julhara tells Joan that Omar plans to declare himself ruler of all of the Arab world at a ceremony in the city of Kadir. Realizing that Al-Julhara is the only one who can stop Omar, Joan decides to escort him to Kadir herself. The pair escape and find Jack, and they flee into the desert in Omar's hijacked F-16 fighter jet. Ralph is captured by Tarak's rebel Sufi tribe who are sworn to protect the Jewel so he can fulfill his people's destiny. After encountering a Nubian mountain tribe, Joan and Jack's romance is rekindled. Joan tells Jack that the jewel is not a gem stone but Al-Julhara. In Kadir, Omar intends to use a smoke-and-mirror special effect provided by a British rock promoter to convince onlookers that he is the prophet who will unite the Arab world. Jack, Joan, and Al-Julhara arrive to expose Omar but are captured. Omar suspends Jack and Joan with ropes over a deep pit (a scenario taken from Joan's biggest-selling novel, The Savage Secret ) while Al-Julhara is in a stockade. Ralph, along with the Sufi tribe, arrives in time to rescue the three prisoners. As Omar takes center stage to address the Arab people, Jack and Joan disrupt the ceremony while the Sufi battle Omar's guards. A fire breaks out, engulfing Omar's stage. Jack and Joan are separated, and Omar corners Joan atop the burning scaffolding. Ralph, using a giant crane, helps Jack reach Joan in the nick of time; he kicks Omar over the side and down into the raging flames, killing him. Al-Julhara rises and safely walks through the blazing inferno, fulfilling the prophecy that he is the true spiritual leader. The following day, Jack and Joan are married by Al-Julhara. While Ralph is genuinely happy for Jack and Joan, he laments once again having gained nothing for his efforts, but Tarak acknowledges that he is a true Sufi friend and presents him with a jeweled dagger as Jack and Joan happily sail away down the Nile.Paul David Magid as Tarak Howard Jay Patterson as Barak Randall Edwin Nelson as Karak Samuel Ross Williams as Arak Timothy Daniel Furst as SarakWith a $21 million budget, principal photography began April 22, 1985 with filming wrapped on July 25, 1985. Location shooting took place at Villefranche-sur-Mer and the Palais des Festivals et des Congrès , Cannes , France, Ait Benhaddou near Ouarzazate and Meknes , Morocco , among other locations, including Zion National Park , Springdale, Utah. At the time, both Kathleen Turner and Michael Douglas only made the sequel because they were contractually obligated to do so, although Douglas was much more invested in the film as its producer. At one point during pre-production, Turner tried to back out of the project because she found the script "terrible, formulaic, sentimental", until 20th Century Fox threatened her with a $25 million lawsuit for breach of contract . Douglas intervened on her behalf and ensured that a rewrite was made. Turner was disappointed that Douglas did not ask Diane Thomas , the writer who had penned the script for Romancing the Stone , to return for the sequel, apparently because he decided her asking price was too high. When Douglas agreed to undertake rewrites to please Turner, Thomas was asked to consult on alterations, but Turner remained disappointed with the script. She elaborated in an interview in 2018: "...ultimately I read the script on a plane to Morocco, where the film was shooting, and I was furious. It didn't have what Michael said it'd have. When I got to the hotel in Fez, Michael and I sat down on the floor with three versions of the script. We were trading pages to get a script that was acceptable to both of us. It was, '"I'll do this if you'll do that."' It was frustrating." Filming in North Africa was dogged with problems from unbearable 120-degree-Fahrenheit heat to problems with the local crew but the most troubling concern was that the director showed that he was not up to the task of helming an action film. After one massive night scene that was hours in setup, and cast and crew in place, it was only then that someone noticed that there was no film in the cameras. As producer, Michael Douglas exploded; the whole debacle had to be re-filmed another day, only after the raw film stock was finally located. More problems with local customs cropped up, with film and equipment mysteriously held up by customs until the requisite bribes were paid. In the end, being only three weeks behind schedule was a minor triumph for Douglas. Approximately two weeks before principal photography began, an aircraft carrying Richard Dawking (production designer) and Brian Coates (production manager) crashed during location scouting over the countryside of Morocco, killing all on board. The film is dedicated to the memory of Dawking and Coates, as well as screenwriter Diane Thomas , who had died in an automobile accident six weeks before the film's release. During filming in Morocco, Douglas and Turner, flying in an executive jet aircraft, had a near-accident when their aircraft wing struck the runway in a heavy landing. The use of a General Dynamics F-16 Fighting Falcon mockup was a key element of the main characters' escaping from a fortified town. The wooden, styrofoam and fibreglass mockup was built on an automobile chassis and powered by a 350ci Chevrolet engine. As with the first film, the novelization of the sequel was credited to Joan Wilder, the character played by Kathleen Turner; both books were actually ghostwritten by Catherine Lanigan. The Jewel of the Nile was the final film released on the RCA SelectaVision CED video format. It was also released in other media formats. " When the Going Gets Tough, the Tough Get Going ", performed by Billy Ocean , and "The Jewel of the Nile", performed by Precious Wilson , play during the film and in the end credits respectively. Douglas, Turner, and DeVito also co-starred with Ocean in the MTV music video of the same name. The soundtrack features 1980s rap group Whodini and their single " Freaks Come Out at Night " as Michael Douglas and company make their way through the desert on camel back as well as "Party (No Sheep Is Safe Tonight)" by The Willesden Dodgers during the campfire party scene. Arista released a soundtrack album on record, cassette and compact disc.While The Jewel of the Nile grossed almost as much as its predecessor, the film was much less successful critically and effectively killed the franchise. Critics felt the film was loaded with numerous plot holes and that it lacked the first film's original charm. The New York Times opened its review by writing, "There's nothing in The Jewel of the Nile that wasn't funnier or more fanciful in Romancing the Stone ." Roger Ebert agreed that "... it is not quite the equal of Romancing the Stone ," but praised the interplay between Douglas and Turner. "It seems clear," he wrote, "that they like each other and are having fun during the parade of ludicrous situations in the movie, and their chemistry is sometimes more entertaining than the contrivances of the plot." Colin Greenland reviewed The Jewel of the Nile for White Dwarf #77, and stated that " The Jewel of the Nile is the sequel to Romancing the Stone , another adventure fantasy with just the right pinch of preposterousness. Against all odds, this is a sequel as enjoyable and endearing as the original." The Jewel of the Nile holds a rating of 48% on Rotten Tomatoes based on 27 reviews. The critical consensus reads: "The sense of romantic spark has waned and the prevalence of stereotypes has grown in Jewel of the Nile , although there is still plenty of swooning action for fans of the first adventure." Then- U.S. President Ronald Reagan viewed this film at Camp David in January 1986. Talk of a third film, again starring Douglas, Turner and DeVito, never got beyond a draft. In The Crimson Eagle , Jack and Joan take their two teenage kids to Thailand where they are blackmailed into stealing a priceless statue. The project languished until 1997, when Douglas as tentative producer announced he was no longer interested. In 2005 and again in 2008, Douglas was working on a second sequel, entitled Racing the Monsoon , although there have been no further developments in recent years. Since 2007, Fox considered a remake of Romancing the Stone with the possibility of a "reboot" of a series. The roles of Jack and Joan would be filled by Taylor Kitsch (or Gerard Butler ) and Katherine Heigl . By 2011, the remake was re-worked as a television series.

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Avian influenza

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Avian influenza

Avian influenza , also known as avian flu , is a bird flu caused by the influenza A virus , which can infect people. [note 1] It is similar to other types of animal flu in that it is caused by a virus strain that has adapted to a specific host . The type with the greatest risk is highly pathogenic avian influenza (HPAI). Though influenza A is adapted to birds, it can also stably adapt and sustain person-to-person transmission. Recent influenza research into the genes of the Spanish flu virus shows it to have genes adapted from both human and avian strains. Pigs can also be infected with human, avian, and swine influenza viruses, allowing for mixtures of genes ( reassortment ) to create a new virus, which can cause an antigenic shift to a new influenza A virus subtype which most people have little to no immune protection against. Avian influenza strains are divided into two types based on their pathogenicity : high pathogenicity (HP) or low pathogenicity (LP). The most well-known HPAI strain, H5N1 , was first isolated from a farmed goose in Guangdong Province, China in 1996, and also has low pathogenic strains found in North America. Companion birds in captivity are unlikely to contract the virus and there has been no report of a companion bird with avian influenza since 2003. Pigeons can contract avian strains, but rarely become ill and are incapable of transmitting the virus efficiently to humans or other animals. The type of influenza known informally as avian or bird flu is caused by viruses adapted to birds . The most widely quoted date for the beginning of recorded history of avian influenza (initially known as fowl plague) was in 1878 when it was differentiated from other diseases that caused high mortality rates in birds. Fowl plague or Avian Flu also included Newcastle disease until as recently as the 1950s. Between 1959 and 1995, there were 15 recorded occasions of the emergence of HPAI viruses in poultry, but losses were minimal. Between 1996 and 2008, HPAI outbreaks in poultry have occurred at least 11 times and 4 of these outbreaks have involved millions of birds. In the 1990s, the world's poultry population grew 76% in developing countries and 23% in developed countries, contributing to the increased prevalence of avian influenza. Before the 1990s, HPAI caused high mortality in poultry, but infections were sporadic and contained. Outbreaks have become more common due to the high density and frequent movement of flocks from intensive poultry production. [ citation needed ] Influenza A/ H5N1 was first isolated from a goose in China in 1996. Human infections were first reported in 1997 in Hong Kong. Since 2003, more than 700 human cases of Asian HPAI H5N1 have been reported to the WHO , primarily from 15 countries in Asia, Africa, the Pacific, Europe, and the Middle East, though over 60 countries have been affected. Between early 2013 and early 2017, 916 lab-confirmed human cases of H7N9 were reported to the World Health Organization (WHO). On 9 January 2017, the National Health and Family Planning Commission of China reported to the WHO 106 cases of H7N9 which occurred from late November through late December, including 35 deaths, 2 potential cases of human-to-human transmission, and 80 of these 106 persons stating that they have visited live poultry markets. The cases are reported from Jiangsu (52), Zhejiang (21), Anhui (14), Guangdong (14), Shanghai (2), Fujian (2) and Hunan (1). Similar sudden increases in the number of human cases of H7N9 have occurred in previous years during December and January. From 2014 through 2015, United States poultry and egg producers experienced the largest outbreak of H5N2 in recorded history with approximately 51 million birds depopulated to control the spread of the disease. From May to June 2015, 25 million birds were culled, equating to 409,836 birds per day, or 284 birds per minute. In total, the 2014-2015 H5N2/H5N8 outbreak cost US$879 million in public expenditures and the United States egg and poultry industry more than US$3 billion to eradicate the disease from poultry production. This was the most costly United States HPAI outbreak to date. By the end of 2020, several outbreaks of various bird flus were reported in Europe. Since mid-October several European countries, including Belgium, Denmark, France, Germany, Ireland, the Netherlands, Sweden, and the United Kingdom have reported outbreaks of highly pathogenic avian influenza (HPAI) viruses, mostly in wild birds. Positive tests were also among poultry and captive birds. According to a report by the European Centre for Disease Prevention and Control (ECDC), three varieties of HPAI viruses were found, A(H5N8), A(H5N5) and A(H5N1), with H5N8 being the most commonly found. In Germany, 29,000 chickens were killed to halt the spread of H5N8. In Belgium, H5N5 was found on a poultry farm according to the World Organization for Animal Health (OIE). The outbreak was reported in Menen, near the border with France, and killed 600 birds and the culling of an additional 151,000 chickens from the flock. Since early 2022, more than 58 million birds in 47 states have died either directly from a bird flu virus infection or been culled (killed) as a result of possible exposure to infected birds. The recent strain has cost the government $661 million with no end to the outbreak in sight despite severe mitigation measures put in place by the industry after the 2015 outbreak. Iowa, the biggest egg producer in the United States, has been the most affected, with almost 16 million birds slaughtered. In January 2023, in Tijuana , a dozen eggs were priced at about $2.30, yet $7.37 in California , and border crossers who declare the eggs at the inspection stations are told the items aren't allowed and must be turned over. In March 2023 Senegal reported an outbreak of the disease on a poultry farm in the village of Potou near the northwestern town of Louga. The disease has killed 500 birds at the farm in Potou, while 1,229 bird deaths have been recorded at the Langue de Barbarie Park and surrounding areas. A week later, in Gambia authorities detected H5N1 bird flu on a wild bird reserve. During September and October 2023 South Africa reported one of its worst outbreaks of bird flu. Millions of chickens were killed over the first few weeks and supplies of poultry meat were threatened and supermarkets across the country were short of eggs. From 2014 through 2015, United States poultry and egg producers experienced the largest outbreak of H5N2 in recorded history with approximately 51 million birds depopulated to control the spread of the disease. From May to June 2015, 25 million birds were culled, equating to 409,836 birds per day, or 284 birds per minute. In total, the 2014-2015 H5N2/H5N8 outbreak cost US$879 million in public expenditures and the United States egg and poultry industry more than US$3 billion to eradicate the disease from poultry production. This was the most costly United States HPAI outbreak to date. By the end of 2020, several outbreaks of various bird flus were reported in Europe. Since mid-October several European countries, including Belgium, Denmark, France, Germany, Ireland, the Netherlands, Sweden, and the United Kingdom have reported outbreaks of highly pathogenic avian influenza (HPAI) viruses, mostly in wild birds. Positive tests were also among poultry and captive birds. According to a report by the European Centre for Disease Prevention and Control (ECDC), three varieties of HPAI viruses were found, A(H5N8), A(H5N5) and A(H5N1), with H5N8 being the most commonly found. In Germany, 29,000 chickens were killed to halt the spread of H5N8. In Belgium, H5N5 was found on a poultry farm according to the World Organization for Animal Health (OIE). The outbreak was reported in Menen, near the border with France, and killed 600 birds and the culling of an additional 151,000 chickens from the flock. Since early 2022, more than 58 million birds in 47 states have died either directly from a bird flu virus infection or been culled (killed) as a result of possible exposure to infected birds. The recent strain has cost the government $661 million with no end to the outbreak in sight despite severe mitigation measures put in place by the industry after the 2015 outbreak. Iowa, the biggest egg producer in the United States, has been the most affected, with almost 16 million birds slaughtered. In January 2023, in Tijuana , a dozen eggs were priced at about $2.30, yet $7.37 in California , and border crossers who declare the eggs at the inspection stations are told the items aren't allowed and must be turned over. In March 2023 Senegal reported an outbreak of the disease on a poultry farm in the village of Potou near the northwestern town of Louga. The disease has killed 500 birds at the farm in Potou, while 1,229 bird deaths have been recorded at the Langue de Barbarie Park and surrounding areas. A week later, in Gambia authorities detected H5N1 bird flu on a wild bird reserve. During September and October 2023 South Africa reported one of its worst outbreaks of bird flu. Millions of chickens were killed over the first few weeks and supplies of poultry meat were threatened and supermarkets across the country were short of eggs. Genetic factors in distinguishing between " human flu viruses" and "avian flu viruses" include: The evolution of avian influenza virus has been influenced by genetic variation in the virus population due to genome segment reassortment and mutation . Also homologous recombination occurs in viral genes , suggesting that genetic variation generated by homologous recombination has also played a role in driving the evolution of the virus and potentially has affected virulence and host range. Out of the three types of influenza viruses ( A , B , and C ), influenza A virus can cause zoonotic infections, with a natural reservoir almost entirely in birds. There are many subtypes of avian influenza viruses, but only some strains of five subtypes have been known to infect humans: H5N1, H7N3, H7N7, H7N9, and H9N2. At least one person, an elderly woman in Jiangxi Province , China, died of pneumonia in December 2013 from the H10N8 strain. She was the first human fatality confirmed to be caused by that strain. Most human cases of the avian flu are a result of either handling dead infected birds or from contact with infected fluids. It can also be spread through contaminated surfaces and droppings. While most wild birds have only a mild form of the H5N1 strain, once domesticated birds such as chickens or turkeys are infected, H5N1 can potentially become much more deadly because the birds are often in close contact. H5N1 is a large threat in Asia with infected poultry due to low hygiene conditions and close quarters. Although it is easy for humans to contract the infection from birds, human-to-human transmission is more difficult without prolonged contact. Public health officials believe strains of avian flu may mutate to become easily transmissible between humans. Spreading of H5N1 from Asia to Europe is much more likely caused by both legal and illegal poultry trades than dispersing through wild bird migrations, being that in recent studies, there were no secondary rises in infection in Asia when wild birds migrate south again from their breeding grounds. Instead, the infection patterns followed transportation such as railroads, roads, and country borders, suggesting poultry trade as being much more likely. While there have been strains of avian flu to exist in the United States, they have been extinguished and have not been known to infect humans. [ citation needed ] Examples of avian influenza A virus strains: Avian influenza is most often spread by contact between infected and healthy birds, though can also be spread indirectly through contaminated equipment. The virus is found in secretions from the nostrils, mouth, and eyes of infected birds as well as their droppings. HPAI infection is spread to people often through direct contact with infected poultry, such as during slaughter or plucking. Though the virus can spread through airborne secretions, the disease itself is not an airborne disease. Highly pathogenic strains spread quickly among flocks and can destroy a flock within 28 hours; the less pathogenic strains may affect egg production but are much less deadly. [ citation needed ] Although it is possible for humans to contract the avian influenza virus from birds, human-to-human transmission is much more difficult without prolonged contact. Public health officials believe strains of avian flu may mutate to become easily transmissible between humans. Some strains of avian influenza are present in the intestinal tract of large numbers of shore birds and water birds, but these strains rarely cause human infection. Five manmade ecosystems have contributed to modern avian influenza virus ecology: integrated indoor commercial poultry, range-raised commercial poultry, live poultry markets, backyard and hobby flocks, and bird collection and trading systems including cockfighting . Indoor commercial poultry has had the largest impact on the spread of HPAI, with the increase in HPAI outbreaks largely the result of increased commercial production since the 1990s. In the early days of the HPAI H5N1 pandemic, village poultry and their owners were frequently implicated in disease transmission. Village poultry, also known as backyard and hobby flocks, are small flocks raised under extensive conditions and often allowed free range between multiple households. Further research suggested these flocks pose less of a threat than intensively raised commercial poultry with homogenous genetic stock and poor biosecurity . Backyard and village poultry also do not travel great distances compared to transport of intensively raised poultry and contribute less to the spread of HPAI. The highly pathogenic influenza A virus subtype H5N1 is an emerging avian influenza virus that is causing global concern as a potential pandemic threat. It is often referred to simply as "bird flu" or "avian influenza", even though it is only one of many subtypes. H5N1 has killed millions of poultry in a growing number of countries throughout Asia, Europe, and Africa. Health experts are concerned that the coexistence of human flu viruses and avian flu viruses (especially H5N1) will provide an opportunity for genetic material to be exchanged between species-specific viruses, possibly creating a new virulent influenza strain that is easily transmissible and lethal to humans. The mortality rate for humans with H5N1 is 60%. Since the first human H5N1 outbreak occurred in 1997, there has been an increasing number of HPAI H5N1 bird-to-human transmissions, leading to clinically severe and fatal human infections. Because a significant species barrier exists between birds and humans, the virus does not easily spread to humans. Some cases of infection were researched to discern whether human-to-human transmission occurred. More research is necessary to understand the pathogenesis and epidemiology of the H5N1 virus in humans. Exposure routes and other disease transmission characteristics, such as genetic and immunological factors that may increase the likelihood of infection, are not clearly understood. The first known transmission of H5N1 to a human occurred in Hong Kong in 1997, when there was an outbreak of 18 human cases; 6 deaths were confirmed. None of the infected people worked with poultry. After culling all of the poultry in the area, no more cases were diagnosed. In 2006, the first human-to-human transmission likely occurred when seven members of a family in Sumatra became infected after contact with a family member who had worked with infected poultry. Although millions of birds have become infected with the virus since its discovery, 359 people have died from H5N1 in twelve countries according to World Health Organization reports as of August 10, 2012. The H5N1 outbreak in Thailand caused massive economic losses, especially among poultry workers. Infected birds were culled and slaughtered. The public lost confidence with the poultry products, thus decreasing the consumption of chicken products. This also elicited a ban from importing countries. Several factors enhanced the virality, including bird migration, cool temperature (increases virus survival) and several festivals at that time. A mutation in the virus was discovered in two Guangdong patients in February 2017 which rendered it more deadly to chickens, inasmuch as it could infect every organ; the risk to humans was not increased. A study published in 2012 in Science Magazine reported on research findings that allowed for the airborne transmission of H5N1 in laboratory ferrets. The study in question created airborne H5N1 via amino acid substitutions that largely mitigated the devastating effects of the disease. This fact was underscored by the 0% fatality rate among the ferrets infected via airborne transmission, as well as the fundamental biology underlying the substitutions. Flu viruses attach to host cells via the hemagluttinin proteins on their envelope. These hemagluttinin proteins bind to sialic acid receptors on host cells, which can fall into two categories. The sialic acid receptors can be either 2,3 or 2,6-linked, with the species of origin largely deciding receptor preference. In influenzas of avian origin 2,3-linkage is preferred, vs. influenzas of human origin in which 2,6-linkage is preferable. 2,3-linked SA receptors in humans are found predominantly in the lower respiratory tract, a fact that is the primary foundation for the deadliness of avian influenzas in humans, and also the key to their lack of airborne transmission. In the study that created an airborne avian influenza among ferrets it was necessary to switch the receptor preference of the host cells to those of 2,6-linkage, found predominantly in humans' upper respiratory tract, in order to create an infection that could shed aerosolized virus particles. Such an infection must occur in the upper respiratory tract of humans, thus fundamentally undercutting the fatal trajectory of the disease. A study published in 2012 in Science Magazine reported on research findings that allowed for the airborne transmission of H5N1 in laboratory ferrets. The study in question created airborne H5N1 via amino acid substitutions that largely mitigated the devastating effects of the disease. This fact was underscored by the 0% fatality rate among the ferrets infected via airborne transmission, as well as the fundamental biology underlying the substitutions. Flu viruses attach to host cells via the hemagluttinin proteins on their envelope. These hemagluttinin proteins bind to sialic acid receptors on host cells, which can fall into two categories. The sialic acid receptors can be either 2,3 or 2,6-linked, with the species of origin largely deciding receptor preference. In influenzas of avian origin 2,3-linkage is preferred, vs. influenzas of human origin in which 2,6-linkage is preferable. 2,3-linked SA receptors in humans are found predominantly in the lower respiratory tract, a fact that is the primary foundation for the deadliness of avian influenzas in humans, and also the key to their lack of airborne transmission. In the study that created an airborne avian influenza among ferrets it was necessary to switch the receptor preference of the host cells to those of 2,6-linkage, found predominantly in humans' upper respiratory tract, in order to create an infection that could shed aerosolized virus particles. Such an infection must occur in the upper respiratory tract of humans, thus fundamentally undercutting the fatal trajectory of the disease. Influenza A virus subtype H7N9 is a novel avian influenza virus first reported to have infected humans in 2013 in China. Most of the reported cases of human infection have resulted in severe respiratory illness. In the month following the report of the first case, more than 100 people had been infected, an unusually high rate for a new infection; a fifth of those patients had died, a fifth had recovered, and the rest remained critically ill. The WHO has identified H7N9 as "...an unusually dangerous virus for humans." As of June 30, 133 cases have been reported, resulting in the deaths of 43. Research regarding background and transmission is ongoing. It has been established that many of the human cases of H7N9 appear to have a link to live bird markets. As of July 2013, there is no evidence of sustained human-to-human transmission. A study group headed by one of the world's leading experts on avian flu reported that several instances of human-to-human infection were suspected. It has been reported that H7N9 virus does not kill poultry, which will make surveillance much more difficult. Researchers have commented on the unusual prevalence of older males among H7N9-infected patients. While several environmental, behavioral, and biological explanations for this pattern have been proposed, as yet, the reason is unknown. Currently no vaccine exists, but the use of influenza antiviral drugs known as neuraminidase inhibitors in cases of early infection may be effective. The number of cases detected after April fell abruptly. The decrease in the number of new human H7N9 cases may have resulted from containment measures taken by Chinese authorities, including closing live bird markets, or from a change in seasons, or possibly a combination of both factors. Studies indicate that avian influenza viruses have a seasonal pattern, thus it is thought that infections may pick up again when the weather turns cooler in China. In the four years from early 2013 to early 2017, 916 lab-confirmed human cases of H7N9 were reported to the WHO. On 9 January 2017, the National Health and Family Planning Commission of China reported to the WHO 106 cases which occurred from late November through December. 29, 2016. The cases are reported from Jiangsu (52), Zhejiang (21), Anhui (14), Guangdong (14), Shanghai (2), Fujian (2) and Hunan (1). 80 of these 106 persons have visited live poultry markets. Of these cases, there have been 35 deaths. In two of the 106 cases, human-to-human transmission could not be ruled out. Affected prefectures in Jiangsu province closed live poultry markets in late December 2016, whereas Zhejiang, Guangdong and Anhui provinces went the route of strengthening live poultry market regulations. Travellers to affected regions are recommended to avoid poultry farms, live bird markets, and surfaces which appear to be contaminated with poultry feces. Similar sudden increases in the number of human cases of H7N9 have occurred in previous years during December and January. Several domestic species have been infected with and shown symptoms of H5N1 viral infection, including cats, dogs, ferrets, pigs, and birds. Attempts are made in the United States to minimize the presence of HPAI in poultry through routine surveillance of poultry flocks in commercial poultry operations. Detection of a HPAI virus may result in immediate culling of the flock. Less pathogenic viruses are controlled by vaccination, which is done primarily in turkey flocks ( ATCvet codes: QI01AA23 ( WHO ) for the inactivated fowl vaccine, QI01CL01 ( WHO ) for the inactivated turkey combination vaccine). Avian influenza in cats can show a variety of symptoms and usually lead to death. Cats are able to get infected by either consuming an infected bird or by contracting the virus from another infected cat. As of April 4, 2024, avian flu has been confirmed in seven dairy herds in Texas, three herds in Kansas, two in New Mexico, and one each in Ohio, Michigan, and Idaho. Since 2022, avian flu has been distributed worldwide by migratory birds. In this current April 2024 outbreak, one agricultural worker in Texas has also tested positive though only with the symptom of eye inflammation. Attempts are made in the United States to minimize the presence of HPAI in poultry through routine surveillance of poultry flocks in commercial poultry operations. Detection of a HPAI virus may result in immediate culling of the flock. Less pathogenic viruses are controlled by vaccination, which is done primarily in turkey flocks ( ATCvet codes: QI01AA23 ( WHO ) for the inactivated fowl vaccine, QI01CL01 ( WHO ) for the inactivated turkey combination vaccine). Avian influenza in cats can show a variety of symptoms and usually lead to death. Cats are able to get infected by either consuming an infected bird or by contracting the virus from another infected cat.As of April 4, 2024, avian flu has been confirmed in seven dairy herds in Texas, three herds in Kansas, two in New Mexico, and one each in Ohio, Michigan, and Idaho. Since 2022, avian flu has been distributed worldwide by migratory birds. In this current April 2024 outbreak, one agricultural worker in Texas has also tested positive though only with the symptom of eye inflammation. In 2005, the formation of the International Partnership on Avian and Pandemic Influenza was announced in order to elevate the importance of avian flu, coordinate efforts, and improve disease reporting and surveillance in order to better respond to future pandemics. New networks of laboratories have emerged to detect and respond to avian flu, such as the Crisis Management Center for Animal Health, the Global Avian Influenza Network for Surveillance, OFFLU , and the Global Early Warning System for major animal diseases. After the 2003 outbreak, WHO member states have also recognized the need for more transparent and equitable sharing of vaccines and other benefits from these networks. Cooperative measures created in response to HPAI have served as a basis for programs related to other emerging and re-emerging infectious diseases. HPAI control has also been used for political ends. In Indonesia, negotiations with global response networks were used to recentralize power and funding to the Ministry of Health. In Vietnam policymakers, with the support of the Food and Agriculture Organization of the United Nations (FAO) , used HPAI control to accelerate the industrialization of livestock production for export by proposing to increase the portion of large-scale commercial farms and reducing the number of poultry keepers from 8 to 2 million by 2010. In 2023, report by the Royal Society for the Protection of Birds (RSPB) and the British Trust for Ornithology 75% decrease in the Great Skua and a 25% reduction in Northern Gannets Backyard poultry production was viewed as "traditional Asian" agricultural practices that contrasted with modern commercial poultry production and seen as a threat to biosecurity. Backyard production appeared to hold greater risk than commercial production due to lack of biosecurity and close contact with humans, though HPAI spread in intensively raised flocks was greater due to high density rearing and genetic homogeneity. Asian culture itself was blamed as the reason why certain interventions, such as those that only looked at placed-based interventions, would fail without looking for multifaceted solutions. Press accounts of avian flu in Indonesia were seen by poultry farmers as conflating suspected cases while the public did see the accounts as informative, though many became de-sensitized to the idea of impending danger or only temporarily changed their poultry-related behavior. Rumors also circulated in Java in 2006. These tended to focus on bird flu being linked to big businesses in order to drive small farmers out of the market by exaggerating the danger of avian influenza, avian flu being introduced by foreigners to force Indonesians to purchase imported chicken and keep Indonesian chicken off the world market, and the government using avian flu as a ploy to attract funds from wealthy countries. Such rumors reflected concerns about big businesses, globalization, and a distrust of the national government in a country where "the amount of decentralization here is breathtaking" according to Steven Bjorge, a WHO epidemiologist in Jakarta in 2006. In the context a decentralized national government that the public did not completely trust, Indonesian Health Minister Siti Fadilah Supari announced in December 2006 that her government would no longer be sharing samples of H5N1 collected from Indonesian patients. This decision came as a shock to the international community as it disrupted the Global Influenza Surveillance Network (GISN) coordinated by the WHO for managing seasonal and pandemic influenza. GISN is based on countries sharing virus specimens freely with the WHO which assesses and eventually sends these samples to pharmaceutical companies in order to produce vaccines that are sold back to these countries. Though this was initially seen as an attempt to protect national sovereignty at all costs, it was instead used for a domestic political struggle. Prior to Indonesia's dispute with the GISN, the Ministry of Health, already weak due to the decentralized nature the government, was experiencing further leakage of funding to state and non-state agencies due to global health interventions. By reasserting control over public health issues and funding by setting itself up as the sole Indonesian representative to the WHO, the Ministry of Health made itself a key player in the management of future international funds relating vaccine production and renegotiated benefits from global surveillance networks. Approximately 20% of the protein consumed in developing countries come from poultry. In the wake of the H5N1 pandemic, millions of poultry were killed. In Vietnam alone, over 50 million domestic birds were killed due to HPAI infection and control attempts. A 2005 report by the FAO totaled economic losses in South East Asia around US$10 billion. This had the greatest impact on small scale commercial and backyard producers relative to total assets compared to industrial chains which primarily experience temporary decreases in exports and loss of consumer confidence. Some governments did provide compensation for culled poultry, it was often far below market value (close to 30% of market value in Vietnam), while others such as Cambodia provide no compensation to farmers at all. As poultry serves as a source of food security and liquid assets, the most vulnerable populations were poor small scale farmers. The loss of birds due to HPAI and culling in Vietnam led to an average loss of 2.3 months of production and US$69–108 for households where many have an income of $2 a day or less. The loss of food security for vulnerable households can be seen in the stunting of children under five in Egypt. Women are another population at risk as in most regions of the world, small flocks are tended to by women. Widespread culling also resulted in the decreased enrollment of girls in school in Turkey. Backyard poultry production was viewed as "traditional Asian" agricultural practices that contrasted with modern commercial poultry production and seen as a threat to biosecurity. Backyard production appeared to hold greater risk than commercial production due to lack of biosecurity and close contact with humans, though HPAI spread in intensively raised flocks was greater due to high density rearing and genetic homogeneity. Asian culture itself was blamed as the reason why certain interventions, such as those that only looked at placed-based interventions, would fail without looking for multifaceted solutions. Press accounts of avian flu in Indonesia were seen by poultry farmers as conflating suspected cases while the public did see the accounts as informative, though many became de-sensitized to the idea of impending danger or only temporarily changed their poultry-related behavior. Rumors also circulated in Java in 2006. These tended to focus on bird flu being linked to big businesses in order to drive small farmers out of the market by exaggerating the danger of avian influenza, avian flu being introduced by foreigners to force Indonesians to purchase imported chicken and keep Indonesian chicken off the world market, and the government using avian flu as a ploy to attract funds from wealthy countries. Such rumors reflected concerns about big businesses, globalization, and a distrust of the national government in a country where "the amount of decentralization here is breathtaking" according to Steven Bjorge, a WHO epidemiologist in Jakarta in 2006. In the context a decentralized national government that the public did not completely trust, Indonesian Health Minister Siti Fadilah Supari announced in December 2006 that her government would no longer be sharing samples of H5N1 collected from Indonesian patients. This decision came as a shock to the international community as it disrupted the Global Influenza Surveillance Network (GISN) coordinated by the WHO for managing seasonal and pandemic influenza. GISN is based on countries sharing virus specimens freely with the WHO which assesses and eventually sends these samples to pharmaceutical companies in order to produce vaccines that are sold back to these countries. Though this was initially seen as an attempt to protect national sovereignty at all costs, it was instead used for a domestic political struggle. Prior to Indonesia's dispute with the GISN, the Ministry of Health, already weak due to the decentralized nature the government, was experiencing further leakage of funding to state and non-state agencies due to global health interventions. By reasserting control over public health issues and funding by setting itself up as the sole Indonesian representative to the WHO, the Ministry of Health made itself a key player in the management of future international funds relating vaccine production and renegotiated benefits from global surveillance networks.Approximately 20% of the protein consumed in developing countries come from poultry. In the wake of the H5N1 pandemic, millions of poultry were killed. In Vietnam alone, over 50 million domestic birds were killed due to HPAI infection and control attempts. A 2005 report by the FAO totaled economic losses in South East Asia around US$10 billion. This had the greatest impact on small scale commercial and backyard producers relative to total assets compared to industrial chains which primarily experience temporary decreases in exports and loss of consumer confidence. Some governments did provide compensation for culled poultry, it was often far below market value (close to 30% of market value in Vietnam), while others such as Cambodia provide no compensation to farmers at all. As poultry serves as a source of food security and liquid assets, the most vulnerable populations were poor small scale farmers. The loss of birds due to HPAI and culling in Vietnam led to an average loss of 2.3 months of production and US$69–108 for households where many have an income of $2 a day or less. The loss of food security for vulnerable households can be seen in the stunting of children under five in Egypt. Women are another population at risk as in most regions of the world, small flocks are tended to by women. Widespread culling also resulted in the decreased enrollment of girls in school in Turkey. People who do not regularly come into contact with birds are not at high risk for contracting avian influenza. Those at high risk include poultry farm workers, animal control workers, wildlife biologists, and ornithologists who handle live birds. Organizations with high-risk workers should have an avian influenza response plan in place before any cases have been discovered. Biosecurity of poultry flocks is also important for prevention. Flocks should be isolated from outside birds, especially wild birds, and their waste; vehicles used around the flock should be regularly disinfected and not shared between farms; and birds from slaughter channels should not be returned to the farm. With proper infection control and use of personal protective equipment (PPE), the chance for infection is low. Protecting the eyes, nose, mouth, and hands is important for prevention because these are the most common ways for the virus to enter the body. Appropriate personal protective equipment includes aprons or coveralls, gloves, boots or boot covers, and a head cover or hair cover. Disposable PPE is recommended. An N-95 respirator and unvented/indirectly vented safety goggles are also part of appropriate PPE. A powered air purifying respirator (PAPR) with hood or helmet and face shield is also an option. Proper reporting of an isolated case can help to prevent spread. The Centers for Disease Control and Prevention (US) recommendation is that if a worker develops symptoms within 10 days of working with infected poultry or potentially contaminated materials, they should seek care and notify their employer, who should notify public health officials. For future avian influenza threats, the WHO suggests a three-phase, five-part plan. Phase 1: Pre-pandemic Reduce opportunities for human infection Strengthen the early warning system Phase 2: Emergence of a pandemic virus Contain or delay spread at the source Phase 3: Pandemic declared and spreading internationally Reduce morbidity, mortality, and social disruption Conduct research to guide response measures Reduce opportunities for human infection Strengthen the early warning system Contain or delay spread at the source Reduce morbidity, mortality, and social disruption Conduct research to guide response measures Vaccines for poultry have been formulated against several of the avian H5N1 influenza varieties. Control measures for HPAI encourage mass vaccinations of poultry though The World Health Organization has compiled a list of known clinical trials of pandemic influenza prototype vaccines, including those against H5N1. In some countries still at high risk for HPAI spread, there is compulsory strategic vaccination though vaccine supply shortages remain a problem. During the initial response to H5N1, a one size fits all recommendation was used for all poultry production systems, though measures for intensively raised birds were not necessarily appropriate for extensively raised birds. When looking at village-raised poultry, it was first assumed that the household was the unit and that flocks did not make contact with other flocks, though more effective measures came into use when the epidemiological unit was the village. Recommendations involve restructuring commercial markets to improve biosecurity against avian influenza. Poultry production zoning is used to limit poultry farming to specific areas outside of urban environments while live poultry markets improve biosecurity by limiting the number of traders holding licenses and subjecting producers and traders to more stringent inspections. These recommendations in combination with requirements to fence and house all poultry, and to limit free ranging flocks, will eventually lead to fewer small commercial producers and backyard producers, costing livelihoods as they are unable to meet the conditions needed to participate. A summary of reports to the World Organisation for Animal Health in 2005 and 2010 suggest that surveillance and under-reporting in developed and developing countries is still a challenge. Often, donor support can focus on HPAI control alone, while similar diseases such as Newcastle disease , acute fowl cholera , infectious laryngotracheitis, and infectious bursal disease still affect poultry populations. When HPAI tests come back negative, a lack of funded testing for differential diagnoses can leave farmers wondering what killed their birds. Since traditional production systems require little investment and serve as a safety net for lower income households, prevention and treatment can be seen as less cost-effective than letting poultry die. Effective control not only requires prior agreements to be made with relevant government agencies, such as seen with Indonesia, they must also not unduly threaten food security. Culling is used in order to decrease the threat of avian influenza transmission by killing potentially infected birds. The FAO manual on HPAI control recommends a zoning strategy which begins with the identification of an infected area (IA) where sick or dead birds have tested positive. All poultry in this zone are culled while the area 1 to 5 km from the outer boundary of the IA is considered the restricted area (RA) placed under strict surveillance. 2 to 10 km from the RA is the control area (CA) that serves as a buffer zone in case of spread. Culling is not recommended beyond the IA unless there is evidence of spread. The manual also provides examples of how control was carried out between 2004 and 2005 to contain H5N1 where all poultry was to be stamped out in a 3 km radius beyond the infected point and beyond that a 5 km radius where all fowl was to be vaccinated. This culling method was indiscriminate as a large proportion of the poultry inside these areas were small backyard flocks which did not travel great enough distances to carry infection to adjacent villages without human effort and may have not been infected at all. Between 2004 and 2005, over 100 million chickens were culled in Asia to contain H5N1. The risk of mass culling of birds and the resulting economic impact led to farmers who were reluctant to report sick poultry. The culls often preempted actual lab testing for H5N1 as avian flu policy justified sacrificing poultry as a safeguard against HPAI spread. In response to these policies, farmers in Vietnam between 2003 and 2004 became more and more unwilling to surrender apparently healthy birds to authorities and stole poultry destined for culls as it stripped poultry of their biosocial and economic worth. By the end of 2005, the government implemented a new policy that targeted high-risk flock in the immediate vicinity of infected farms and instituted voluntary culling with compensation in the case of a local outbreak. Not only did culling result in severe economic impacts especially for small scale farmers, culling itself may be an ineffective preventative measure. In the short-term, mass culling achieves its goals of limiting the immediate spread of HPAI, it has been found to impede the evolution of host resistance which is important for the long-term success of HPAI control. Mass culling also selects for elevated influenza virulence and results in the greater mortality of birds overall. Effective culling strategies must be selective as well as considerate of economic impacts to optimize epidemiological control and minimize economic and agricultural destruction. Prevention and control programs must take into account local understandings of people-poultry relations. In the past, programs that have focused on singular, place-based understandings of disease transmission have been ineffective. In the case of Northern Vietnam, health workers saw poultry as commodities with an environment that was under the control of people. Poultry existed in the context of farms, markets, slaughterhouses, and roads while humans were indirectly the primary transmitters of avian flu, placing the burden of disease control on people. Farmers saw their free ranging poultry in an environment dominated by nonhuman forces that they could not exert control over. There were a host of nonhuman actors such as wild birds and weather patterns whose relationships with the poultry fostered the disease and absolved farmers of complete responsibility for disease control. Attempts at singular, place-based controls sought to teach farmers to identify areas where their behavior could change without looking at poultry behaviors. Behavior recommendations by Vietnam's National Steering Committee for Avian Influenza Control and Prevention (NSCAI) were drawn from the FAO Principles of Biosecurity. These included restrictions from entering areas where poultry are kept by erecting barriers to segregate poultry from non-human contact, limits on human movement of poultry and poultry-related products ideally to transporters, and recommendations for farmers to wash hands and footwear before and after contact with poultry. Farmers, pointed to wind and environmental pollution as reasons poultry would get sick. NSCAI recommendations also would disrupt longstanding livestock production practices as gates impede sales by restricting assessment of birds by appearance and offend customers by limiting outside human contact. Instead of incorporating local knowledge into recommendations, cultural barriers were used as scapegoats for failed interventions. Prevention and control methods have been more effective when also considering the social, political, and ecological agents in play. During the initial response to H5N1, a one size fits all recommendation was used for all poultry production systems, though measures for intensively raised birds were not necessarily appropriate for extensively raised birds. When looking at village-raised poultry, it was first assumed that the household was the unit and that flocks did not make contact with other flocks, though more effective measures came into use when the epidemiological unit was the village. Recommendations involve restructuring commercial markets to improve biosecurity against avian influenza. Poultry production zoning is used to limit poultry farming to specific areas outside of urban environments while live poultry markets improve biosecurity by limiting the number of traders holding licenses and subjecting producers and traders to more stringent inspections. These recommendations in combination with requirements to fence and house all poultry, and to limit free ranging flocks, will eventually lead to fewer small commercial producers and backyard producers, costing livelihoods as they are unable to meet the conditions needed to participate. A summary of reports to the World Organisation for Animal Health in 2005 and 2010 suggest that surveillance and under-reporting in developed and developing countries is still a challenge. Often, donor support can focus on HPAI control alone, while similar diseases such as Newcastle disease , acute fowl cholera , infectious laryngotracheitis, and infectious bursal disease still affect poultry populations. When HPAI tests come back negative, a lack of funded testing for differential diagnoses can leave farmers wondering what killed their birds. Since traditional production systems require little investment and serve as a safety net for lower income households, prevention and treatment can be seen as less cost-effective than letting poultry die. Effective control not only requires prior agreements to be made with relevant government agencies, such as seen with Indonesia, they must also not unduly threaten food security. Culling is used in order to decrease the threat of avian influenza transmission by killing potentially infected birds. The FAO manual on HPAI control recommends a zoning strategy which begins with the identification of an infected area (IA) where sick or dead birds have tested positive. All poultry in this zone are culled while the area 1 to 5 km from the outer boundary of the IA is considered the restricted area (RA) placed under strict surveillance. 2 to 10 km from the RA is the control area (CA) that serves as a buffer zone in case of spread. Culling is not recommended beyond the IA unless there is evidence of spread. The manual also provides examples of how control was carried out between 2004 and 2005 to contain H5N1 where all poultry was to be stamped out in a 3 km radius beyond the infected point and beyond that a 5 km radius where all fowl was to be vaccinated. This culling method was indiscriminate as a large proportion of the poultry inside these areas were small backyard flocks which did not travel great enough distances to carry infection to adjacent villages without human effort and may have not been infected at all. Between 2004 and 2005, over 100 million chickens were culled in Asia to contain H5N1. The risk of mass culling of birds and the resulting economic impact led to farmers who were reluctant to report sick poultry. The culls often preempted actual lab testing for H5N1 as avian flu policy justified sacrificing poultry as a safeguard against HPAI spread. In response to these policies, farmers in Vietnam between 2003 and 2004 became more and more unwilling to surrender apparently healthy birds to authorities and stole poultry destined for culls as it stripped poultry of their biosocial and economic worth. By the end of 2005, the government implemented a new policy that targeted high-risk flock in the immediate vicinity of infected farms and instituted voluntary culling with compensation in the case of a local outbreak. Not only did culling result in severe economic impacts especially for small scale farmers, culling itself may be an ineffective preventative measure. In the short-term, mass culling achieves its goals of limiting the immediate spread of HPAI, it has been found to impede the evolution of host resistance which is important for the long-term success of HPAI control. Mass culling also selects for elevated influenza virulence and results in the greater mortality of birds overall. Effective culling strategies must be selective as well as considerate of economic impacts to optimize epidemiological control and minimize economic and agricultural destruction.Prevention and control programs must take into account local understandings of people-poultry relations. In the past, programs that have focused on singular, place-based understandings of disease transmission have been ineffective. In the case of Northern Vietnam, health workers saw poultry as commodities with an environment that was under the control of people. Poultry existed in the context of farms, markets, slaughterhouses, and roads while humans were indirectly the primary transmitters of avian flu, placing the burden of disease control on people. Farmers saw their free ranging poultry in an environment dominated by nonhuman forces that they could not exert control over. There were a host of nonhuman actors such as wild birds and weather patterns whose relationships with the poultry fostered the disease and absolved farmers of complete responsibility for disease control. Attempts at singular, place-based controls sought to teach farmers to identify areas where their behavior could change without looking at poultry behaviors. Behavior recommendations by Vietnam's National Steering Committee for Avian Influenza Control and Prevention (NSCAI) were drawn from the FAO Principles of Biosecurity. These included restrictions from entering areas where poultry are kept by erecting barriers to segregate poultry from non-human contact, limits on human movement of poultry and poultry-related products ideally to transporters, and recommendations for farmers to wash hands and footwear before and after contact with poultry. Farmers, pointed to wind and environmental pollution as reasons poultry would get sick. NSCAI recommendations also would disrupt longstanding livestock production practices as gates impede sales by restricting assessment of birds by appearance and offend customers by limiting outside human contact. Instead of incorporating local knowledge into recommendations, cultural barriers were used as scapegoats for failed interventions. Prevention and control methods have been more effective when also considering the social, political, and ecological agents in play.

Wiki

Avian influenza

https://api.wikimedia.org/core/v1/wikipedia/en/page/Influenza_A_virus_subtype_H5N1/html

Influenza A virus subtype H5N1

Influenza A virus subtype H5N1 (A/H5N1) is a subtype of the influenza A virus which can cause illness in humans and many other species. A bird-adapted strain of H5N1, called HPAI A(H5N1) for highly pathogenic avian influenza virus of type A of subtype H5N1 , is the highly pathogenic causative agent of H5N1 flu , commonly known as avian influenza ("bird flu"). It is enzootic (maintained in the population) in many bird populations, especially in Southeast Asia . One strain of HPAI A(H5N1) is spreading globally after first appearing in Asia. It is epizootic (an epidemic in nonhumans) and panzootic (affecting animals of many species, especially over a wide area), killing tens of millions of birds and spurring the culling of hundreds of millions of others to stem its spread. Many references to "bird flu" and H5N1 in the popular media refer to this strain. According to the World Health Organization (WHO) and the United Nations Food and Agriculture Organization (FAO), H5N1 pathogenicity is gradually continuing to rise in endemic areas, but the avian influenza disease situation in farmed birds is being held in check by vaccination, and there is "no evidence of sustained human-to-human transmission" of the virus. Eleven outbreaks of H5N1 were reported worldwide in June 2008, in five countries (China, Egypt, Indonesia, Pakistan and Vietnam) compared to 65 outbreaks in June 2006, and 55 in June 2007. The global HPAI situation significantly improved in the first half of 2008, but FAO reports that imperfect disease surveillance systems mean that occurrence of the virus remains underestimated and underreported. As of March 2024, the WHO reported a total of 888 confirmed human cases which resulted in the deaths of 463 people since 2003. Several H5N1 vaccines have been developed and approved, and stockpiled by a number of countries, including the United States (in its National Stockpile ), Britain, France, Canada, and Australia, for use in an emergency. HPAI A(H5N1) is considered an avian disease, although there is some evidence of limited human-to-human transmission of the virus. A risk factor for contracting the virus is handling of infected poultry, but transmission of the virus from infected birds to humans has been characterized as inefficient. Still, around 60% of humans known to have been infected with the Asian strain of HPAI A(H5N1) have died from it, and H5N1 may mutate or reassort into a strain capable of efficient human-to-human transmission. In 2003, virologist Robert G. Webster published an article titled "The world is teetering on the edge of a pandemic that could kill a large fraction of the human population" in American Scientist . He called for adequate resources to fight what he sees as a major world threat to possibly billions of lives. On September 29, 2005, David Nabarro , the newly appointed Senior United Nations System Coordinator for Avian and Human Influenza, warned the world that an outbreak of avian influenza could kill anywhere between 5 million and 150 million people. Due to the high lethality and virulence of HPAI A(H5N1), its endemic presence, its increasingly large host reservoir, and its significant ongoing mutations, in 2006, the H5N1 virus has been regarded to be the world's largest pandemic threat, and billions of dollars are being spent researching H5N1 and preparing for a potential influenza pandemic . At least 12 companies and 17 governments are developing prepandemic influenza vaccines in 28 different clinical trials that, if successful, could turn a deadly pandemic infection into a nondeadly one. Full-scale production of a vaccine that could prevent any illness at all from the strain would require at least three months after the virus's emergence to begin, but it is hoped that vaccine production could increase until one billion doses were produced by one year after the initial identification of the virus. H5N1 may cause more than one influenza pandemic , as it is expected to continue mutating in birds regardless of whether humans develop herd immunity to a future pandemic strain. Influenza pandemics from its genetic offspring may include influenza A virus subtypes other than H5N1. While genetic analysis of the H5N1 virus shows that influenza pandemics from its genetic offspring can easily be far more lethal than the Spanish flu pandemic, planning for a future influenza pandemic is based on what can be done and there is no higher Pandemic Severity Index level than a Category 5 pandemic which, roughly speaking, is any pandemic as bad as the Spanish flu or worse; and for which all intervention measures are to be used. In general, humans who catch a humanized influenza A virus (a human flu virus of type A) usually have symptoms that include fever , cough , sore throat , muscle aches , conjunctivitis , and, in severe cases, breathing problems and pneumonia that may be fatal. The severity of the infection depends in large part on the state of the infected persons' immune systems and whether they had been exposed to the strain before (in which case they would be partially immune). No one knows if these or other symptoms will be the symptoms of a humanized H5N1 flu. The avian influenza hemagglutinin binds alpha 2–3 sialic acid receptors, while human influenza hemagglutinins bind alpha 2–6 sialic acid receptors. This means when the H5N1 strain infects humans, it will replicate in the lower respiratory tract, and consequently will cause viral pneumonia . There is as yet no human form of H5N1, so all humans who have caught it so far have caught avian H5N1. The reported mortality rate of highly pathogenic H5N1 avian influenza in a human is high; WHO data indicate 60% of cases classified as H5N1 resulted in death. However, there is some evidence the actual mortality rate of avian flu could be much lower, as there may be many people with milder symptoms who do not seek treatment and are not counted. In one case, a boy with H5N1 experienced diarrhea followed rapidly by a coma without developing respiratory or flu-like symptoms. There have been studies of the levels of cytokines in humans infected by the H5N1 flu virus. Of particular concern is elevated levels of tumor necrosis factor-alpha , a protein associated with tissue destruction at sites of infection and increased production of other cytokines. Flu virus-induced increases in the level of cytokines is also associated with flu symptoms, including fever, chills, vomiting and headache. Tissue damage associated with pathogenic flu virus infection can ultimately result in death. The inflammatory cascade triggered by H5N1 has been called a ' cytokine storm ' by some, because of what seems to be a positive feedback process of damage to the body resulting from immune system stimulation. H5N1 induces higher levels of cytokines than the more common flu virus types. Clinical signs of H5N1 in birds range from mild—decrease in egg production, nasal discharge, coughing and sneezing—to severe, including loss of coordination, energy, and appetite; soft-shelled or misshapen eggs; purple discoloration of the wattles, head, eyelids, combs, and hocks; and diarrhea. Sometimes the first noticeable sign is sudden death. Clinical signs of H5N1 in birds range from mild—decrease in egg production, nasal discharge, coughing and sneezing—to severe, including loss of coordination, energy, and appetite; soft-shelled or misshapen eggs; purple discoloration of the wattles, head, eyelids, combs, and hocks; and diarrhea. Sometimes the first noticeable sign is sudden death. The first known strain of HPAI A(H5N1) (called A/chicken/Scotland/59) killed two flocks of chickens in Scotland in 1959, but that strain was very different from the highly pathogenic strain of H5N1. The dominant strain of HPAI A(H5N1) in 2004 evolved from 1999 to 2002 creating the Z genotype. It has also been called "Asian lineage HPAI A(H5N1)". Asian lineage HPAI A(H5N1) is divided into two antigenic clades. "Clade 1 includes human and bird isolates from Vietnam , Thailand , and Cambodia and bird isolates from Laos and Malaysia . Clade 2 viruses were first identified in bird isolates from China , Indonesia , Japan , and South Korea before spreading westward to the Middle East , Europe , and Africa . The clade 2 viruses have been primarily responsible for human H5N1 infections that have occurred during late 2005 and 2006, according to WHO. Genetic analysis has identified six subclades of clade 2, three of which have a distinct geographic distribution and have been implicated in human infections: Map A 2007 study focused on the EMA subclade has shed further light on the EMA mutations. "The 36 new isolates reported here greatly expand the amount of whole-genome sequence data available from recent avian influenza (H5N1) isolates. Before our project, GenBank contained only 5 other complete genomes from Europe for the 2004–2006 period, and it contained no whole genomes from the Middle East or northern Africa. Our analysis showed several new findings. First, all European, Middle Eastern, and African samples fall into a clade that is distinct from other contemporary Asian clades, all of which share common ancestry with the original 1997 Hong Kong strain. Phylogenetic trees built on each of the 8 segments show a consistent picture of 3 lineages, as illustrated by the HA tree shown in Figure 1. Two of the clades contain exclusively Vietnamese isolates; the smaller of these, with 5 isolates, we label V1; the larger clade, with 9 isolates, is V2. The remaining 22 isolates all fall into a third, clearly distinct clade, labeled EMA, which comprises samples from Europe, the Middle East, and Africa. Trees for the other 7 segments display a similar topology, with clades V1, V2, and EMA clearly separated in each case. Analyses of all available complete influenza (H5N1) genomes and of 589 HA sequences placed the EMA clade as distinct from the major clades circulating in People's Republic of China, Indonesia, and Southeast Asia." H5N1 isolates are identified like this actual HPAI A(H5N1) example, A/chicken/Nakorn-Patom/Thailand/CU-K2/04(H5N1) : Other examples include: A/duck/Hong Kong/308/78(H5N3), A/avian/NY/01(H5N2), A/chicken/Mexico/31381-3/94(H5N2), and A/ shoveler /Egypt/03(H5N2). As with other avian flu viruses, H5N1 has strains called "highly pathogenic" (HP) and "low-pathogenic" (LP). Avian influenza viruses that cause HPAI are highly virulent , and mortality rates in infected flocks often approach 100%. LPAI viruses have negligible virulence, but these viruses can serve as progenitors to HPAI viruses. The strain of H5N1 responsible for the deaths of birds across the world is an HPAI strain; all other strains of H5N1, including a North American strain that causes no disease at all in any species, are LPAI strains. All HPAI strains identified to date have involved H5 and H7 subtypes. The distinction concerns pathogenicity in poultry, not humans. Normally, a highly pathogenic avian virus is not highly pathogenic to either humans or nonpoultry birds. This [ which? ] deadly strain of H5N1 is unusual in being deadly to so many species, including some, like domestic cats, never previously susceptible to any influenza virus . [ failed verification ] H5N1 is a subtype of the species Influenza A virus of the genus Alphainfluenzavirus of the family Orthomyxoviridae . Like all other influenza A subtypes, the H5N1 subtype is an RNA virus . It has a segmented genome of eight negative sense, single-strands of RNA , abbreviated as PB2, PB1, PA, HA, NP, NA, MP and NS. [ citation needed ] HA codes for hemagglutinin , an antigenic glycoprotein found on the surface of the influenza viruses and is responsible for binding the virus to the cell that is being infected. NA codes for neuraminidase , an antigenic glycosylated enzyme found on the surface of the influenza viruses. It facilitates the release of progeny viruses from infected cells. The hemagglutinin (HA) and neuraminidase (NA) RNA strands specify the structure of proteins that are most medically relevant as targets for antiviral drugs and antibodies . HA and NA are also used as the basis for the naming of the different subtypes of influenza A viruses. This is where the H and N come from in H5N1 . Low pathogenic avian influenza H5N1 (LPAI H5N1), also called "North American" H5N1, commonly occurs in wild birds. In most cases, it causes minor sickness or no noticeable signs of disease in birds. It is not known to affect humans at all. The only concern about it is that it is possible for it to be transmitted to poultry and in poultry mutate into a highly pathogenic strain. 1966 – LPAI H5N1 A/Turkey/Ontario/6613/1966(H5N1) was detected in a flock of infected turkeys in Ontario, Canada. 1975 – LPAI H5N1 was detected in a wild mallard duck and a wild blue goose in Wisconsin. 1981 and 1985 – LPAI H5N1 was detected in ducks by the University of Minnesota conducting a sampling procedure in which sentinel ducks were monitored in cages placed in the wild for a short period of time. 1983 – LPAI H5N1 was detected in ring-billed gulls in Pennsylvania. 1986 – LPAI H5N1 was detected in a wild mallard duck in Ohio. 2005 – LPAI H5N1 was detected in ducks in Manitoba, Canada. 2008 – LPAI H5N1 was detected in ducks in New Zealand. 2009 – LPAI H5N1 was detected in commercial poultry in British Columbia. "In the past, there was no requirement for reporting or tracking LPAI H5 or H7 detections in wild birds so states and universities tested wild bird samples independently of USDA. Because of this, the above list of previous detections might not be all inclusive of past LPAI H5N1 detections. However, the World Organization for Animal Health ( OIE ) recently changed its requirement of reporting detections of avian influenza. Effective in 2006, all confirmed LPAI H5 and H7 AI subtypes must be reported to the OIE because of their potential to mutate into highly pathogenic strains. Therefore, USDA now tracks these detections in wild birds, backyard flocks, commercial flocks and live bird markets." Influenza viruses have a relatively high mutation rate that is characteristic of RNA viruses . The segmentation of its genome facilitates genetic recombination by segment reassortment in hosts infected with two different strains of influenza viruses at the same time. A previously uncontagious strain may then be able to pass between humans, one of several possible paths to a pandemic. [ citation needed ] The ability of various influenza strains to show species-selectivity is largely due to variation in the hemagglutinin genes. Genetic mutations in the hemagglutinin gene that cause single amino acid substitutions can significantly alter the ability of viral hemagglutinin proteins to bind to receptors on the surface of host cells. Such mutations in avian H5N1 viruses can change virus strains from being inefficient at infecting human cells to being as efficient in causing human infections as more common human influenza virus types. This doesn't mean that one amino acid substitution can cause a pandemic, but it does mean that one amino acid substitution can cause an avian flu virus that is not pathogenic in humans to become pathogenic in humans. [ citation needed ] Influenza A virus subtype H3N2 is endemic in pigs in China, and has been detected in pigs in Vietnam, increasing fears of the emergence of new variant strains. The dominant strain of annual flu virus in January 2006 was H3N2 , which is now resistant to the standard antiviral drugs amantadine and rimantadine . The possibility of H5N1 and H3N2 exchanging genes through reassortment is a major concern. If a reassortment in H5N1 occurs, it might remain an H5N1 subtype, or it could shift subtypes, as H2N2 did when it evolved into the Hong Kong Flu strain of H3N2 . Both the H2N2 and H3N2 pandemic strains contained avian influenza virus RNA segments. "While the pandemic human influenza viruses of 1957 (H2N2) and 1968 (H3N2) clearly arose through reassortment between human and avian viruses, the influenza virus causing the 'Spanish flu' in 1918 appears to be entirely derived from an avian source". H5N1 isolates are identified like this actual HPAI A(H5N1) example, A/chicken/Nakorn-Patom/Thailand/CU-K2/04(H5N1) : Other examples include: A/duck/Hong Kong/308/78(H5N3), A/avian/NY/01(H5N2), A/chicken/Mexico/31381-3/94(H5N2), and A/ shoveler /Egypt/03(H5N2). As with other avian flu viruses, H5N1 has strains called "highly pathogenic" (HP) and "low-pathogenic" (LP). Avian influenza viruses that cause HPAI are highly virulent , and mortality rates in infected flocks often approach 100%. LPAI viruses have negligible virulence, but these viruses can serve as progenitors to HPAI viruses. The strain of H5N1 responsible for the deaths of birds across the world is an HPAI strain; all other strains of H5N1, including a North American strain that causes no disease at all in any species, are LPAI strains. All HPAI strains identified to date have involved H5 and H7 subtypes. The distinction concerns pathogenicity in poultry, not humans. Normally, a highly pathogenic avian virus is not highly pathogenic to either humans or nonpoultry birds. This [ which? ] deadly strain of H5N1 is unusual in being deadly to so many species, including some, like domestic cats, never previously susceptible to any influenza virus . [ failed verification ]H5N1 is a subtype of the species Influenza A virus of the genus Alphainfluenzavirus of the family Orthomyxoviridae . Like all other influenza A subtypes, the H5N1 subtype is an RNA virus . It has a segmented genome of eight negative sense, single-strands of RNA , abbreviated as PB2, PB1, PA, HA, NP, NA, MP and NS. [ citation needed ] HA codes for hemagglutinin , an antigenic glycoprotein found on the surface of the influenza viruses and is responsible for binding the virus to the cell that is being infected. NA codes for neuraminidase , an antigenic glycosylated enzyme found on the surface of the influenza viruses. It facilitates the release of progeny viruses from infected cells. The hemagglutinin (HA) and neuraminidase (NA) RNA strands specify the structure of proteins that are most medically relevant as targets for antiviral drugs and antibodies . HA and NA are also used as the basis for the naming of the different subtypes of influenza A viruses. This is where the H and N come from in H5N1 .Low pathogenic avian influenza H5N1 (LPAI H5N1), also called "North American" H5N1, commonly occurs in wild birds. In most cases, it causes minor sickness or no noticeable signs of disease in birds. It is not known to affect humans at all. The only concern about it is that it is possible for it to be transmitted to poultry and in poultry mutate into a highly pathogenic strain. 1966 – LPAI H5N1 A/Turkey/Ontario/6613/1966(H5N1) was detected in a flock of infected turkeys in Ontario, Canada. 1975 – LPAI H5N1 was detected in a wild mallard duck and a wild blue goose in Wisconsin. 1981 and 1985 – LPAI H5N1 was detected in ducks by the University of Minnesota conducting a sampling procedure in which sentinel ducks were monitored in cages placed in the wild for a short period of time. 1983 – LPAI H5N1 was detected in ring-billed gulls in Pennsylvania. 1986 – LPAI H5N1 was detected in a wild mallard duck in Ohio. 2005 – LPAI H5N1 was detected in ducks in Manitoba, Canada. 2008 – LPAI H5N1 was detected in ducks in New Zealand. 2009 – LPAI H5N1 was detected in commercial poultry in British Columbia. "In the past, there was no requirement for reporting or tracking LPAI H5 or H7 detections in wild birds so states and universities tested wild bird samples independently of USDA. Because of this, the above list of previous detections might not be all inclusive of past LPAI H5N1 detections. However, the World Organization for Animal Health ( OIE ) recently changed its requirement of reporting detections of avian influenza. Effective in 2006, all confirmed LPAI H5 and H7 AI subtypes must be reported to the OIE because of their potential to mutate into highly pathogenic strains. Therefore, USDA now tracks these detections in wild birds, backyard flocks, commercial flocks and live bird markets." Influenza viruses have a relatively high mutation rate that is characteristic of RNA viruses . The segmentation of its genome facilitates genetic recombination by segment reassortment in hosts infected with two different strains of influenza viruses at the same time. A previously uncontagious strain may then be able to pass between humans, one of several possible paths to a pandemic. [ citation needed ] The ability of various influenza strains to show species-selectivity is largely due to variation in the hemagglutinin genes. Genetic mutations in the hemagglutinin gene that cause single amino acid substitutions can significantly alter the ability of viral hemagglutinin proteins to bind to receptors on the surface of host cells. Such mutations in avian H5N1 viruses can change virus strains from being inefficient at infecting human cells to being as efficient in causing human infections as more common human influenza virus types. This doesn't mean that one amino acid substitution can cause a pandemic, but it does mean that one amino acid substitution can cause an avian flu virus that is not pathogenic in humans to become pathogenic in humans. [ citation needed ] Influenza A virus subtype H3N2 is endemic in pigs in China, and has been detected in pigs in Vietnam, increasing fears of the emergence of new variant strains. The dominant strain of annual flu virus in January 2006 was H3N2 , which is now resistant to the standard antiviral drugs amantadine and rimantadine . The possibility of H5N1 and H3N2 exchanging genes through reassortment is a major concern. If a reassortment in H5N1 occurs, it might remain an H5N1 subtype, or it could shift subtypes, as H2N2 did when it evolved into the Hong Kong Flu strain of H3N2 . Both the H2N2 and H3N2 pandemic strains contained avian influenza virus RNA segments. "While the pandemic human influenza viruses of 1957 (H2N2) and 1968 (H3N2) clearly arose through reassortment between human and avian viruses, the influenza virus causing the 'Spanish flu' in 1918 appears to be entirely derived from an avian source". There are several H5N1 vaccines for several of the avian H5N1 varieties, but the continual mutation of H5N1 renders them of limited use to date: while vaccines can sometimes provide cross-protection against related flu strains, the best protection would be from a vaccine specifically produced for any future pandemic flu virus strain. Daniel R. Lucey , co-director of the Biohazardous Threats and Emerging Diseases graduate program at Georgetown University has made this point, "There is no H5N1 pandemic so there can be no pandemic vaccine ". However, "pre-pandemic vaccines" have been created; are being refined and tested; and do have some promise both in furthering research and preparedness for the next pandemic. Vaccine manufacturing companies are being encouraged to increase capacity so that if a pandemic vaccine is needed, facilities will be available for rapid production of large amounts of a vaccine specific to a new pandemic strain. "The United States is collaborating closely with eight international organizations, including the World Health Organization (WHO), the Food and Agriculture Organization of the United Nations (FAO), the World Organization for Animal Health (OIE), and 88 foreign governments to address the situation through planning, greater monitoring, and full transparency in reporting and investigating avian influenza occurrences. The United States and these international partners have led global efforts to encourage countries to heighten surveillance for outbreaks in poultry and significant numbers of deaths in migratory birds and to rapidly introduce containment measures. The U.S. Agency for International Development (USAID) and the U.S. Department of State , the U.S. Department of Health and Human Services (HHS), and Agriculture (USDA) are coordinating future international response measures on behalf of the White House with departments and agencies across the federal government". Together steps are being taken to "minimize the risk of further spread in animal populations", "reduce the risk of human infections", and "further support pandemic planning and preparedness". Ongoing detailed mutually coordinated onsite surveillance and analysis of human and animal H5N1 avian flu outbreaks are being conducted and reported by the USGS National Wildlife Health Center, the Centers for Disease Control and Prevention , the World Health Organization , the European Commission , and others. There are several H5N1 vaccines for several of the avian H5N1 varieties, but the continual mutation of H5N1 renders them of limited use to date: while vaccines can sometimes provide cross-protection against related flu strains, the best protection would be from a vaccine specifically produced for any future pandemic flu virus strain. Daniel R. Lucey , co-director of the Biohazardous Threats and Emerging Diseases graduate program at Georgetown University has made this point, "There is no H5N1 pandemic so there can be no pandemic vaccine ". However, "pre-pandemic vaccines" have been created; are being refined and tested; and do have some promise both in furthering research and preparedness for the next pandemic. Vaccine manufacturing companies are being encouraged to increase capacity so that if a pandemic vaccine is needed, facilities will be available for rapid production of large amounts of a vaccine specific to a new pandemic strain."The United States is collaborating closely with eight international organizations, including the World Health Organization (WHO), the Food and Agriculture Organization of the United Nations (FAO), the World Organization for Animal Health (OIE), and 88 foreign governments to address the situation through planning, greater monitoring, and full transparency in reporting and investigating avian influenza occurrences. The United States and these international partners have led global efforts to encourage countries to heighten surveillance for outbreaks in poultry and significant numbers of deaths in migratory birds and to rapidly introduce containment measures. The U.S. Agency for International Development (USAID) and the U.S. Department of State , the U.S. Department of Health and Human Services (HHS), and Agriculture (USDA) are coordinating future international response measures on behalf of the White House with departments and agencies across the federal government". Together steps are being taken to "minimize the risk of further spread in animal populations", "reduce the risk of human infections", and "further support pandemic planning and preparedness". Ongoing detailed mutually coordinated onsite surveillance and analysis of human and animal H5N1 avian flu outbreaks are being conducted and reported by the USGS National Wildlife Health Center, the Centers for Disease Control and Prevention , the World Health Organization , the European Commission , and others. There is no highly effective treatment for H5N1 flu, but oseltamivir (commercially marketed by Roche as Tamiflu) can sometimes inhibit the influenza virus from spreading inside the user's body. This drug has become a focus for some governments and organizations trying to prepare for a possible H5N1 pandemic. On April 20, 2006, Roche AG announced that a stockpile of three million treatment courses of Tamiflu are waiting at the disposal of the World Health Organization to be used in case of a flu pandemic; separately Roche donated two million courses to the WHO for use in developing nations that may be affected by such a pandemic but lack the ability to purchase large quantities of the drug. However, WHO expert Hassan al-Bushra has said: Animal and lab studies suggest that Relenza ( zanamivir ), which is in the same class of drugs as Tamiflu, may also be effective against H5N1. In a study performed on mice in 2000, "zanamivir was shown to be efficacious in treating avian influenza viruses H9N2, H6N1 , and H5N1 transmissible to mammals". In addition, mice studies suggest the combination of zanamivir, celecoxib and mesalazine looks promising producing a 50% survival rate compared to no survival in the placebo arm. While no one knows if zanamivir will be useful or not on a yet to exist pandemic strain of H5N1, it might be useful to stockpile zanamivir as well as oseltamivir in the event of an H5N1 influenza pandemic. Neither oseltamivir nor zanamivir can be manufactured in quantities that would be meaningful once efficient human transmission starts. In September, 2006, a WHO scientist announced that studies had confirmed cases of H5N1 strains resistant to Tamiflu and Amantadine. Tamiflu-resistant strains have also appeared in the EU , which remain sensitive to Relenza. The earliest infections of humans by H5N1 coincided with an epizootic (an epidemic in nonhumans) of H5N1 influenza in Hong Kong's poultry population in 1997. This panzootic (a disease affecting animals of many species, especially over a wide area) outbreak was stopped by the killing of the entire domestic poultry population within the territory. However, the disease has continued to spread; outbreaks were reported in Asia again in 2003. On December 21, 2009, the WHO announced a total of 447 cases which resulted in the deaths of 263. H5N1 is easily transmissible between birds, facilitating a potential global spread of H5N1 . While H5N1 undergoes mutation and reassortment, creating variations which can infect species not previously known to carry the virus, not all of these variant forms can infect humans. H5N1 as an avian virus preferentially binds to a type of galactose receptors that populate the avian respiratory tract from the nose to the lungs and are virtually absent in humans, occurring only in and around the alveoli , structures deep in the lungs where oxygen is passed to the blood. Therefore, the virus is not easily expelled by coughing and sneezing, the usual route of transmission. H5N1 is mainly spread by domestic poultry , both through the movements of infected birds and poultry products and through the use of infected poultry manure as fertilizer or feed. Humans with H5N1 have typically caught it from chickens, which were in turn infected by other poultry or waterfowl. Migrating waterfowl (wild ducks , geese and swans ) carry H5N1, often without becoming sick. Many species of birds and mammals can be infected with HPAI A(H5N1), but the role of animals other than poultry and waterfowl as disease-spreading hosts is unknown. According to a report by the World Health Organization , H5N1 may be spread indirectly. The report stated the virus may sometimes stick to surfaces or get kicked up in fertilizer dust to infect people. H5N1 has mutated into a variety of strains with differing pathogenic profiles, some pathogenic to one species but not others, some pathogenic to multiple species. Each specific known genetic variation is traceable to a virus isolate of a specific case of infection. Through antigenic drift , H5N1 has mutated into dozens of highly pathogenic varieties divided into genetic clades which are known from specific isolates, but all belong to genotype Z of avian influenza virus H5N1, now the dominant genotype. H5N1 isolates found in Hong Kong in 1997 and 2001 were not consistently transmitted efficiently among birds and did not cause significant disease in these animals. In 2002, new isolates of H5N1 were appearing within the bird population of Hong Kong. These new isolates caused acute disease, including severe neurological dysfunction and death in ducks . This was the first reported case of lethal influenza virus infection in wild aquatic birds since 1961. Genotype Z emerged in 2002 through reassortment from earlier highly pathogenic genotypes of H5N1 that first infected birds in China in 1996, and first infected humans in Hong Kong in 1997. Genotype Z is endemic in birds in Southeast Asia, has created at least two clades that can infect humans, and is spreading across the globe in bird populations. Mutations occurring within this genotype are increasing their pathogenicity. Birds are also able to shed the virus for longer periods of time before their death, increasing the transmissibility of the virus. Infected birds transmit H5N1 through their saliva , nasal secretions , feces and blood . Other animals may become infected with the virus through direct contact with these bodily fluids or through contact with surfaces contaminated with them. H5N1 remains infectious after over 30 days at 0 °C (32 °F) (over one month at freezing temperature) or 6 days at 37 °C (99 °F) (one week at human body temperature); at ordinary temperatures it lasts in the environment for weeks. In Arctic temperatures, it does not degrade at all. Because migratory birds are among the carriers of the highly pathogenic H5N1 virus, it is spreading to all parts of the world. H5N1 is different from all previously known highly pathogenic avian flu viruses in its ability to be spread by animals other than poultry. In October 2004, researchers discovered H5N1 is far more dangerous than was previously believed. Waterfowl were revealed to be directly spreading this highly pathogenic strain to chickens , crows , pigeons , and other birds, and the virus was increasing its ability to infect mammals, as well. From this point on, avian flu experts increasingly referred to containment as a strategy that can delay, but not ultimately prevent, a future avian flu pandemic. "Since 1997, studies of influenza A (H5N1) indicate that these viruses continue to evolve, with changes in antigenicity and internal gene constellations; an expanded host range in avian species and the ability to infect felids; enhanced pathogenicity in experimentally infected mice and ferrets, in which they cause systemic infections; and increased environmental stability." The New York Times , in an article on transmission of H5N1 through smuggled birds, reports Wade Hagemeijer of Wetlands International stating, "We believe it is spread by both bird migration and trade, but that trade, particularly illegal trade, is more important". On September 29, 2007, researchers reported the H5N1 bird flu virus can also pass through a pregnant woman's placenta to infect the fetus. They also found evidence of what doctors had long suspected—the virus not only affects the lungs, but also passes throughout the body into the gastrointestinal tract, the brain, liver, and blood cells. In May 2013, North Korea confirmed a H5N1 bird flu outbreak that forced authorities to kill over 160,000 ducks in Pyongyang . A major outbreak of a new strain of H5N1 in wild birds and poultry appeared in Russia in August 2020 and quickly spread to other parts of Europe by October. Over the winter of 2021 and 2022 avian flu spread among the population of barnacle geese on the Solway Firth, UK, with estimates of up to a third of the Svalbard population being lost; pink-footed geese were also affected there and it seems carried the virus to new sites in northern Scotland. The disease was confirmed in sandwich terns in South Africa in April 2022. In late spring 2022 avian flu outbreaks affected many species of wild bird in the United Kingdom, with heavy losses reported among seabirds returning to breed at colonies in the Northern Isles and Outer Hebrides, including great skuas (bonxie) for which outbreaks had initially been reported in 2021 (Scotland hosts c. 60% of the world's breeding population) – the 2022 census on St Kilda showed a 64% decline on 2019 with 106 dead birds recorded so far (to 6 June), gannets (1000+ birds reported dead at the Shetlands' Hermaness colony alone, where there are around 26,000 breeding pairs), with many more gannets being reported dead at other colonies ( Troup Head , Bass Rock , and St Kilda ); the range of species also seems to be expanding, with reports for many species of wildfowl, seabirds (auks, terns and gulls) and scavenging species (corvids and raptors). Elsewhere in Europe the virus killed hundreds (574+) of Dalmatian pelicans in Greece, and in Israel around 6000 common cranes were found dead at Hula in December 2021. A report by Scientific Task Force on Avian Influenza and Wild Birds on: "H5N1 Highly Pathogenic Avian Influenza in poultry and wild birds: Winter of 2021/2022 with focus on mass mortality of wild birds in UK and Israel" summarises the situation up to 24 January 2022 and mentions that "H5N8 HPAI is still responsible for poultry and wild bird cases mainly in Asia, H5N1 has now in effect replaced this subtype in Africa and Eurasia in both poultry and wild birds". The 2022–2023 season was also the worst recorded outbreak in the United Kingdom, with the British government requiring a so-called "poultry lockdown" which required that farmers keep their birds indoors. Meanwhile, an outbreak of H5N1 on a Spanish mink farm led researchers to believe that they had observed the first case of mammal-to-mammal transmission of H5N1. Human cases were reported in Spain in November 2022, and in the UK in May 2023. By November 2020, large outbreaks of the new strain of H5N1 had started to spread into wild birds and farmed poultry across Asia. In February 2023, human cases were reported in Cambodia. Large losses of poultry and wild birds to H5N1 started to occur in Africa in November 2021 and continued through 2022. Similar to 2021 reports, outbreaks were noted from gannet colonies in Canada, with thousands of birds dead in June 2022, as well as common eiders and great black-backed gulls . Prior to that there were reports of spread in wild birds in over 30 states in the US, including major mortalities in a double-crested cormorant colony in Barrington, Illinois , the virus also spreading to scavengers including three bald eagles in Georgia. Mass die-offs of both birds and mammals were noted in Peru during the 2022–2023 season. In particular, the Peruvian government reported the deaths of approximately 63,000 birds as well as 716 sea lions , with the WHO noting that mammalian spillovers needed to be "monitored closely". In the United States, the 2022–2023 avian outbreak was the worst since H5N1 was first detected. Ecuador entered into a three-month "animal-health emergency" on 29 November 2022, just days after its first case was reported, whereas Argentina and Uruguay both declared "national sanitary emergencies" on 15 February 2023, after their respective first cases were discovered. On 22 May 2023, Brazil, as the world's largest exporter of chicken meat, declared a 180-day emergency following several cases detected in wild birds and created an emergency operations center to plan for and mitigate potential further spread of H5N1. Human cases were reported in Ecuador and Chile. In March 2024, H5N1 infections were recorded for the first time in deceased and sick livestock located in the United States. Goats and cows in three states became ill after exposure to wild birds and culled poultry. In early April, H5N1 was reported to have spread amongst dairy cow herds in multiple states of the USA, indicating cow-to-cow spread. A dairy worker in Texas also became infected, with conjunctivitis being the main symptom. H5N1 was detected in dead birds on the Antarctic mainland for the first time in February 2024. Novel, contagious strains of H5N1 were created by Ron Fouchier of the Erasmus Medical Center in Rotterdam, the Netherlands, who first presented his work to the public at an influenza conference in Malta in September 2011. Three mutations were introduced into the H5N1 virus genome, and the virus was then passed from the noses of infected ferrets to the noses of uninfected ones, which was repeated 10 times. After these 10 passages the H5N1 virus had acquired the ability of transmission between ferrets via aerosols or respiratory droplets. After Fouchier offered an article describing this work to the leading academic journal Science , the US National Science Advisory Board for Biosecurity (NSABB) recommended against publication of the full details of the study, and the one submitted to Nature by Yoshihiro Kawaoka of the University of Wisconsin describing related work. However, after additional consultations at the World Health Organization and by the NSABB, the NSABB reversed its position and recommended publication of revised versions of the two papers. However, then the Dutch government declared that this type of manuscripts required Fouchier to apply for an export permit in the light of EU directive 428/2009 on dual use goods. [note 1] After much controversy surrounding the publishing of his research, Fouchier complied (under formal protest) with Dutch government demands to obtain a special permit for submitting his manuscript, and his research appeared in a special issue of the journal Science devoted to H5N1. The papers by Fouchier and Kawaoka conclude that it is entirely possible that a natural chain of mutations could lead to an H5N1 virus acquiring the capability of airborne transmission between mammals, and that a H5N1 influenza pandemic would not be impossible. In May 2013, it was reported that scientists at the Harbin Veterinary Research Institute in Harbin , China, had created H5N1 strains which passed between guinea pigs . In response to Fouchier and Kawaoka's work, a number of scientists expressed concerns with the risks of creating novel potential pandemic pathogens, culminating in the formation of the Cambridge Working Group , a consensus statement calling for an assessment of the risks and benefits of such research. Although mammals, including humans, had become infected with H5N1 bird flu strains in the past, these cases had ostensibly been caused by direct exposure to infected birds, such as through consumption of birds by wildlife or exposure to infected poultry by farmers. In contrast, the October 2022 mammalian outbreak of H5N1 on a Spanish mink farm showed evidence of being the first recorded case of mammal-to-mammal transmission, with 4 percent of the farm's mink population dying from H5N1-related haemorrhagic pneumonia. The mink respiratory tract is particularly well suited to act as a pathway of viral transmission into humans, which has concerned public health professionals due to the production of all but one approved human vaccine requiring the eggs of chickens, which H5N1 kills at a 90–100 percent fatality rate. Infected mink in Spain were also found to have exhibited the "PB2" viral mutation found when H5N1 jumped into pigs over a decade prior, adding to fears that farms could be acting as incubators and/or reservoirs of the virus, similar to the role of minks in SARS-CoV-2 . As of January 2023, fifteen species of wild and captive mammals had become infected with H5N1 throughout the United States. A mass Caspian seal die-off in December 2022, with 700 infected seals found dead along the Caspian Sea coastline of Russia's Dagestan republic , worried researchers regarding the possibility that wild mammal-to-mammal spread had begun. A similar mass die-off of 95% of southern elephant seal pups in 2023 also raised concerns of mammal-to-mammal spread, as nursing pups would have had less exposure to birds. In April 2024, spread of H5N1 amongst dairy cow herds in five states of the USA strongly indicated the presence of cow-to-cow transmission. As of April 2024, the WHO reported a total of 889 confirmed human cases which resulted in the deaths of 463 people since 2003. [ failed verification ] Following the February 2023 H5N1 death of an 11-year-old girl from Cambodia 's Prey Veng province , her father was confirmed positive for the virus and several close contacts also began showing signs of infection. On 24 February 2023, the WHO expressed concern that the virus had potentially begun to spread among humans and ordered the production of a new human vaccine for H5N1. Following the confirmed infections, the WHO began working with the Cambodian government to determine whether both individuals had gotten the virus directly from infected poultry or if it had indeed been a case of human-to-human transmission. Further sequencing determined that at least one of the two cases was from an older H5N1 clade, 2.3.2.1c, which had circulated as a common H5N1 strain in Cambodia for many years, rather than the more recent clade 2.3.4.4b, which had caused mass poultry deaths since 2020. This older clade had jumped to humans in the past yet hadn't previously resulted in any known human-to-human transmission. On March 1, 2023, as Taiwan raised its travel alert for Cambodia, the WHO and the U.S. CDC, in concert with Cambodian authorities, determined that both of the individuals had been infected through direct contact with poultry. H5N1 is easily transmissible between birds, facilitating a potential global spread of H5N1 . While H5N1 undergoes mutation and reassortment, creating variations which can infect species not previously known to carry the virus, not all of these variant forms can infect humans. H5N1 as an avian virus preferentially binds to a type of galactose receptors that populate the avian respiratory tract from the nose to the lungs and are virtually absent in humans, occurring only in and around the alveoli , structures deep in the lungs where oxygen is passed to the blood. Therefore, the virus is not easily expelled by coughing and sneezing, the usual route of transmission. H5N1 is mainly spread by domestic poultry , both through the movements of infected birds and poultry products and through the use of infected poultry manure as fertilizer or feed. Humans with H5N1 have typically caught it from chickens, which were in turn infected by other poultry or waterfowl. Migrating waterfowl (wild ducks , geese and swans ) carry H5N1, often without becoming sick. Many species of birds and mammals can be infected with HPAI A(H5N1), but the role of animals other than poultry and waterfowl as disease-spreading hosts is unknown. According to a report by the World Health Organization , H5N1 may be spread indirectly. The report stated the virus may sometimes stick to surfaces or get kicked up in fertilizer dust to infect people. H5N1 has mutated into a variety of strains with differing pathogenic profiles, some pathogenic to one species but not others, some pathogenic to multiple species. Each specific known genetic variation is traceable to a virus isolate of a specific case of infection. Through antigenic drift , H5N1 has mutated into dozens of highly pathogenic varieties divided into genetic clades which are known from specific isolates, but all belong to genotype Z of avian influenza virus H5N1, now the dominant genotype. H5N1 isolates found in Hong Kong in 1997 and 2001 were not consistently transmitted efficiently among birds and did not cause significant disease in these animals. In 2002, new isolates of H5N1 were appearing within the bird population of Hong Kong. These new isolates caused acute disease, including severe neurological dysfunction and death in ducks . This was the first reported case of lethal influenza virus infection in wild aquatic birds since 1961. Genotype Z emerged in 2002 through reassortment from earlier highly pathogenic genotypes of H5N1 that first infected birds in China in 1996, and first infected humans in Hong Kong in 1997. Genotype Z is endemic in birds in Southeast Asia, has created at least two clades that can infect humans, and is spreading across the globe in bird populations. Mutations occurring within this genotype are increasing their pathogenicity. Birds are also able to shed the virus for longer periods of time before their death, increasing the transmissibility of the virus.Infected birds transmit H5N1 through their saliva , nasal secretions , feces and blood . Other animals may become infected with the virus through direct contact with these bodily fluids or through contact with surfaces contaminated with them. H5N1 remains infectious after over 30 days at 0 °C (32 °F) (over one month at freezing temperature) or 6 days at 37 °C (99 °F) (one week at human body temperature); at ordinary temperatures it lasts in the environment for weeks. In Arctic temperatures, it does not degrade at all. Because migratory birds are among the carriers of the highly pathogenic H5N1 virus, it is spreading to all parts of the world. H5N1 is different from all previously known highly pathogenic avian flu viruses in its ability to be spread by animals other than poultry. In October 2004, researchers discovered H5N1 is far more dangerous than was previously believed. Waterfowl were revealed to be directly spreading this highly pathogenic strain to chickens , crows , pigeons , and other birds, and the virus was increasing its ability to infect mammals, as well. From this point on, avian flu experts increasingly referred to containment as a strategy that can delay, but not ultimately prevent, a future avian flu pandemic. "Since 1997, studies of influenza A (H5N1) indicate that these viruses continue to evolve, with changes in antigenicity and internal gene constellations; an expanded host range in avian species and the ability to infect felids; enhanced pathogenicity in experimentally infected mice and ferrets, in which they cause systemic infections; and increased environmental stability." The New York Times , in an article on transmission of H5N1 through smuggled birds, reports Wade Hagemeijer of Wetlands International stating, "We believe it is spread by both bird migration and trade, but that trade, particularly illegal trade, is more important". On September 29, 2007, researchers reported the H5N1 bird flu virus can also pass through a pregnant woman's placenta to infect the fetus. They also found evidence of what doctors had long suspected—the virus not only affects the lungs, but also passes throughout the body into the gastrointestinal tract, the brain, liver, and blood cells. In May 2013, North Korea confirmed a H5N1 bird flu outbreak that forced authorities to kill over 160,000 ducks in Pyongyang . A major outbreak of a new strain of H5N1 in wild birds and poultry appeared in Russia in August 2020 and quickly spread to other parts of Europe by October. Over the winter of 2021 and 2022 avian flu spread among the population of barnacle geese on the Solway Firth, UK, with estimates of up to a third of the Svalbard population being lost; pink-footed geese were also affected there and it seems carried the virus to new sites in northern Scotland. The disease was confirmed in sandwich terns in South Africa in April 2022. In late spring 2022 avian flu outbreaks affected many species of wild bird in the United Kingdom, with heavy losses reported among seabirds returning to breed at colonies in the Northern Isles and Outer Hebrides, including great skuas (bonxie) for which outbreaks had initially been reported in 2021 (Scotland hosts c. 60% of the world's breeding population) – the 2022 census on St Kilda showed a 64% decline on 2019 with 106 dead birds recorded so far (to 6 June), gannets (1000+ birds reported dead at the Shetlands' Hermaness colony alone, where there are around 26,000 breeding pairs), with many more gannets being reported dead at other colonies ( Troup Head , Bass Rock , and St Kilda ); the range of species also seems to be expanding, with reports for many species of wildfowl, seabirds (auks, terns and gulls) and scavenging species (corvids and raptors). Elsewhere in Europe the virus killed hundreds (574+) of Dalmatian pelicans in Greece, and in Israel around 6000 common cranes were found dead at Hula in December 2021. A report by Scientific Task Force on Avian Influenza and Wild Birds on: "H5N1 Highly Pathogenic Avian Influenza in poultry and wild birds: Winter of 2021/2022 with focus on mass mortality of wild birds in UK and Israel" summarises the situation up to 24 January 2022 and mentions that "H5N8 HPAI is still responsible for poultry and wild bird cases mainly in Asia, H5N1 has now in effect replaced this subtype in Africa and Eurasia in both poultry and wild birds". The 2022–2023 season was also the worst recorded outbreak in the United Kingdom, with the British government requiring a so-called "poultry lockdown" which required that farmers keep their birds indoors. Meanwhile, an outbreak of H5N1 on a Spanish mink farm led researchers to believe that they had observed the first case of mammal-to-mammal transmission of H5N1. Human cases were reported in Spain in November 2022, and in the UK in May 2023. By November 2020, large outbreaks of the new strain of H5N1 had started to spread into wild birds and farmed poultry across Asia. In February 2023, human cases were reported in Cambodia. Large losses of poultry and wild birds to H5N1 started to occur in Africa in November 2021 and continued through 2022. Similar to 2021 reports, outbreaks were noted from gannet colonies in Canada, with thousands of birds dead in June 2022, as well as common eiders and great black-backed gulls . Prior to that there were reports of spread in wild birds in over 30 states in the US, including major mortalities in a double-crested cormorant colony in Barrington, Illinois , the virus also spreading to scavengers including three bald eagles in Georgia. Mass die-offs of both birds and mammals were noted in Peru during the 2022–2023 season. In particular, the Peruvian government reported the deaths of approximately 63,000 birds as well as 716 sea lions , with the WHO noting that mammalian spillovers needed to be "monitored closely". In the United States, the 2022–2023 avian outbreak was the worst since H5N1 was first detected. Ecuador entered into a three-month "animal-health emergency" on 29 November 2022, just days after its first case was reported, whereas Argentina and Uruguay both declared "national sanitary emergencies" on 15 February 2023, after their respective first cases were discovered. On 22 May 2023, Brazil, as the world's largest exporter of chicken meat, declared a 180-day emergency following several cases detected in wild birds and created an emergency operations center to plan for and mitigate potential further spread of H5N1. Human cases were reported in Ecuador and Chile. In March 2024, H5N1 infections were recorded for the first time in deceased and sick livestock located in the United States. Goats and cows in three states became ill after exposure to wild birds and culled poultry. In early April, H5N1 was reported to have spread amongst dairy cow herds in multiple states of the USA, indicating cow-to-cow spread. A dairy worker in Texas also became infected, with conjunctivitis being the main symptom. H5N1 was detected in dead birds on the Antarctic mainland for the first time in February 2024. A major outbreak of a new strain of H5N1 in wild birds and poultry appeared in Russia in August 2020 and quickly spread to other parts of Europe by October. Over the winter of 2021 and 2022 avian flu spread among the population of barnacle geese on the Solway Firth, UK, with estimates of up to a third of the Svalbard population being lost; pink-footed geese were also affected there and it seems carried the virus to new sites in northern Scotland. The disease was confirmed in sandwich terns in South Africa in April 2022. In late spring 2022 avian flu outbreaks affected many species of wild bird in the United Kingdom, with heavy losses reported among seabirds returning to breed at colonies in the Northern Isles and Outer Hebrides, including great skuas (bonxie) for which outbreaks had initially been reported in 2021 (Scotland hosts c. 60% of the world's breeding population) – the 2022 census on St Kilda showed a 64% decline on 2019 with 106 dead birds recorded so far (to 6 June), gannets (1000+ birds reported dead at the Shetlands' Hermaness colony alone, where there are around 26,000 breeding pairs), with many more gannets being reported dead at other colonies ( Troup Head , Bass Rock , and St Kilda ); the range of species also seems to be expanding, with reports for many species of wildfowl, seabirds (auks, terns and gulls) and scavenging species (corvids and raptors). Elsewhere in Europe the virus killed hundreds (574+) of Dalmatian pelicans in Greece, and in Israel around 6000 common cranes were found dead at Hula in December 2021. A report by Scientific Task Force on Avian Influenza and Wild Birds on: "H5N1 Highly Pathogenic Avian Influenza in poultry and wild birds: Winter of 2021/2022 with focus on mass mortality of wild birds in UK and Israel" summarises the situation up to 24 January 2022 and mentions that "H5N8 HPAI is still responsible for poultry and wild bird cases mainly in Asia, H5N1 has now in effect replaced this subtype in Africa and Eurasia in both poultry and wild birds". The 2022–2023 season was also the worst recorded outbreak in the United Kingdom, with the British government requiring a so-called "poultry lockdown" which required that farmers keep their birds indoors. Meanwhile, an outbreak of H5N1 on a Spanish mink farm led researchers to believe that they had observed the first case of mammal-to-mammal transmission of H5N1. Human cases were reported in Spain in November 2022, and in the UK in May 2023. By November 2020, large outbreaks of the new strain of H5N1 had started to spread into wild birds and farmed poultry across Asia. In February 2023, human cases were reported in Cambodia. Large losses of poultry and wild birds to H5N1 started to occur in Africa in November 2021 and continued through 2022. Similar to 2021 reports, outbreaks were noted from gannet colonies in Canada, with thousands of birds dead in June 2022, as well as common eiders and great black-backed gulls . Prior to that there were reports of spread in wild birds in over 30 states in the US, including major mortalities in a double-crested cormorant colony in Barrington, Illinois , the virus also spreading to scavengers including three bald eagles in Georgia. Mass die-offs of both birds and mammals were noted in Peru during the 2022–2023 season. In particular, the Peruvian government reported the deaths of approximately 63,000 birds as well as 716 sea lions , with the WHO noting that mammalian spillovers needed to be "monitored closely". In the United States, the 2022–2023 avian outbreak was the worst since H5N1 was first detected. Ecuador entered into a three-month "animal-health emergency" on 29 November 2022, just days after its first case was reported, whereas Argentina and Uruguay both declared "national sanitary emergencies" on 15 February 2023, after their respective first cases were discovered. On 22 May 2023, Brazil, as the world's largest exporter of chicken meat, declared a 180-day emergency following several cases detected in wild birds and created an emergency operations center to plan for and mitigate potential further spread of H5N1. Human cases were reported in Ecuador and Chile. In March 2024, H5N1 infections were recorded for the first time in deceased and sick livestock located in the United States. Goats and cows in three states became ill after exposure to wild birds and culled poultry. In early April, H5N1 was reported to have spread amongst dairy cow herds in multiple states of the USA, indicating cow-to-cow spread. A dairy worker in Texas also became infected, with conjunctivitis being the main symptom. H5N1 was detected in dead birds on the Antarctic mainland for the first time in February 2024. Novel, contagious strains of H5N1 were created by Ron Fouchier of the Erasmus Medical Center in Rotterdam, the Netherlands, who first presented his work to the public at an influenza conference in Malta in September 2011. Three mutations were introduced into the H5N1 virus genome, and the virus was then passed from the noses of infected ferrets to the noses of uninfected ones, which was repeated 10 times. After these 10 passages the H5N1 virus had acquired the ability of transmission between ferrets via aerosols or respiratory droplets. After Fouchier offered an article describing this work to the leading academic journal Science , the US National Science Advisory Board for Biosecurity (NSABB) recommended against publication of the full details of the study, and the one submitted to Nature by Yoshihiro Kawaoka of the University of Wisconsin describing related work. However, after additional consultations at the World Health Organization and by the NSABB, the NSABB reversed its position and recommended publication of revised versions of the two papers. However, then the Dutch government declared that this type of manuscripts required Fouchier to apply for an export permit in the light of EU directive 428/2009 on dual use goods. [note 1] After much controversy surrounding the publishing of his research, Fouchier complied (under formal protest) with Dutch government demands to obtain a special permit for submitting his manuscript, and his research appeared in a special issue of the journal Science devoted to H5N1. The papers by Fouchier and Kawaoka conclude that it is entirely possible that a natural chain of mutations could lead to an H5N1 virus acquiring the capability of airborne transmission between mammals, and that a H5N1 influenza pandemic would not be impossible. In May 2013, it was reported that scientists at the Harbin Veterinary Research Institute in Harbin , China, had created H5N1 strains which passed between guinea pigs . In response to Fouchier and Kawaoka's work, a number of scientists expressed concerns with the risks of creating novel potential pandemic pathogens, culminating in the formation of the Cambridge Working Group , a consensus statement calling for an assessment of the risks and benefits of such research. Although mammals, including humans, had become infected with H5N1 bird flu strains in the past, these cases had ostensibly been caused by direct exposure to infected birds, such as through consumption of birds by wildlife or exposure to infected poultry by farmers. In contrast, the October 2022 mammalian outbreak of H5N1 on a Spanish mink farm showed evidence of being the first recorded case of mammal-to-mammal transmission, with 4 percent of the farm's mink population dying from H5N1-related haemorrhagic pneumonia. The mink respiratory tract is particularly well suited to act as a pathway of viral transmission into humans, which has concerned public health professionals due to the production of all but one approved human vaccine requiring the eggs of chickens, which H5N1 kills at a 90–100 percent fatality rate. Infected mink in Spain were also found to have exhibited the "PB2" viral mutation found when H5N1 jumped into pigs over a decade prior, adding to fears that farms could be acting as incubators and/or reservoirs of the virus, similar to the role of minks in SARS-CoV-2 . As of January 2023, fifteen species of wild and captive mammals had become infected with H5N1 throughout the United States. A mass Caspian seal die-off in December 2022, with 700 infected seals found dead along the Caspian Sea coastline of Russia's Dagestan republic , worried researchers regarding the possibility that wild mammal-to-mammal spread had begun. A similar mass die-off of 95% of southern elephant seal pups in 2023 also raised concerns of mammal-to-mammal spread, as nursing pups would have had less exposure to birds. In April 2024, spread of H5N1 amongst dairy cow herds in five states of the USA strongly indicated the presence of cow-to-cow transmission. Novel, contagious strains of H5N1 were created by Ron Fouchier of the Erasmus Medical Center in Rotterdam, the Netherlands, who first presented his work to the public at an influenza conference in Malta in September 2011. Three mutations were introduced into the H5N1 virus genome, and the virus was then passed from the noses of infected ferrets to the noses of uninfected ones, which was repeated 10 times. After these 10 passages the H5N1 virus had acquired the ability of transmission between ferrets via aerosols or respiratory droplets. After Fouchier offered an article describing this work to the leading academic journal Science , the US National Science Advisory Board for Biosecurity (NSABB) recommended against publication of the full details of the study, and the one submitted to Nature by Yoshihiro Kawaoka of the University of Wisconsin describing related work. However, after additional consultations at the World Health Organization and by the NSABB, the NSABB reversed its position and recommended publication of revised versions of the two papers. However, then the Dutch government declared that this type of manuscripts required Fouchier to apply for an export permit in the light of EU directive 428/2009 on dual use goods. [note 1] After much controversy surrounding the publishing of his research, Fouchier complied (under formal protest) with Dutch government demands to obtain a special permit for submitting his manuscript, and his research appeared in a special issue of the journal Science devoted to H5N1. The papers by Fouchier and Kawaoka conclude that it is entirely possible that a natural chain of mutations could lead to an H5N1 virus acquiring the capability of airborne transmission between mammals, and that a H5N1 influenza pandemic would not be impossible. In May 2013, it was reported that scientists at the Harbin Veterinary Research Institute in Harbin , China, had created H5N1 strains which passed between guinea pigs . In response to Fouchier and Kawaoka's work, a number of scientists expressed concerns with the risks of creating novel potential pandemic pathogens, culminating in the formation of the Cambridge Working Group , a consensus statement calling for an assessment of the risks and benefits of such research. Although mammals, including humans, had become infected with H5N1 bird flu strains in the past, these cases had ostensibly been caused by direct exposure to infected birds, such as through consumption of birds by wildlife or exposure to infected poultry by farmers. In contrast, the October 2022 mammalian outbreak of H5N1 on a Spanish mink farm showed evidence of being the first recorded case of mammal-to-mammal transmission, with 4 percent of the farm's mink population dying from H5N1-related haemorrhagic pneumonia. The mink respiratory tract is particularly well suited to act as a pathway of viral transmission into humans, which has concerned public health professionals due to the production of all but one approved human vaccine requiring the eggs of chickens, which H5N1 kills at a 90–100 percent fatality rate. Infected mink in Spain were also found to have exhibited the "PB2" viral mutation found when H5N1 jumped into pigs over a decade prior, adding to fears that farms could be acting as incubators and/or reservoirs of the virus, similar to the role of minks in SARS-CoV-2 . As of January 2023, fifteen species of wild and captive mammals had become infected with H5N1 throughout the United States. A mass Caspian seal die-off in December 2022, with 700 infected seals found dead along the Caspian Sea coastline of Russia's Dagestan republic , worried researchers regarding the possibility that wild mammal-to-mammal spread had begun. A similar mass die-off of 95% of southern elephant seal pups in 2023 also raised concerns of mammal-to-mammal spread, as nursing pups would have had less exposure to birds. In April 2024, spread of H5N1 amongst dairy cow herds in five states of the USA strongly indicated the presence of cow-to-cow transmission. As of April 2024, the WHO reported a total of 889 confirmed human cases which resulted in the deaths of 463 people since 2003. [ failed verification ] Following the February 2023 H5N1 death of an 11-year-old girl from Cambodia 's Prey Veng province , her father was confirmed positive for the virus and several close contacts also began showing signs of infection. On 24 February 2023, the WHO expressed concern that the virus had potentially begun to spread among humans and ordered the production of a new human vaccine for H5N1. Following the confirmed infections, the WHO began working with the Cambodian government to determine whether both individuals had gotten the virus directly from infected poultry or if it had indeed been a case of human-to-human transmission. Further sequencing determined that at least one of the two cases was from an older H5N1 clade, 2.3.2.1c, which had circulated as a common H5N1 strain in Cambodia for many years, rather than the more recent clade 2.3.4.4b, which had caused mass poultry deaths since 2020. This older clade had jumped to humans in the past yet hadn't previously resulted in any known human-to-human transmission. On March 1, 2023, as Taiwan raised its travel alert for Cambodia, the WHO and the U.S. CDC, in concert with Cambodian authorities, determined that both of the individuals had been infected through direct contact with poultry. Following the February 2023 H5N1 death of an 11-year-old girl from Cambodia 's Prey Veng province , her father was confirmed positive for the virus and several close contacts also began showing signs of infection. On 24 February 2023, the WHO expressed concern that the virus had potentially begun to spread among humans and ordered the production of a new human vaccine for H5N1. Following the confirmed infections, the WHO began working with the Cambodian government to determine whether both individuals had gotten the virus directly from infected poultry or if it had indeed been a case of human-to-human transmission. Further sequencing determined that at least one of the two cases was from an older H5N1 clade, 2.3.2.1c, which had circulated as a common H5N1 strain in Cambodia for many years, rather than the more recent clade 2.3.4.4b, which had caused mass poultry deaths since 2020. This older clade had jumped to humans in the past yet hadn't previously resulted in any known human-to-human transmission. On March 1, 2023, as Taiwan raised its travel alert for Cambodia, the WHO and the U.S. CDC, in concert with Cambodian authorities, determined that both of the individuals had been infected through direct contact with poultry. Following the February 2023 H5N1 death of an 11-year-old girl from Cambodia 's Prey Veng province , her father was confirmed positive for the virus and several close contacts also began showing signs of infection. On 24 February 2023, the WHO expressed concern that the virus had potentially begun to spread among humans and ordered the production of a new human vaccine for H5N1. Following the confirmed infections, the WHO began working with the Cambodian government to determine whether both individuals had gotten the virus directly from infected poultry or if it had indeed been a case of human-to-human transmission. Further sequencing determined that at least one of the two cases was from an older H5N1 clade, 2.3.2.1c, which had circulated as a common H5N1 strain in Cambodia for many years, rather than the more recent clade 2.3.4.4b, which had caused mass poultry deaths since 2020. This older clade had jumped to humans in the past yet hadn't previously resulted in any known human-to-human transmission. On March 1, 2023, as Taiwan raised its travel alert for Cambodia, the WHO and the U.S. CDC, in concert with Cambodian authorities, determined that both of the individuals had been infected through direct contact with poultry. H5N1 has had a significant effect on human society , especially the financial , political , social , and personal responses to both actual and predicted deaths in birds , humans , and other animals . Billions of dollars are being raised and spent to research H5N1 and prepare for a potential avian influenza pandemic . Over $10 billion have been spent and over 200 million birds have been killed to try to contain H5N1. People have reacted by buying less chicken, causing poultry sales and prices to fall. Many individuals have stockpiled supplies for a possible flu pandemic. International health officials and other experts have pointed out that many unknown questions still hover around the disease. Dr. David Nabarro , Chief Avian Flu Coordinator for the United Nations, and former Chief of Crisis Response for the World Health Organization has described himself as "quite scared" about H5N1's potential impact on humans. Nabarro has been accused of being alarmist before, and on his first day in his role for the United Nations, he proclaimed the avian flu could kill 150 million people. In an interview with the International Herald Tribune , Nabarro compares avian flu to AIDS in Africa, warning that underestimations led to inappropriate focus for research and intervention. In February 2020 an outbreak of H5N1 avian flu occurred in Shuangqing District of Shaoyang City , in the Hunan province . After poultry had become ill from the virus the city killed close to 18,000 chickens to prevent the spread of the illness. Hunan borders Hubei province where Wuhan is located, the epicenter of the coronavirus pandemic .

Wiki

Avian influenza

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Influenza A virus

See text Influenza A virus ( IAV ) is a pathogen that causes the flu in birds and some mammals , including humans. It is an RNA virus whose subtypes have been isolated from wild birds. Occasionally, it is transmitted from wild to domestic birds, and this may cause severe disease, outbreaks, or human influenza pandemics . Each virus subtype includes a wide variety of strains with differing pathogenic profiles; some may cause disease only in one species but others to multiple ones. Because the viral genome is segmented, subtypes are neither strains nor lineages, as the subtype designation refers to proteins encoded by only two of the eight genome segments. A filtered and purified influenza A vaccine for humans has been developed and many countries have stockpiled it to allow a quick administration to the population in the event of an avian influenza pandemic . In 2011, researchers reported the discovery of an antibody effective against all types of the influenza A virus. Influenza A virus is the only species of the genus Alphainfluenzavirus of the virus family Orthomyxoviridae . There are two methods of classification, one based on surface proteins (originally serotypes ), and the other based on its behavior, mainly the host animal . There are two proteins on the surface of the viral envelope: The hemagglutinin is central to the virus's recognizing and binding to target cells, and also to its then infecting the cell with its RNA . The neuraminidase, on the other hand, is critical for the subsequent release of the daughter virus particles created within the infected cell so they can spread to other cells. [ citation needed ] Different influenza virus genomes encode different hemagglutinin and neuraminidase proteins. Based on how the different H and N proteins react to antisera , scientists defined 18 types of hemaglutinin and 11 types of neuraminidase. In modern days, determination of serotype is more commonly done by polymerase chain reaction . For example, " H5N1 " designates an influenza A subtype that has a type-5 hemagglutinin (H) protein and a type-1 neuraminidase (N) protein. Further variations exist within the subtypes and can lead to very significant differences in the virus's behavior. [lower-alpha 1] By definition, the subtyping scheme only takes into account the two outer proteins, not the at least 8 proteins internal to the virus. Variants are sometimes named according to the species (host) in which the strain is endemic or to which it is adapted. The main variants named using this convention are: [ citation needed ] Variants have also sometimes been named according to their deadliness in poultry, especially chickens: [ citation needed ] Low pathogenic avian influenza (LPAI) Highly pathogenic avian influenza (HPAI), also called deadly flu or death flu Using subtyping and host range is not sufficient to uniquely identify an influenza A virus (or a lineage of them sharing a common ancestor). To unambiguously describe a specific collection of viruses, researchers use the Influenza virus nomenclature , which describes, among other things, the serotype, time, and place of collection. Some examples include: A/Rio de Janeiro/62434/2021 (H3N2) . The starting A indicates that the virus is an influenza A virus. Rio de Janeiro indicates the place of collection. 62434 is a sequence number. 2021 indicates that the sample is collected in 2021. (H3N2) indicates the type of the virus: a H3N2 virus. A/swine/South Dakota/152B/2009 (H1N2) This example shows an additional field before the place: swine . It indicates that the sample was collected from a pig. A/California/04/2009 A(H1N1)pdm09 . This example carries an unusual designation in the last part: instead of a usual (H1N1) , it uses A(H1N1)pdm09 . This is because the CDC found it necessary to distinguish the Pandemic H1N1/09 virus lineage from older H1N1 viruses. The starting A indicates that the virus is an influenza A virus. Rio de Janeiro indicates the place of collection. 62434 is a sequence number. 2021 indicates that the sample is collected in 2021. (H3N2) indicates the type of the virus: a H3N2 virus. This example shows an additional field before the place: swine . It indicates that the sample was collected from a pig. Some variants [lower-alpha 2] are informally identified and named according to the isolate they resemble, thus are presumed to share lineage (example Fujian flu virus-like); according to their typical host (example human flu virus); according to their subtype (example H3N2); and according to their deadliness (example LP, low pathogenic). So a flu from a virus similar to the isolate A/Fujian/411/2002 (H3N2) is called Fujian flu, human flu, and H3N2 flu. [ citation needed ] Most known strains are extinct strains. For example, the annual flu subtype H3N2 no longer contains the strain that caused the Hong Kong flu , A/Hong Kong/1/1968 (H3N2) . The World Health Organization recommends flu shots for the 2023-2024 flu season in northern hemisphere to use the A/Darwin/9/2021 (H3N2) -like virus. There are two proteins on the surface of the viral envelope: The hemagglutinin is central to the virus's recognizing and binding to target cells, and also to its then infecting the cell with its RNA . The neuraminidase, on the other hand, is critical for the subsequent release of the daughter virus particles created within the infected cell so they can spread to other cells. [ citation needed ] Different influenza virus genomes encode different hemagglutinin and neuraminidase proteins. Based on how the different H and N proteins react to antisera , scientists defined 18 types of hemaglutinin and 11 types of neuraminidase. In modern days, determination of serotype is more commonly done by polymerase chain reaction . For example, " H5N1 " designates an influenza A subtype that has a type-5 hemagglutinin (H) protein and a type-1 neuraminidase (N) protein. Further variations exist within the subtypes and can lead to very significant differences in the virus's behavior. [lower-alpha 1] By definition, the subtyping scheme only takes into account the two outer proteins, not the at least 8 proteins internal to the virus. Variants are sometimes named according to the species (host) in which the strain is endemic or to which it is adapted. The main variants named using this convention are: [ citation needed ] Variants have also sometimes been named according to their deadliness in poultry, especially chickens: [ citation needed ] Low pathogenic avian influenza (LPAI) Highly pathogenic avian influenza (HPAI), also called deadly flu or death fluUsing subtyping and host range is not sufficient to uniquely identify an influenza A virus (or a lineage of them sharing a common ancestor). To unambiguously describe a specific collection of viruses, researchers use the Influenza virus nomenclature , which describes, among other things, the serotype, time, and place of collection. Some examples include: A/Rio de Janeiro/62434/2021 (H3N2) . The starting A indicates that the virus is an influenza A virus. Rio de Janeiro indicates the place of collection. 62434 is a sequence number. 2021 indicates that the sample is collected in 2021. (H3N2) indicates the type of the virus: a H3N2 virus. A/swine/South Dakota/152B/2009 (H1N2) This example shows an additional field before the place: swine . It indicates that the sample was collected from a pig. A/California/04/2009 A(H1N1)pdm09 . This example carries an unusual designation in the last part: instead of a usual (H1N1) , it uses A(H1N1)pdm09 . This is because the CDC found it necessary to distinguish the Pandemic H1N1/09 virus lineage from older H1N1 viruses. The starting A indicates that the virus is an influenza A virus. Rio de Janeiro indicates the place of collection. 62434 is a sequence number. 2021 indicates that the sample is collected in 2021. (H3N2) indicates the type of the virus: a H3N2 virus. This example shows an additional field before the place: swine . It indicates that the sample was collected from a pig. Some variants [lower-alpha 2] are informally identified and named according to the isolate they resemble, thus are presumed to share lineage (example Fujian flu virus-like); according to their typical host (example human flu virus); according to their subtype (example H3N2); and according to their deadliness (example LP, low pathogenic). So a flu from a virus similar to the isolate A/Fujian/411/2002 (H3N2) is called Fujian flu, human flu, and H3N2 flu. [ citation needed ] Most known strains are extinct strains. For example, the annual flu subtype H3N2 no longer contains the strain that caused the Hong Kong flu , A/Hong Kong/1/1968 (H3N2) . The World Health Organization recommends flu shots for the 2023-2024 flu season in northern hemisphere to use the A/Darwin/9/2021 (H3N2) -like virus. The annual flu (also called "seasonal flu" or "human flu") in the US "results in approximately 36,000 deaths and more than 200,000 hospitalizations each year. In addition to this human toll, influenza is annually responsible for a total cost of over $10 billion in the U.S." Globally the toll of influenza virus is estimated at 290,000–645,000 deaths annually, exceeding previous estimates. The annually updated, trivalent influenza vaccine consists of hemagglutinin (HA) surface glycoprotein components from influenza H3N2 , H1N1 , and B influenza viruses. Measured resistance to the standard antiviral drugs amantadine and rimantadine in H3N2 has increased from 1% in 1994 to 12% in 2003 to 91% in 2005. [ citation needed ] "Contemporary human H3N2 influenza viruses are now endemic in pigs in southern China and can reassort with avian H5N1 viruses in this intermediate host." FI6 , an antibody that targets the hemagglutinin protein, was discovered in 2011. FI6 is the only known antibody effective against all 16 subtypes of the influenza A virus. FI6 , an antibody that targets the hemagglutinin protein, was discovered in 2011. FI6 is the only known antibody effective against all 16 subtypes of the influenza A virus. Influenza A viruses are negative-sense , single-stranded, segmented RNA virus . The several subtypes are labeled according to an H number (for the type of hemagglutinin ) and an N number (for the type of neuraminidase ). There are 18 different known H antigens (H1 to H18) and 11 different known N antigens (N1 to N11). H17N10 was isolated from fruit bats in 2012. H18N11 was discovered in a Peruvian bat in 2013. Influenza type A viruses are very similar in structure to influenza viruses types B, C, and D. The virus particle (also called the virion) is 80–120 nanometers in diameter such that the smallest virions adopt an elliptical shape. The length of each particle varies considerably, owing to the fact that influenza is pleomorphic, and can be in excess of many tens of micrometers, producing filamentous virions. Confusion about the nature of influenza virus pleomorphy stems from the observation that lab adapted strains typically lose the ability to form filaments and that these lab adapted strains were the first to be visualized by electron microscopy. Despite these varied shapes, the virions of all influenza type A viruses are similar in composition. They are all made up of a viral envelope containing two main types of proteins, wrapped around a central core. The two large proteins found on the outside of viral particles are hemagglutinin (HA) and neuraminidase (NA). HA is a protein that mediates binding of the virion to target cells and entry of the viral genome into the target cell. NA is involved in release from the abundant non-productive attachment sites present in mucus as well as the release of progeny virions from infected cells. These proteins are usually the targets for antiviral drugs. Furthermore, they are also the antigen proteins to which a host's antibodies can bind and trigger an immune response. Influenza type A viruses are categorized into subtypes based on the type of these two proteins on the surface of the viral envelope. There are 16 subtypes of HA and 9 subtypes of NA known, but only H 1, 2 and 3, and N 1 and 2 are commonly found in humans. The central core of a virion contains the viral genome and other viral proteins that package and protect the genetic material. Unlike the genomes of most organisms (including humans, animals, plants, and bacteria) which are made up of double-stranded DNA, many viral genomes are made up of a different, single-stranded nucleic acid called RNA. Unusually for a virus, though, the influenza type A virus genome is not a single piece of RNA; instead, it consists of segmented pieces of negative-sense RNA, each piece containing either one or two genes which code for a gene product (protein). The term negative-sense RNA just implies that the RNA genome cannot be translated into protein directly; it must first be transcribed to positive-sense RNA before it can be translated into protein products. The segmented nature of the genome allows for the exchange of entire genes between different viral strains. The entire Influenza A virus genome is 13,588 bases long and is contained on eight RNA segments that code for at least 10 but up to 14 proteins, depending on the strain. The relevance or presence of alternate gene products can vary: Segment 1 encodes RNA polymerase subunit (PB2). Segment 2 encodes RNA polymerase subunit (PB1) and the PB1-F2 protein, which induces cell death, by using different reading frames from the same RNA segment. Segment 3 encodes RNA polymerase subunit (PA) and the PA-X protein, which has a role in host transcription shutoff. Segment 4 encodes for HA (hemagglutinin). About 500 molecules of hemagglutinin are needed to make one virion. HA determines the extent and severity of a viral infection in a host organism. Segment 5 encodes NP, which is a nucleoprotein. Segment 6 encodes NA (neuraminidase). About 100 molecules of neuraminidase are needed to make one virion. Segment 7 encodes two matrix proteins (M1 and M2) by using different reading frames from the same RNA segment. About 3,000 matrix protein molecules are needed to make one virion. Segment 8 encodes two distinct non-structural proteins (NS1 and NEP) by using different reading frames from the same RNA segment. The RNA segments of the viral genome have complementary base sequences at the terminal ends, allowing them to bond to each other with hydrogen bonds. Transcription of the viral (-) sense genome (vRNA) can only proceed after the PB2 protein binds to host capped RNAs, allowing for the PA subunit to cleave several nucleotides after the cap. This host-derived cap and accompanied nucleotides serve as the primer for viral transcription initiation. Transcription proceeds along the vRNA until a stretch of several uracil bases is reached, initiating a 'stuttering' whereby the nascent viral mRNA is poly-adenylated, producing a mature transcript for nuclear export and translation by host machinery. The RNA synthesis takes place in the cell nucleus, while the synthesis of proteins takes place in the cytoplasm. Once the viral proteins are assembled into virions, the assembled virions leave the nucleus and migrate towards the cell membrane. The host cell membrane has patches of viral transmembrane proteins (HA, NA, and M2) and an underlying layer of the M1 protein which assist the assembled virions to budding through the membrane, releasing finished enveloped viruses into the extracellular fluid. The subtypes of influenza A virus are estimated to have diverged 2,000 years ago. Influenza viruses A and B are estimated to have diverged from a single ancestor around 4,000 years ago, while the ancestor of influenza viruses A and B and the ancestor of influenza virus C are estimated to have diverged from a common ancestor around 8,000 years ago. Influenza virus is able to undergo multiplicity reactivation after inactivation by UV radiation, or by ionizing radiation. If any of the eight RNA strands that make up the genome contains damage that prevents replication or expression of an essential gene, the virus is not viable when it alone infects a cell (a single infection). However, when two or more damaged viruses infect the same cell (multiple infection), viable progeny viruses can be produced provided each of the eight genomic segments is present in at least one undamaged copy. That is, multiplicity reactivation can occur. [ citation needed ] Upon infection, influenza virus induces a host response involving increased production of reactive oxygen species, and this can damage the virus genome. If, under natural conditions, virus survival is ordinarily vulnerable to the challenge of oxidative damage, then multiplicity reactivation is likely selectively advantageous as a kind of genomic repair process. It has been suggested that multiplicity reactivation involving segmented RNA genomes may be similar to the earliest evolved form of sexual interaction in the RNA world that likely preceded the DNA world. "Human influenza virus" usually refers to those subtypes that spread widely among humans. H1N1, H1N2, and H3N2 are the only known influenza A virus subtypes currently circulating among humans. Genetic factors in distinguishing between "human flu viruses" and "avian influenza viruses" include: Human flu symptoms usually include fever, cough, sore throat , muscle aches , conjunctivitis and, in severe cases, breathing problems and pneumonia that may be fatal. The severity of the infection will depend in large part on the state of the infected person's immune system and if the victim has been exposed to the strain before, and is therefore partially immune. Follow-up studies on the impact of statins on influenza virus replication show that pre-treatment of cells with atorvastatin suppresses virus growth in culture. Highly pathogenic H5N1 avian influenza in a human is far worse, killing 50% of humans who catch it. In one case, a boy with H5N1 experienced diarrhea followed rapidly by a coma without developing respiratory or flu-like symptoms. The influenza A virus subtypes that have been confirmed in humans, ordered by the number of known human pandemic deaths, are: H10N3 In May 2021, in Zhenjiang , China H10N3 was reported for the first time in humans. One person was infected. According to Jeffery Taubenberger : All influenza A pandemics since [the Spanish flu pandemic], and indeed almost all cases of influenza A worldwide (excepting human infections from avian viruses such as H5N1 and H7N7), have been caused by descendants of the 1918 virus, including "drifted" H1N1 viruses and reassorted H2N2 and H3N2 viruses. The latter are composed of key genes from the 1918 virus, updated by subsequently incorporated avian influenza genes that code for novel surface proteins, making the 1918 virus indeed the "mother" of all pandemics. Researchers from the National Institutes of Health used data from the Influenza Genome Sequencing Project and concluded that during the ten-year period examined, most of the time the hemagglutinin gene in H3N2 showed no significant excess of mutations in the antigenic regions while an increasing variety of strains accumulated. This resulted in one of the variants eventually achieving higher fitness, becoming dominant, and in a brief interval of rapid evolution , rapidly sweeping through the population and eliminating most other variants. In the short-term evolution of influenza A virus, a 2006 study found that stochastic, or random, processes are key factors. Influenza A virus HA antigenic evolution appears to be characterized more by punctuated, sporadic jumps as opposed to a constant rate of antigenic change. Using phylogenetic analysis of 413 complete genomes of human influenza A viruses that were collected throughout the state of New York, the authors of Nelson et al. 2006 were able to show that genetic diversity, and not antigenic drift, shaped the short-term evolution of influenza A via random migration and reassortment. The evolution of these viruses is dominated more by the random importation of genetically different viral strains from other geographic locations and less by natural selection. Within a given season, adaptive evolution is infrequent and had an overall weak effect as evidenced from the data gathered from the 413 genomes. Phylogenetic analysis revealed the different strains were derived from newly imported genetic material as opposed to isolates that had been circulating in New York in previous seasons. Therefore, the gene flow in and out of this population, and not natural selection, was more important in the short term. [ citation needed ]According to Jeffery Taubenberger : All influenza A pandemics since [the Spanish flu pandemic], and indeed almost all cases of influenza A worldwide (excepting human infections from avian viruses such as H5N1 and H7N7), have been caused by descendants of the 1918 virus, including "drifted" H1N1 viruses and reassorted H2N2 and H3N2 viruses. The latter are composed of key genes from the 1918 virus, updated by subsequently incorporated avian influenza genes that code for novel surface proteins, making the 1918 virus indeed the "mother" of all pandemics. Researchers from the National Institutes of Health used data from the Influenza Genome Sequencing Project and concluded that during the ten-year period examined, most of the time the hemagglutinin gene in H3N2 showed no significant excess of mutations in the antigenic regions while an increasing variety of strains accumulated. This resulted in one of the variants eventually achieving higher fitness, becoming dominant, and in a brief interval of rapid evolution , rapidly sweeping through the population and eliminating most other variants. In the short-term evolution of influenza A virus, a 2006 study found that stochastic, or random, processes are key factors. Influenza A virus HA antigenic evolution appears to be characterized more by punctuated, sporadic jumps as opposed to a constant rate of antigenic change. Using phylogenetic analysis of 413 complete genomes of human influenza A viruses that were collected throughout the state of New York, the authors of Nelson et al. 2006 were able to show that genetic diversity, and not antigenic drift, shaped the short-term evolution of influenza A via random migration and reassortment. The evolution of these viruses is dominated more by the random importation of genetically different viral strains from other geographic locations and less by natural selection. Within a given season, adaptive evolution is infrequent and had an overall weak effect as evidenced from the data gathered from the 413 genomes. Phylogenetic analysis revealed the different strains were derived from newly imported genetic material as opposed to isolates that had been circulating in New York in previous seasons. Therefore, the gene flow in and out of this population, and not natural selection, was more important in the short term. [ citation needed ]Fowl act as natural asymptomatic carriers of influenza A viruses. Prior to the current [ when? ] H5N1 epizootic, strains of influenza A virus had been demonstrated to be transmitted from wildfowl to only birds, pigs, horses, seals , whales and humans; and only between humans and pigs and between humans and domestic fowl; and not other pathways such as domestic fowl to horse. Wild aquatic birds are the natural hosts for a large variety of influenza A viruses. Occasionally, viruses are transmitted from these birds to other species and may then cause devastating outbreaks in domestic poultry or give rise to human influenza pandemics. H5N1 has been shown to be transmitted to tigers, leopards, and domestic cats that were fed uncooked domestic fowl (chickens) with the virus. H3N8 viruses from horses have crossed over and caused outbreaks in dogs. Laboratory mice have been infected successfully with a variety of avian flu genotypes. Influenza A viruses spread in the air and in manure , and survives longer in cold weather. They can also be transmitted by contaminated feed, water, equipment, and clothing; however, there is no evidence the virus can survive in well-cooked meat. Symptoms in animals vary, but virulent strains can cause death within a few days. Avian influenza viruses that the World Organisation for Animal Health and others test for to control poultry disease include H5N1 , H7N2 , H1N7 , H7N3 , H13N6 , H5N9 , H11N6, H3N8 , H9N2 , H5N2 , H4N8, H10N7 , H2N2 , H8N4, H14N5, H6N5, and H12N5. [ citation needed ] *Outbreaks with significant spread to numerous farms, resulting in great economic losses. Most other outbreaks involved little or no spread from the initially infected farms. More than 400 harbor seal deaths were recorded in New England between December 1979 and October 1980, from acute pneumonia caused by the influenza virus, A/Seal/Mass/1/180 (H7N7). Swine influenza (or "pig influenza") refers to a subset of Orthomyxoviridae that create influenza and are endemic in pigs. The species of Orthomyxoviridae that can cause flu in pigs are influenza A virus and influenza C virus , but not all genotypes of these two species infect pigs. The known subtypes of influenza A virus that create influenza and are endemic in pigs are H1N1, H1N2, H3N1 and H3N2. In 1997, H3N2 viruses from humans entered the pig population, causing widespread disease among pigs. Horse flu (or "equine influenza") refers to varieties of influenza A virus that affect horses. Horse flu viruses were only isolated in 1956. The two main types of virus are called equine-1 (H7N7), which commonly affects horse heart muscle, and equine-2 (H3N8), which is usually more severe. H3N8 viruses from horses have infected dogs. Dog flu (or "canine influenza") refers to varieties of influenza A virus that affect dogs. The equine influenza virus H3N8 was found to infect and kill – with respiratory illness – greyhound race dogs at a Florida racetrack in January 2004. Bat flu (or "Bat influenza") refers to the H17N10 and H18N11 influenza A virus strains that were discovered in Central and South American fruit bats as well as a H9N2 virus isolated from the Egyptian fruit bat. Until now it is unclear whether these bat-derived viruses are circulating in any non-bat species and whether they pose a zoonotic threat. Initial characterization of the H18N11 subtype, however, suggests that this bat influenza virus is not well adapted to any other species than bats. H3N8 is now endemic in birds, horses and dogs.Fowl act as natural asymptomatic carriers of influenza A viruses. Prior to the current [ when? ] H5N1 epizootic, strains of influenza A virus had been demonstrated to be transmitted from wildfowl to only birds, pigs, horses, seals , whales and humans; and only between humans and pigs and between humans and domestic fowl; and not other pathways such as domestic fowl to horse. Wild aquatic birds are the natural hosts for a large variety of influenza A viruses. Occasionally, viruses are transmitted from these birds to other species and may then cause devastating outbreaks in domestic poultry or give rise to human influenza pandemics. H5N1 has been shown to be transmitted to tigers, leopards, and domestic cats that were fed uncooked domestic fowl (chickens) with the virus. H3N8 viruses from horses have crossed over and caused outbreaks in dogs. Laboratory mice have been infected successfully with a variety of avian flu genotypes. Influenza A viruses spread in the air and in manure , and survives longer in cold weather. They can also be transmitted by contaminated feed, water, equipment, and clothing; however, there is no evidence the virus can survive in well-cooked meat. Symptoms in animals vary, but virulent strains can cause death within a few days. Avian influenza viruses that the World Organisation for Animal Health and others test for to control poultry disease include H5N1 , H7N2 , H1N7 , H7N3 , H13N6 , H5N9 , H11N6, H3N8 , H9N2 , H5N2 , H4N8, H10N7 , H2N2 , H8N4, H14N5, H6N5, and H12N5. [ citation needed ] *Outbreaks with significant spread to numerous farms, resulting in great economic losses. Most other outbreaks involved little or no spread from the initially infected farms. More than 400 harbor seal deaths were recorded in New England between December 1979 and October 1980, from acute pneumonia caused by the influenza virus, A/Seal/Mass/1/180 (H7N7). Swine influenza (or "pig influenza") refers to a subset of Orthomyxoviridae that create influenza and are endemic in pigs. The species of Orthomyxoviridae that can cause flu in pigs are influenza A virus and influenza C virus , but not all genotypes of these two species infect pigs. The known subtypes of influenza A virus that create influenza and are endemic in pigs are H1N1, H1N2, H3N1 and H3N2. In 1997, H3N2 viruses from humans entered the pig population, causing widespread disease among pigs. Horse flu (or "equine influenza") refers to varieties of influenza A virus that affect horses. Horse flu viruses were only isolated in 1956. The two main types of virus are called equine-1 (H7N7), which commonly affects horse heart muscle, and equine-2 (H3N8), which is usually more severe. H3N8 viruses from horses have infected dogs. Dog flu (or "canine influenza") refers to varieties of influenza A virus that affect dogs. The equine influenza virus H3N8 was found to infect and kill – with respiratory illness – greyhound race dogs at a Florida racetrack in January 2004.Bat flu (or "Bat influenza") refers to the H17N10 and H18N11 influenza A virus strains that were discovered in Central and South American fruit bats as well as a H9N2 virus isolated from the Egyptian fruit bat. Until now it is unclear whether these bat-derived viruses are circulating in any non-bat species and whether they pose a zoonotic threat. Initial characterization of the H18N11 subtype, however, suggests that this bat influenza virus is not well adapted to any other species than bats. H3N8 is now endemic in birds, horses and dogs.Influenza A virus has the following subtypes: [ citation needed ]

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Avian influenza

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Influenza pandemic

An influenza pandemic is an epidemic of an influenza virus that spreads across a large region (either multiple continents or worldwide) and infects a large proportion of the population. There have been six major influenza epidemics in the last 140 years, with the 1918 flu pandemic being the most severe; this is estimated to have been responsible for the deaths of 50–100 million people. The 2009 swine flu pandemic resulted in under 300,000 deaths and is considered relatively mild. These pandemics occur irregularly. Influenza pandemics occur when a new strain of the influenza virus is transmitted to humans from another animal species. Species that are thought to be important in the emergence of new human strains are pigs , chickens and ducks . These novel strains are unaffected by any immunity people may have to older strains of human influenza and can therefore spread extremely rapidly and infect very large numbers of people. Influenza A viruses can occasionally be transmitted from wild birds to other species, causing outbreaks in domestic poultry, and may give rise to human influenza pandemics. The propagation of influenza viruses throughout the world is thought to be in part by bird migrations , though commercial shipments of live bird products might also be implicated, as well as human travel patterns. [ citation needed ] The World Health Organization (WHO) has produced a six-stage classification that describes the process by which a novel influenza virus moves from the first few infections in humans through to a pandemic. This starts with the virus mostly infecting animals, with a few cases where animals infect people, then moves through the stage where the virus begins to spread directly between people, and ends with a pandemic when infections from the new virus have spread worldwide. One strain of virus that may produce a pandemic in the future is a highly pathogenic variation of the H5N1 subtype of influenza A virus . On 11 June 2009, a new strain of H1N1 influenza was declared to be a pandemic (Stage 6) by the WHO after evidence of spreading in the southern hemisphere. The 13 November 2009 worldwide update by the WHO stated that "[a]s of 8 November 2009, worldwide more than 206 countries and overseas territories or communities have reported [503,536] laboratory confirmed cases of pandemic influenza H1N1 2009, including over 6,250 deaths." Influenza, commonly known as the flu, is an infectious disease of birds and mammals . It was thought to be caused by comets, earthquakes, volcanoes, cosmic dust, the rising and setting of the sun, vapors arising from the air and ground, or a blast from the stars. Now we know that it is caused by an RNA virus of the family Orthomyxoviridae (the influenza viruses). In humans, common symptoms of influenza infection are fever, sore throat, muscle pains , severe headache, coughing, and weakness and fatigue . In more serious cases, influenza causes pneumonia , which can be fatal, particularly in young children and the elderly. While sometimes confused with the common cold , influenza is a much more severe disease and is caused by a different type of virus. Although nausea and vomiting can be produced, especially in children, these symptoms are more characteristic of the unrelated gastroenteritis , which is sometimes called "stomach flu" or "24-hour flu." Typically, influenza is transmitted from infected mammals through the air by coughs or sneezes, creating aerosols containing the virus, and from infected birds through their droppings . Influenza can also be transmitted by saliva , nasal secretions , feces, and blood. Healthy individuals can become infected if they breathe in a virus-laden aerosol directly, or if they touch their eyes, nose or mouth after touching any of the aforementioned bodily fluids (or surfaces contaminated with those fluids). Flu viruses can remain infectious for about one week at human body temperature, over 30 days at 0 °C (32 °F) , and indefinitely at very low temperatures (such as lakes in northeast Siberia ). Most influenza strains can be inactivated easily by disinfectants and detergents . Flu spreads around the world in seasonal epidemics. Ten pandemics were recorded before the Spanish flu of 1918. Three influenza pandemics occurred during the 20th century and killed tens of millions of people, with each of these pandemics being caused by the appearance of a new strain of the virus in humans. Often, these new strains result from the spread of an existing flu virus to humans from other animal species , so close proximity between humans and animals can promote epidemics. In addition, epidemiological factors, such as the WWI practice of packing soldiers with severe influenza illness into field hospitals while soldiers with mild illness stayed outside on the battlefield, are an important determinant of whether or not a new strain of influenza virus will spur a pandemic. (During the 1918 Spanish flu pandemic, this practice served to promote the evolution of more virulent viral strains over those that produced mild illness.) When it first killed humans in Asia in the 1990s, a deadly avian strain of H5N1 posed a great risk for a new influenza pandemic; however, this virus did not mutate to spread easily between people. [ permanent dead link ] Vaccinations against influenza are most commonly given to high-risk humans in industrialized countries and to farmed poultry. The most common human vaccine is the trivalent influenza vaccine that contains purified and inactivated material from three viral strains. Typically this vaccine includes material from two influenza A virus subtypes and one influenza B virus strain. A vaccine formulated for one year may be ineffective in the following year, since the influenza virus changes rapidly over time and different strains become dominant. Antiviral drugs can be used to treat influenza, with neuraminidase inhibitors being particularly effective. [ citation needed ]Variants of Influenza A virus are identified and named according to the isolate that they are like and thus are presumed to share lineage (example Fujian flu virus like); according to their typical host (example Human flu virus); according to their subtype (example H3N2 ); and according to their deadliness (e.g., Low Pathogenic as discussed below). So, a flu from a virus similar to the isolate A/Fujian/411/2002(H3N2) is called Fujian flu, human flu, and H3N2 flu. [ citation needed ] Variants are sometimes named according to the species (host) the strain is endemic in or adapted to. Some variants named using this convention are: Avian variants have also sometimes been named according to their deadliness in poultry, especially chickens: Low Pathogenic Avian Influenza (LPAI) Highly Pathogenic Avian Influenza (HPAI), also called: deadly flu or death flu The Influenza A virus subtypes are labeled according to an H number (for hemagglutinin ) and an N number (for neuraminidase ). Each subtype virus has mutated into a variety of strains with differing pathogenic profiles; some pathogenic to one species but not others, some pathogenic to multiple species. Most known strains are extinct strains. For example, the annual flu subtype H3N2 no longer contains the strain that caused the Hong Kong flu . Influenza A viruses are negative sense, single-stranded, segmented RNA viruses. "There are 16 different HA antigens (H1 to H16) and nine different NA antigens (N1 to N9) for influenza A. Until recently, 15 HA types had been recognized, but recently two new types were isolated: a new type (H16) was isolated from black-headed gulls caught in Sweden and the Netherlands in 1999 and reported in the literature in 2005." "The other, H17, was isolated from fruit bats caught in Guatemala and reported in the literature in 2013." Some pandemics are relatively minor such as the one in 1957 called Asian flu (1–4 million dead, depending on source). Others have a higher Pandemic Severity Index whose severity warrants more comprehensive social isolation measures. The 1918 pandemic killed tens of millions and sickened hundreds of millions; the loss of this many people in the population caused upheaval and psychological damage to many people. There were not enough doctors, hospital rooms, or medical supplies for the living as they contracted the disease. Dead bodies were often left unburied as few people were available to deal with them. There can be great social disruption as well as a sense of fear. Efforts to deal with pandemics can leave a great deal to be desired because of human selfishness, lack of trust, illegal behavior, and ignorance. For example, in the 1918 pandemic: "This horrific disconnect between reassurances and reality destroyed the credibility of those in authority. People felt they had no one to turn to, no one to rely on, no one to trust." A letter from a physician at one U.S. Army camp in the 1918 pandemic said: It is only a matter of a few hours then until death comes [...]. It is horrible. One can stand it to see one, two or twenty men die, but to see these poor devils dropping like flies [...]. We have been averaging about 100 deaths per day [...]. Pneumonia means in about all cases death [...]. We have lost an outrageous number of Nurses and Drs. It takes special trains to carry away the dead. For several days there were no coffins and the bodies piled up something fierce [...]. Flu pandemics typically come in waves. The 1889–1890 and 1918–1920 flu pandemics each came in three or four waves of increasing lethality. Within a wave, mortality was greater at the beginning of the wave. Mortality varies widely in a pandemic. In the 1918 pandemic: In U.S. Army camps where reasonably reliable statistics were kept, case mortality often exceeded 5 percent, and in some circumstances exceeded 10 percent. In the British Army in India, case mortality for white troops was 9.6 percent, for Indian troops 21.9 percent. In isolated human populations, the virus killed at even higher rates. In the Fiji islands, it killed 14 percent of the entire population in 16 days. In Labrador and Alaska, it killed at least one-third of the entire native population. Flu pandemics typically come in waves. The 1889–1890 and 1918–1920 flu pandemics each came in three or four waves of increasing lethality. Within a wave, mortality was greater at the beginning of the wave. Mortality varies widely in a pandemic. In the 1918 pandemic: In U.S. Army camps where reasonably reliable statistics were kept, case mortality often exceeded 5 percent, and in some circumstances exceeded 10 percent. In the British Army in India, case mortality for white troops was 9.6 percent, for Indian troops 21.9 percent. In isolated human populations, the virus killed at even higher rates. In the Fiji islands, it killed 14 percent of the entire population in 16 days. In Labrador and Alaska, it killed at least one-third of the entire native population. A 1921 book lists nine influenza pandemics prior to the 1889–1890 flu, the first in 1510 . A more modern source lists six. The 1889–1890 pandemic, often referred to as the Asiatic flu or Russian flu , killed about 1 million people out of a world population of about 1.5 billion. It was long believed to be caused by an influenza A subtype (most often H2N2), but recent analysis largely brought on by the 2002-2004 SARS outbreak and the COVID-19 pandemic determined the outbreak to be more likely caused by a coronavirus. The 1918 flu pandemic, commonly referred to as the Spanish flu , was a category 5 influenza pandemic caused by an unusually severe and deadly Influenza A virus strain of subtype H1N1 . The Spanish flu pandemic lasted from 1918 to 1920. Various estimates say it killed between 17 million and 100 million people This pandemic has been described as "the greatest medical holocaust in history" and may have killed as many people as the Black Death , although the Black Death is estimated to have killed over a fifth of the world's population at the time, a significantly higher proportion. This huge death toll was caused by an extremely high infection rate of up to 50% and the extreme severity of the symptoms, suspected to be caused by cytokine storms . Indeed, symptoms in 1918 were so unusual that initially influenza was misdiagnosed as dengue, cholera , or typhoid. One observer wrote, "One of the most striking of the complications was hemorrhage from mucous membranes, especially from the nose, stomach, and intestine. Bleeding from the ears and petechial hemorrhages in the skin also occurred." The majority of deaths were from bacterial pneumonia , a secondary infection caused by influenza, but the virus also killed people directly, causing massive hemorrhages and edema in the lung. The Spanish flu pandemic was truly global, spreading even to the Arctic and remote Pacific islands. The unusually severe disease killed between 10 and 20% of those infected, as opposed to the more usual flu epidemic mortality rate of 0.1%. Another unusual feature of this pandemic was that it mostly killed young adults, with 99% of pandemic influenza deaths occurring in people under 65, and more than half in young adults 20 to 40 years old. This is unusual since influenza is normally most deadly to the very young (under age 2) and the very old (over age 70). The total mortality of the 1918–1920 pandemic is estimated to be between 17 and 100 million people, constituting approximately 1–6% of the world's population. As many as 25 million may have been killed in the first 25 weeks; in contrast, HIV/AIDS has killed 25 million in its first 25 years . The Asian flu was a category 2 flu pandemic outbreak caused by a strain of H2N2 that originated in China in early 1957, lasting until 1958. The virus originated from a mutation in wild ducks combining with a pre-existing human strain. The virus was first identified in Guizhou in late February; by mid-March it had spread across the entire mainland. It was not until the virus had reached Hong Kong in April, however, that the world was alerted to the unusual situation, when the international press began to report on the outbreak. The World Health Organization was officially informed when the virus arrived in Singapore , which operated the only influenza surveillance laboratory in Southeast Asia , in early May. From that point on, as the virus continued to sweep the region, the WHO remained attuned to the developing outbreak and helped coordinate the global response for the duration of the pandemic. This was the first pandemic to occur during what is considered the "era of modern virology". One significant development since the 1918 pandemic was the identification of the causative agent behind the flu. Later, it was recognized that the influenza virus changes over time, typically only slightly (a process called " antigenic drift "), sometimes significantly enough to result in a new subtype (" antigenic shift "). Within weeks of the report out of Hong Kong, laboratories in the United States , the United Kingdom , and Australia had analyzed the virus and concluded that it was a novel strain of influenza A. Chinese researchers had already come to a similar conclusion in March, but as China was not a member of the WHO nor a part of its network of National Influenza Centers , this information did not reach the rest of the world, a fact which the WHO would lament after the pandemic. The virus swept across the Middle East , Africa , and the Southern Hemisphere in the middle months of the year, causing widespread outbreaks. By the end of September, nearly the entire inhabited world had been infected or at least seeded with the virus. Around this time, extensive epidemics developed in the Northern Hemisphere following the opening of schools, generally peaking in North America and Europe in October. Some countries experienced a second wave in the final months of the year; Japan experienced a particularly severe resurgence in October. Influenza activity had largely subsided by the end of the year and remained apparently low during the first months of 1958, though some countries, such as the United States, experienced another rise in mortality from respiratory disease, of unclear origin. The disease tended to resemble seasonal influenza in its presentation; the WHO described it at the time as "uniformly benign". However, there was the potential for complications, of which there was some variability. Most deaths were a result of bacterial pneumonia, though cases of this condition were attenuated through the use of antibiotics that did not exist in 1918. There were also detailed accounts of fatal primary influenza pneumonia, with no indication of bacterial infection. Those with underlying conditions such as cardiovascular disease were at greater risk of developing these pneumonias; pregnant women were also vulnerable to complications. In general, the elderly experienced the greatest rates of mortality. Estimates of worldwide deaths vary widely depending on the source, ranging from 1 million to 4 million. Mortality in the US has been estimated between 60,000 and 80,000 deaths. Pandemic impact continued over several years in many countries, with Latin America experiencing considerable excess mortality through 1959. Chile experienced notably severe mortality over the course of two waves during this period. This was the most publicized influenza epidemic at the time of its occurrence. As the first pandemic to occur in the context of a global surveillance network, it was also the first time that preparations could be made ahead of an anticipated epidemic. Vaccination efforts were undertaken in some countries such as the US, though it is doubtful how successful such campaigns were with altering the courses of individual epidemics, mainly due to the timing of when the vaccines became widely available and how many people were able to be effectively immunized before the peak. The Hong Kong flu was a category 2 flu pandemic caused by a strain of H3N2 descended from H2N2 by antigenic shift , in which genes from multiple subtypes reassorted to form a new virus. This pandemic killed an estimated 1–4 million people worldwide. Those over 65 had the greatest death rates. In the US, there were about 100,000 deaths. The 1977 Russian flu was a relatively benign flu pandemic, mostly affecting population younger than the age of 26 or 25. It is estimated that 700,000 people died due to the pandemic worldwide. The cause was H1N1 virus strain, which was not seen after 1957 until its re-appearance in China and the Soviet Union in 1977. Genetic analysis and several unusual characteristics of the pandemic have prompted speculation that the virus was released to the public through a laboratory accident. [ excessive citations ] An epidemic of influenza-like illness of unknown causation occurred in Mexico in March–April 2009 . On 24 April 2009, following the isolation of an A/H1N1 influenza in seven ill patients in the southwest US, the WHO issued a statement on the outbreak of "influenza like illness" that confirmed cases of A/H1N1 influenza had been reported in Mexico, and that 20 confirmed cases of the disease had been reported in the US. The next day, the number of confirmed cases rose to 40 in the US, 26 in Mexico, six in Canada, and one in Spain. The disease spread rapidly through the rest of the spring, and by 3 May, a total of 787 confirmed cases had been reported worldwide. On 11 June 2009, the ongoing outbreak of Influenza A/H1N1, commonly referred to as swine flu, was officially declared by the WHO to be the first influenza pandemic of the 21st century and a new strain of Influenza A virus subtype H1N1 first identified in April 2009. It is thought to be a mutation (reassortment) of four known strains of influenza A virus subtype H1N1: one endemic in humans, one endemic in birds, and two endemic in pigs (swine). The rapid spread of this new virus was likely due to a general lack of pre-existing antibody-mediated immunity in the human population. On 1 November 2009, a worldwide update by the WHO stated that "199 countries and overseas territories/communities have officially reported a total of over 482,300 laboratory confirmed cases of the influenza pandemic H1N1 infection, that included 6,071 deaths." By the end of the pandemic, declared on 10 August 2010, there were more than 18,000 laboratory-confirmed deaths from H1N1. Due to inadequate surveillance and lack of healthcare in many countries, the actual total of cases and deaths was likely much higher than reported. Experts, including the WHO, have since agreed that an estimated 284,500 people were killed by the disease, about 15 times the number of deaths in the initial death toll. The 1889–1890 pandemic, often referred to as the Asiatic flu or Russian flu , killed about 1 million people out of a world population of about 1.5 billion. It was long believed to be caused by an influenza A subtype (most often H2N2), but recent analysis largely brought on by the 2002-2004 SARS outbreak and the COVID-19 pandemic determined the outbreak to be more likely caused by a coronavirus. The 1918 flu pandemic, commonly referred to as the Spanish flu , was a category 5 influenza pandemic caused by an unusually severe and deadly Influenza A virus strain of subtype H1N1 . The Spanish flu pandemic lasted from 1918 to 1920. Various estimates say it killed between 17 million and 100 million people This pandemic has been described as "the greatest medical holocaust in history" and may have killed as many people as the Black Death , although the Black Death is estimated to have killed over a fifth of the world's population at the time, a significantly higher proportion. This huge death toll was caused by an extremely high infection rate of up to 50% and the extreme severity of the symptoms, suspected to be caused by cytokine storms . Indeed, symptoms in 1918 were so unusual that initially influenza was misdiagnosed as dengue, cholera , or typhoid. One observer wrote, "One of the most striking of the complications was hemorrhage from mucous membranes, especially from the nose, stomach, and intestine. Bleeding from the ears and petechial hemorrhages in the skin also occurred." The majority of deaths were from bacterial pneumonia , a secondary infection caused by influenza, but the virus also killed people directly, causing massive hemorrhages and edema in the lung. The Spanish flu pandemic was truly global, spreading even to the Arctic and remote Pacific islands. The unusually severe disease killed between 10 and 20% of those infected, as opposed to the more usual flu epidemic mortality rate of 0.1%. Another unusual feature of this pandemic was that it mostly killed young adults, with 99% of pandemic influenza deaths occurring in people under 65, and more than half in young adults 20 to 40 years old. This is unusual since influenza is normally most deadly to the very young (under age 2) and the very old (over age 70). The total mortality of the 1918–1920 pandemic is estimated to be between 17 and 100 million people, constituting approximately 1–6% of the world's population. As many as 25 million may have been killed in the first 25 weeks; in contrast, HIV/AIDS has killed 25 million in its first 25 years . The Asian flu was a category 2 flu pandemic outbreak caused by a strain of H2N2 that originated in China in early 1957, lasting until 1958. The virus originated from a mutation in wild ducks combining with a pre-existing human strain. The virus was first identified in Guizhou in late February; by mid-March it had spread across the entire mainland. It was not until the virus had reached Hong Kong in April, however, that the world was alerted to the unusual situation, when the international press began to report on the outbreak. The World Health Organization was officially informed when the virus arrived in Singapore , which operated the only influenza surveillance laboratory in Southeast Asia , in early May. From that point on, as the virus continued to sweep the region, the WHO remained attuned to the developing outbreak and helped coordinate the global response for the duration of the pandemic. This was the first pandemic to occur during what is considered the "era of modern virology". One significant development since the 1918 pandemic was the identification of the causative agent behind the flu. Later, it was recognized that the influenza virus changes over time, typically only slightly (a process called " antigenic drift "), sometimes significantly enough to result in a new subtype (" antigenic shift "). Within weeks of the report out of Hong Kong, laboratories in the United States , the United Kingdom , and Australia had analyzed the virus and concluded that it was a novel strain of influenza A. Chinese researchers had already come to a similar conclusion in March, but as China was not a member of the WHO nor a part of its network of National Influenza Centers , this information did not reach the rest of the world, a fact which the WHO would lament after the pandemic. The virus swept across the Middle East , Africa , and the Southern Hemisphere in the middle months of the year, causing widespread outbreaks. By the end of September, nearly the entire inhabited world had been infected or at least seeded with the virus. Around this time, extensive epidemics developed in the Northern Hemisphere following the opening of schools, generally peaking in North America and Europe in October. Some countries experienced a second wave in the final months of the year; Japan experienced a particularly severe resurgence in October. Influenza activity had largely subsided by the end of the year and remained apparently low during the first months of 1958, though some countries, such as the United States, experienced another rise in mortality from respiratory disease, of unclear origin. The disease tended to resemble seasonal influenza in its presentation; the WHO described it at the time as "uniformly benign". However, there was the potential for complications, of which there was some variability. Most deaths were a result of bacterial pneumonia, though cases of this condition were attenuated through the use of antibiotics that did not exist in 1918. There were also detailed accounts of fatal primary influenza pneumonia, with no indication of bacterial infection. Those with underlying conditions such as cardiovascular disease were at greater risk of developing these pneumonias; pregnant women were also vulnerable to complications. In general, the elderly experienced the greatest rates of mortality. Estimates of worldwide deaths vary widely depending on the source, ranging from 1 million to 4 million. Mortality in the US has been estimated between 60,000 and 80,000 deaths. Pandemic impact continued over several years in many countries, with Latin America experiencing considerable excess mortality through 1959. Chile experienced notably severe mortality over the course of two waves during this period. This was the most publicized influenza epidemic at the time of its occurrence. As the first pandemic to occur in the context of a global surveillance network, it was also the first time that preparations could be made ahead of an anticipated epidemic. Vaccination efforts were undertaken in some countries such as the US, though it is doubtful how successful such campaigns were with altering the courses of individual epidemics, mainly due to the timing of when the vaccines became widely available and how many people were able to be effectively immunized before the peak. The Hong Kong flu was a category 2 flu pandemic caused by a strain of H3N2 descended from H2N2 by antigenic shift , in which genes from multiple subtypes reassorted to form a new virus. This pandemic killed an estimated 1–4 million people worldwide. Those over 65 had the greatest death rates. In the US, there were about 100,000 deaths. The 1977 Russian flu was a relatively benign flu pandemic, mostly affecting population younger than the age of 26 or 25. It is estimated that 700,000 people died due to the pandemic worldwide. The cause was H1N1 virus strain, which was not seen after 1957 until its re-appearance in China and the Soviet Union in 1977. Genetic analysis and several unusual characteristics of the pandemic have prompted speculation that the virus was released to the public through a laboratory accident. [ excessive citations ]An epidemic of influenza-like illness of unknown causation occurred in Mexico in March–April 2009 . On 24 April 2009, following the isolation of an A/H1N1 influenza in seven ill patients in the southwest US, the WHO issued a statement on the outbreak of "influenza like illness" that confirmed cases of A/H1N1 influenza had been reported in Mexico, and that 20 confirmed cases of the disease had been reported in the US. The next day, the number of confirmed cases rose to 40 in the US, 26 in Mexico, six in Canada, and one in Spain. The disease spread rapidly through the rest of the spring, and by 3 May, a total of 787 confirmed cases had been reported worldwide. On 11 June 2009, the ongoing outbreak of Influenza A/H1N1, commonly referred to as swine flu, was officially declared by the WHO to be the first influenza pandemic of the 21st century and a new strain of Influenza A virus subtype H1N1 first identified in April 2009. It is thought to be a mutation (reassortment) of four known strains of influenza A virus subtype H1N1: one endemic in humans, one endemic in birds, and two endemic in pigs (swine). The rapid spread of this new virus was likely due to a general lack of pre-existing antibody-mediated immunity in the human population. On 1 November 2009, a worldwide update by the WHO stated that "199 countries and overseas territories/communities have officially reported a total of over 482,300 laboratory confirmed cases of the influenza pandemic H1N1 infection, that included 6,071 deaths." By the end of the pandemic, declared on 10 August 2010, there were more than 18,000 laboratory-confirmed deaths from H1N1. Due to inadequate surveillance and lack of healthcare in many countries, the actual total of cases and deaths was likely much higher than reported. Experts, including the WHO, have since agreed that an estimated 284,500 people were killed by the disease, about 15 times the number of deaths in the initial death toll. "Human influenza virus" usually refers to those subtypes that spread widely among humans. H1N1, H1N2 , and H3N2 are the only known Influenza A virus subtypes currently circulating among humans. Genetic factors in distinguishing between "human flu viruses" and "avian influenza viruses" include: "About 52 key genetic changes distinguish avian influenza strains from those that spread easily among people, according to researchers in Taiwan, who analyzed the genes of more than 400 A type flu viruses." "How many mutations would make an avian virus capable of infecting humans efficiently, or how many mutations would render an influenza virus a pandemic strain, is difficult to predict. We have examined sequences from the 1918 strain, which is the only pandemic influenza virus that could be entirely derived from avian strains. Of the 52 species-associated positions, 16 have residues typical for human strains; the others remained as avian signatures. The result supports the hypothesis that the 1918 pandemic virus is more closely related to the avian influenza A virus than are other human influenza viruses." Highly pathogenic H5N1 avian influenza kills 50% of humans that catch it. In one case, a boy with H5N1 experienced diarrhea followed rapidly by a coma without developing respiratory or flu-like symptoms. The Influenza A virus subtypes that have been confirmed in humans, ordered by the number of known human pandemic deaths, are: [ citation needed ] H1N1 is currently endemic in both human and pig populations. A variant of H1N1 was responsible for the Spanish flu pandemic that killed some 50 million to 100 million people worldwide over about a year in 1918 and 1919. Controversy arose in October 2005, after the H1N1 genome was published in the journal, Science . Many fear that this information could be used for bioterrorism . When he compared the 1918 virus with today's human flu viruses, Dr. Taubenberger noticed that it had alterations in just 25 to 30 of the virus's 4,400 amino acids. Those few changes turned a bird virus into a killer that could spread from person to person. In mid-April 2009, an H1N1 variant appeared in Mexico, with its center in Mexico City. By 26 April the variant had spread widely; with cases reported in Canada, the US, New Zealand, the UK, France, Spain and Israel. On 29 April the WHO raised the worldwide pandemic phase to 5. On 11 June 2009 the WHO raised the worldwide pandemic phase to 6, which means that the H1N1 swine flu has reached pandemic proportions, with nearly 30,000 confirmed cases worldwide. A 13 November 2009 worldwide update by the WHO states that "206 countries and overseas territories/communities have officially reported over 503,536 laboratory confirmed cases of the influenza pandemic H1N1 infection, including 6,250 deaths." The Asian Flu was a pandemic outbreak of H2N2 avian influenza that originated in China in 1957, spread worldwide that same year during which an influenza vaccine was developed, lasted until 1958 and caused between one and four million deaths. [ citation needed ] H3N2 is currently endemic in both human and pig populations. It evolved from H2N2 by antigenic shift and caused the Hong Kong flu pandemic that killed up to 750,000. "An early-onset, severe form of influenza A H3N2 made headlines when it claimed the lives of several children in the United States in late 2003." The dominant strain of annual flu in January 2006 is H3N2. Measured resistance to the standard antiviral drugs amantadine and rimantadine in H3N2 has increased from 1% in 1994 to 12% in 2003 to 91% in 2005. [C]ontemporary human H3N2 influenza viruses are now endemic in pigs in southern China and can reassort with avian H5N1 viruses in this intermediate host. H7N7 has unusual zoonotic potential. In 2003 in Netherlands 89 people were confirmed to have H7N7 influenza virus infection following an outbreak in poultry on several farms. One death was recorded. H1N2 is currently endemic in both human and pig populations. The new H1N2 strain appears to have resulted from the reassortment of the genes of the currently circulating influenza H1N1 and H3N2 subtypes. The hemagglutinin protein of the H1N2 virus is similar to that of the currently circulating H1N1 viruses and the neuraminidase protein is similar to that of the current H3N2 viruses. In 2014, the CDC adopted the Pandemic Severity Assessment Framework (PSAF) to assess the severity of pandemics. The PSAF superseded the 2007 linear Pandemic Severity Index, which assumed 30% spread and measured case fatality rate (CFR) to assess the severity and evolution of the pandemic. Historically, measures of pandemic severity were based on the case fatality rate. However, the case fatality rate might not be an adequate measure of pandemic severity during a pandemic response because: Deaths may lag several weeks behind cases, making the case fatality rate an underestimate The total number of cases may not be known, making the case fatality rate an overestimate A single case fatality rate for the entire population may obscure the effect on vulnerable sub-populations, such as children, the elderly, those with chronic conditions, and members of certain racial and ethnic minorities Fatalities alone may not account for the full effects of the pandemic, such as absenteeism or demand on healthcare services To account for the limitations of measuring the case fatality rate alone, the PSAF rates severity of a disease outbreak on two dimensions: clinical severity of illness in infected persons; and the transmissibility of the infection in the population. Each dimension can be measured using more than one measure, which are scaled to allow comparison of the different measures.In 2014, the CDC adopted the Pandemic Severity Assessment Framework (PSAF) to assess the severity of pandemics. The PSAF superseded the 2007 linear Pandemic Severity Index, which assumed 30% spread and measured case fatality rate (CFR) to assess the severity and evolution of the pandemic. Historically, measures of pandemic severity were based on the case fatality rate. However, the case fatality rate might not be an adequate measure of pandemic severity during a pandemic response because: Deaths may lag several weeks behind cases, making the case fatality rate an underestimate The total number of cases may not be known, making the case fatality rate an overestimate A single case fatality rate for the entire population may obscure the effect on vulnerable sub-populations, such as children, the elderly, those with chronic conditions, and members of certain racial and ethnic minorities Fatalities alone may not account for the full effects of the pandemic, such as absenteeism or demand on healthcare services To account for the limitations of measuring the case fatality rate alone, the PSAF rates severity of a disease outbreak on two dimensions: clinical severity of illness in infected persons; and the transmissibility of the infection in the population. Each dimension can be measured using more than one measure, which are scaled to allow comparison of the different measures.The World Health Organization (WHO) developed a global influenza preparedness plan, which defines the stages of a pandemic, outlines WHO's role and makes recommendations for national measures before and during a pandemic. This included a classification system for assessing the progress of an outbreak. Phases 1–3 correlate with preparedness, including capacity development and response planning activities, while phases 4–6 clearly signal the need for response and mitigation efforts. In February 2020, WHO announced that it no longer uses this six-phase classification model: "For the sake of clarification, WHO does not use the old system of 6 phases—that ranged from phase 1 (no reports of animal influenza causing human infections) to phase 6 (a pandemic)—that some people may be familiar with from H1N1 in 2009." In 2014, the United States Centers for Disease Control and Prevention (CDC) introduced the Pandemic Intervals Framework for assessing influenza outbreaks. It includes two pre-pandemic intervals: - Investigation Recognition and four pandemic intervals, Initiation Acceleration Deceleration Preparation This section contains strategies to prevent a flu pandemic by a Council on Foreign Relations panel. If influenza remains an animal problem with limited human-to-human transmission it is not a pandemic, though it continues to pose a risk. To prevent the situation from progressing to a pandemic, the following short-term strategies have been put forward: [ citation needed ] Culling and vaccinating livestock Vaccinating poultry workers against common flu Limiting travel in areas where the virus is found The rationale for vaccinating poultry workers against common flu is that it reduces the probability of common influenza virus recombining with avian H5N1 virus to form a pandemic strain. Longer-term strategies proposed for regions where highly pathogenic H5N1 is endemic in wild birds have included: The main ways available to tackle a flu pandemic initially are behavioural. Doing so requires a good public health communication strategy and the ability to track public concerns, attitudes and behaviour. For example, the Flu TElephone Survey Template (FluTEST) was developed for the UK Department of Health as a set of questions for use in national surveys during a flu pandemic. The Institute of Medicine has published a number of reports and summaries of workshops on public policy issues related to influenza pandemics. They are collected in Pandemic Influenza: A Guide to Recent Institute of Medicine Studies and Workshops , and some strategies from these reports are included in the list above. Relevant learning from the 2009 flu pandemic in the UK was published in Health Technology Assessment , volume 14, issue 34. Asymptomatic transmission appears to play a small role, but was not well studied by 2009. There are two groups of antiviral drugs available for the treatment and prophylaxis of influenza: neuraminidase inhibitors such as Oseltamivir (trade name Tamiflu) and Zanamivir (trade name Relenza), and adamantanes such as amantadine and rimantadine. Due to the high rate of side effects and risk of antiviral resistance, use of adamantanes to fight influenza is limited. Many nations, as well as the World Health Organization, are working to stockpile antiviral drugs in preparation for a possible pandemic. Oseltamivir is the most commonly sought drug, since it is available in pill form. Zanamivir is also considered for use, but it must be inhaled. Other anti-viral drugs are less likely to be effective against pandemic influenza. Both Tamiflu and Relenza are in short supply, and production capabilities are limited in the medium term. Some doctors say that co-administration of Tamiflu with probenecid could double supplies. There also is the potential of viruses to evolve drug resistance. Some H5N1-infected persons treated with oseltamivir have developed resistant strains of that virus. A vaccine probably would not be available in the initial stages of population infection. To date, there is no known mechanism to develop a vaccine to protect against a virus which does not yet exist. The avian flu virus H5N1 has the potential to mutate into a pandemic strain, but so do other types of flu virus. Once a potential virus is identified and a vaccine is approved, it normally takes five to six months before the vaccine becomes available. The capability to produce vaccines varies widely from country to country; only 19 countries are listed as "influenza vaccine manufacturers" according to the World Health Organization. It is estimated that, in a best scenario situation, 750 million doses could be produced each year, whereas it is likely that each individual would need two doses of the vaccine to become immuno-competent. Distribution to and inside countries would probably be problematic. Several countries, however, have well-developed plans for producing large quantities of vaccine. For example, Canadian health authorities say that they are developing the capacity to produce 32 million doses within four months, enough vaccine to inoculate every person in the country. Another concern is whether countries which do not manufacture vaccines themselves, including those where a pandemic strain is likely to originate, will be able to purchase vaccine to protect their population. Cost considerations aside, they fear that the countries with vaccine-manufacturing capability will reserve production to protect their own populations and not release vaccines to other countries until their own population is protected. Indonesia has refused to share samples of H5N1 strains which have infected and killed its citizens until it receives assurances that it will have access to vaccines produced with those samples. So far, it has not received those assurances. However, in September 2009, Australia, Brazil, France, Italy, New Zealand, Norway, Switzerland, the UK, and the USA agreed to make 10 percent of their H1N1 vaccine supply available to less-developed countries. There are two serious technical problems associated with the development of a vaccine against H5N1. The first problem is this: seasonal influenza vaccines require a single injection of 15 μg haemagluttinin in order to give protection; H5 seems to evoke only a weak immune response and a large multicentre trial found that two injections of 90 µg H5 given 28 days apart provided protection in only 54% of people. Even if it is considered that 54% is an acceptable level of protection, the world is currently capable of producing only 900 million doses at a strength of 15 μg (assuming that all production were immediately converted to manufacturing H5 vaccine); if two injections of 90 μg are needed then this capacity drops to only 70 million. Trials using adjuvants such as alum , AS03 , AS04 or MF59 to try and lower the dose of vaccine are urgently needed. The second problem is this: there are two circulating clades of virus, clade 1 is the virus originally isolated in Vietnam, clade 2 is the virus isolated in Indonesia. Vaccine research has mostly been focused on clade 1 viruses, but the clade 2 virus is antigenically distinct and a clade 1 vaccine will probably not protect against a pandemic caused by clade 2 virus. [ citation needed ] Since 2009, most vaccine development efforts have been focused on the current pandemic influenza virus H1N1. As of July 2009, more than 70 known clinical trials have been completed or are ongoing for pandemic influenza vaccines. In September 2009, the US Food and Drug Administration approved four vaccines against the 2009 H1N1 influenza virus, and expected the initial vaccine lots to be available within the following month. The World Health Organization (WHO) developed a global influenza preparedness plan, which defines the stages of a pandemic, outlines WHO's role and makes recommendations for national measures before and during a pandemic. This included a classification system for assessing the progress of an outbreak. Phases 1–3 correlate with preparedness, including capacity development and response planning activities, while phases 4–6 clearly signal the need for response and mitigation efforts. In February 2020, WHO announced that it no longer uses this six-phase classification model: "For the sake of clarification, WHO does not use the old system of 6 phases—that ranged from phase 1 (no reports of animal influenza causing human infections) to phase 6 (a pandemic)—that some people may be familiar with from H1N1 in 2009." In 2014, the United States Centers for Disease Control and Prevention (CDC) introduced the Pandemic Intervals Framework for assessing influenza outbreaks. It includes two pre-pandemic intervals: - Investigation Recognition and four pandemic intervals, Initiation Acceleration Deceleration Preparation This section contains strategies to prevent a flu pandemic by a Council on Foreign Relations panel. If influenza remains an animal problem with limited human-to-human transmission it is not a pandemic, though it continues to pose a risk. To prevent the situation from progressing to a pandemic, the following short-term strategies have been put forward: [ citation needed ] Culling and vaccinating livestock Vaccinating poultry workers against common flu Limiting travel in areas where the virus is found The rationale for vaccinating poultry workers against common flu is that it reduces the probability of common influenza virus recombining with avian H5N1 virus to form a pandemic strain. Longer-term strategies proposed for regions where highly pathogenic H5N1 is endemic in wild birds have included:The main ways available to tackle a flu pandemic initially are behavioural. Doing so requires a good public health communication strategy and the ability to track public concerns, attitudes and behaviour. For example, the Flu TElephone Survey Template (FluTEST) was developed for the UK Department of Health as a set of questions for use in national surveys during a flu pandemic. The Institute of Medicine has published a number of reports and summaries of workshops on public policy issues related to influenza pandemics. They are collected in Pandemic Influenza: A Guide to Recent Institute of Medicine Studies and Workshops , and some strategies from these reports are included in the list above. Relevant learning from the 2009 flu pandemic in the UK was published in Health Technology Assessment , volume 14, issue 34. Asymptomatic transmission appears to play a small role, but was not well studied by 2009. There are two groups of antiviral drugs available for the treatment and prophylaxis of influenza: neuraminidase inhibitors such as Oseltamivir (trade name Tamiflu) and Zanamivir (trade name Relenza), and adamantanes such as amantadine and rimantadine. Due to the high rate of side effects and risk of antiviral resistance, use of adamantanes to fight influenza is limited. Many nations, as well as the World Health Organization, are working to stockpile antiviral drugs in preparation for a possible pandemic. Oseltamivir is the most commonly sought drug, since it is available in pill form. Zanamivir is also considered for use, but it must be inhaled. Other anti-viral drugs are less likely to be effective against pandemic influenza. Both Tamiflu and Relenza are in short supply, and production capabilities are limited in the medium term. Some doctors say that co-administration of Tamiflu with probenecid could double supplies. There also is the potential of viruses to evolve drug resistance. Some H5N1-infected persons treated with oseltamivir have developed resistant strains of that virus. A vaccine probably would not be available in the initial stages of population infection. To date, there is no known mechanism to develop a vaccine to protect against a virus which does not yet exist. The avian flu virus H5N1 has the potential to mutate into a pandemic strain, but so do other types of flu virus. Once a potential virus is identified and a vaccine is approved, it normally takes five to six months before the vaccine becomes available. The capability to produce vaccines varies widely from country to country; only 19 countries are listed as "influenza vaccine manufacturers" according to the World Health Organization. It is estimated that, in a best scenario situation, 750 million doses could be produced each year, whereas it is likely that each individual would need two doses of the vaccine to become immuno-competent. Distribution to and inside countries would probably be problematic. Several countries, however, have well-developed plans for producing large quantities of vaccine. For example, Canadian health authorities say that they are developing the capacity to produce 32 million doses within four months, enough vaccine to inoculate every person in the country. Another concern is whether countries which do not manufacture vaccines themselves, including those where a pandemic strain is likely to originate, will be able to purchase vaccine to protect their population. Cost considerations aside, they fear that the countries with vaccine-manufacturing capability will reserve production to protect their own populations and not release vaccines to other countries until their own population is protected. Indonesia has refused to share samples of H5N1 strains which have infected and killed its citizens until it receives assurances that it will have access to vaccines produced with those samples. So far, it has not received those assurances. However, in September 2009, Australia, Brazil, France, Italy, New Zealand, Norway, Switzerland, the UK, and the USA agreed to make 10 percent of their H1N1 vaccine supply available to less-developed countries. There are two serious technical problems associated with the development of a vaccine against H5N1. The first problem is this: seasonal influenza vaccines require a single injection of 15 μg haemagluttinin in order to give protection; H5 seems to evoke only a weak immune response and a large multicentre trial found that two injections of 90 µg H5 given 28 days apart provided protection in only 54% of people. Even if it is considered that 54% is an acceptable level of protection, the world is currently capable of producing only 900 million doses at a strength of 15 μg (assuming that all production were immediately converted to manufacturing H5 vaccine); if two injections of 90 μg are needed then this capacity drops to only 70 million. Trials using adjuvants such as alum , AS03 , AS04 or MF59 to try and lower the dose of vaccine are urgently needed. The second problem is this: there are two circulating clades of virus, clade 1 is the virus originally isolated in Vietnam, clade 2 is the virus isolated in Indonesia. Vaccine research has mostly been focused on clade 1 viruses, but the clade 2 virus is antigenically distinct and a clade 1 vaccine will probably not protect against a pandemic caused by clade 2 virus. [ citation needed ] Since 2009, most vaccine development efforts have been focused on the current pandemic influenza virus H1N1. As of July 2009, more than 70 known clinical trials have been completed or are ongoing for pandemic influenza vaccines. In September 2009, the US Food and Drug Administration approved four vaccines against the 2009 H1N1 influenza virus, and expected the initial vaccine lots to be available within the following month. The main ways available to tackle a flu pandemic initially are behavioural. Doing so requires a good public health communication strategy and the ability to track public concerns, attitudes and behaviour. For example, the Flu TElephone Survey Template (FluTEST) was developed for the UK Department of Health as a set of questions for use in national surveys during a flu pandemic. The Institute of Medicine has published a number of reports and summaries of workshops on public policy issues related to influenza pandemics. They are collected in Pandemic Influenza: A Guide to Recent Institute of Medicine Studies and Workshops , and some strategies from these reports are included in the list above. Relevant learning from the 2009 flu pandemic in the UK was published in Health Technology Assessment , volume 14, issue 34. Asymptomatic transmission appears to play a small role, but was not well studied by 2009. There are two groups of antiviral drugs available for the treatment and prophylaxis of influenza: neuraminidase inhibitors such as Oseltamivir (trade name Tamiflu) and Zanamivir (trade name Relenza), and adamantanes such as amantadine and rimantadine. Due to the high rate of side effects and risk of antiviral resistance, use of adamantanes to fight influenza is limited. Many nations, as well as the World Health Organization, are working to stockpile antiviral drugs in preparation for a possible pandemic. Oseltamivir is the most commonly sought drug, since it is available in pill form. Zanamivir is also considered for use, but it must be inhaled. Other anti-viral drugs are less likely to be effective against pandemic influenza. Both Tamiflu and Relenza are in short supply, and production capabilities are limited in the medium term. Some doctors say that co-administration of Tamiflu with probenecid could double supplies. There also is the potential of viruses to evolve drug resistance. Some H5N1-infected persons treated with oseltamivir have developed resistant strains of that virus.A vaccine probably would not be available in the initial stages of population infection. To date, there is no known mechanism to develop a vaccine to protect against a virus which does not yet exist. The avian flu virus H5N1 has the potential to mutate into a pandemic strain, but so do other types of flu virus. Once a potential virus is identified and a vaccine is approved, it normally takes five to six months before the vaccine becomes available. The capability to produce vaccines varies widely from country to country; only 19 countries are listed as "influenza vaccine manufacturers" according to the World Health Organization. It is estimated that, in a best scenario situation, 750 million doses could be produced each year, whereas it is likely that each individual would need two doses of the vaccine to become immuno-competent. Distribution to and inside countries would probably be problematic. Several countries, however, have well-developed plans for producing large quantities of vaccine. For example, Canadian health authorities say that they are developing the capacity to produce 32 million doses within four months, enough vaccine to inoculate every person in the country. Another concern is whether countries which do not manufacture vaccines themselves, including those where a pandemic strain is likely to originate, will be able to purchase vaccine to protect their population. Cost considerations aside, they fear that the countries with vaccine-manufacturing capability will reserve production to protect their own populations and not release vaccines to other countries until their own population is protected. Indonesia has refused to share samples of H5N1 strains which have infected and killed its citizens until it receives assurances that it will have access to vaccines produced with those samples. So far, it has not received those assurances. However, in September 2009, Australia, Brazil, France, Italy, New Zealand, Norway, Switzerland, the UK, and the USA agreed to make 10 percent of their H1N1 vaccine supply available to less-developed countries. There are two serious technical problems associated with the development of a vaccine against H5N1. The first problem is this: seasonal influenza vaccines require a single injection of 15 μg haemagluttinin in order to give protection; H5 seems to evoke only a weak immune response and a large multicentre trial found that two injections of 90 µg H5 given 28 days apart provided protection in only 54% of people. Even if it is considered that 54% is an acceptable level of protection, the world is currently capable of producing only 900 million doses at a strength of 15 μg (assuming that all production were immediately converted to manufacturing H5 vaccine); if two injections of 90 μg are needed then this capacity drops to only 70 million. Trials using adjuvants such as alum , AS03 , AS04 or MF59 to try and lower the dose of vaccine are urgently needed. The second problem is this: there are two circulating clades of virus, clade 1 is the virus originally isolated in Vietnam, clade 2 is the virus isolated in Indonesia. Vaccine research has mostly been focused on clade 1 viruses, but the clade 2 virus is antigenically distinct and a clade 1 vaccine will probably not protect against a pandemic caused by clade 2 virus. [ citation needed ] Since 2009, most vaccine development efforts have been focused on the current pandemic influenza virus H1N1. As of July 2009, more than 70 known clinical trials have been completed or are ongoing for pandemic influenza vaccines. In September 2009, the US Food and Drug Administration approved four vaccines against the 2009 H1N1 influenza virus, and expected the initial vaccine lots to be available within the following month. According to The New York Times as of March 2006, "governments worldwide have spent billions planning for a potential influenza pandemic: buying medicines, running disaster drills, [and] developing strategies for tighter border controls" due to the H5N1 threat. [T]he United States is collaborating closely with eight international organizations, including the World Health Organization (WHO), the Food and Agriculture Organization of the United Nations (FAO), the World Organization for Animal Health (OIE), and 88 foreign governments to address the situation through planning, greater monitoring, and full transparency in reporting and investigating avian influenza occurrences. The United States and these international partners have led global efforts to encourage countries to heighten surveillance for outbreaks in poultry and significant numbers of deaths in migratory birds and to rapidly introduce containment measures. The U.S. Agency for International Development (USAID) and the U.S. Departments of State , Health and Human Services (HHS), and Agriculture (USDA) are coordinating future international response measures on behalf of the White House with departments and agencies across the federal government. Together steps are being taken to "minimize the risk of further spread in animal populations", "reduce the risk of human infections", and "further support pandemic planning and preparedness". Ongoing detailed mutually coordinated onsite surveillance and analysis of human and animal H5N1 avian flu outbreaks are being conducted and reported by the USGS National Wildlife Health Center, the CDC, the ECDC , the World Health Organization, the European Commission , the National Influenza Centers, and others. [ failed verification ] In September 2005, David Nabarro , a lead UN health official, warned that a bird flu outbreak could happen at any time and had the potential to kill 5–150 million people. The World Health Organization (WHO), believing that the world was closer to another influenza pandemic than it has been any time since 1968, when the last of the 20th century's three pandemics swept the globe, has developed guidelines on pandemic influenza preparedness and response. The March 2005 plan includes guidance on roles and responsibilities in preparedness and response; information on pandemic phases; and recommended actions for before, during, and after a pandemic. "[E]fforts by the federal government to prepare for pandemic influenza at the national level include a $100 million DHHS initiative in 2003 to build U.S. vaccine production. Several agencies within Department of Health and Human Services (DHHS)—including the Office of the Secretary, the Food and Drug Administration (FDA), CDC , and the National Institute of Allergy and Infectious Diseases (NIAID)—are in the process of working with vaccine manufacturers to facilitate production of pilot vaccine lots for both H5N1 and H9N2 strains as well as contracting for the manufacturing of 2 million doses of an H5N1 vaccine. This H5N1 vaccine production will provide a critical pilot test of the pandemic vaccine system; it will also be used for clinical trials to evaluate dose and immunogenicity and can provide initial vaccine for early use in the event of an emerging pandemic." Each state and territory of the United States has a specific pandemic flu plan which covers avian flu, swine flu (H1N1), and other potential influenza epidemics. The state plans together with a professionally vetted search engine of flu related research, policies, and plans, is available at the current portal: Pandemic Flu Search Archived 18 November 2019 at the Wayback Machine . On 26 August 2004, Secretary of Health and Human Services, Tommy Thompson released a draft Pandemic Influenza Response and Preparedness Plan, which outlined a coordinated national strategy to prepare for and respond to an influenza pandemic. Public comments were accepted for 60 days. In a speech before the United Nations General Assembly on 14 September 2005, President George W. Bush announced the creation of the International Partnership on Avian and Pandemic Influenza . The Partnership brings together nations and international organizations to improve global readiness by: elevating the issue on national agendas; coordinating efforts among donor and affected nations; mobilizing and leveraging resources; increasing transparency in disease reporting and surveillance; and building capacity to identify, contain and respond to a pandemic influenza. On 5 October 2005, Democratic Senators Harry Reid , Evan Bayh , Dick Durbin , Ted Kennedy , Barack Obama , and Tom Harkin introduced the Pandemic Preparedness and Response Act as a proposal to deal with a possible outbreak. On 27 October 2005, the Department of Health and Human Services awarded a $62.5 million contract to Chiron Corporation to manufacture an avian influenza vaccine designed to protect against the H5N1 influenza virus strain. This followed a previous awarded $100 million contract to Sanofi Pasteur , the vaccines business of Sanofi , for avian flu vaccine. In October 2005, Bush urged bird flu vaccine manufacturers to increase their production. On 1 November 2005, Bush unveiled the National Strategy To Safeguard Against The Danger of Pandemic Influenza. He also submitted a request to Congress for $7.1 billion to begin implementing the plan. The request includes $251 million to detect and contain outbreaks before they spread around the world; $2.8 billion to accelerate development of cell-culture technology; $800 million for development of new treatments and vaccines; $1.519 billion for the Departments of Health and Human Services ( HHS ) and Defense to purchase influenza vaccines; $1.029 billion to stockpile antiviral medications; and $644 million to ensure that all levels of government are prepared to respond to a pandemic outbreak. On 6 March 2006, Mike Leavitt , Secretary of Health and Human Services, said U.S. health agencies are continuing to develop vaccine alternatives that will protect against the evolving avian influenza virus. The U.S. government, bracing for the possibility that migrating birds could carry a deadly strain of bird flu to North America, plans to test nearly eight times as many wild birds starting in April 2006 as have been tested in the past decade. On 8 March 2006, Dr. David Nabarro , senior UN coordinator for avian and human influenza, said that given the flight patterns of wild birds that have been spreading avian influenza (bird flu) from Asia to Europe and Africa, birds infected with the H5N1 virus could reach the Americas within the next six to 12 months. July 5, 2006, ( CIDRAP News) – "In an update on pandemic influenza preparedness efforts, the federal government said last week it had stockpiled enough vaccine against H5N1 avian influenza virus to inoculate about 4 million people and enough antiviral medication to treat about 6.3 million." The Public Health Agency of Canada follows the WHO's categories, but has expanded them. The avian flu scare of 2006 prompted The Canadian Public Health Agency to release an updated Pandemic Influenza Plan for Health Officials. This document was created to address the growing concern over the hazards faced by public health officials when exposed to sick or dying patients. [ citation needed ] Since the Nipah virus outbreak in 1999, the Malaysian Health Ministry have put in place processes to be better prepared to protect the Malaysian population from the threat of infectious diseases. Malaysia was fully prepared during the severe acute respiratory syndrome (SARS) situation (Malaysia was not a SARS-affected country) and the episode of the H5N1 outbreak in 2004. The Malaysian government has developed a National Influenza Pandemic Preparedness Plan (NIPPP) which serves as a time bound guide for preparedness and response plan for influenza pandemic. It provides a policy and strategic framework for a multisectoral response and contains specific advice and actions to be undertaken by the Ministry of Health at the different levels, other governmental departments and agencies and non-governmental organizations to ensure that resources are mobilized and used most efficiently before, during and after a pandemic episode.In September 2005, David Nabarro , a lead UN health official, warned that a bird flu outbreak could happen at any time and had the potential to kill 5–150 million people. The World Health Organization (WHO), believing that the world was closer to another influenza pandemic than it has been any time since 1968, when the last of the 20th century's three pandemics swept the globe, has developed guidelines on pandemic influenza preparedness and response. The March 2005 plan includes guidance on roles and responsibilities in preparedness and response; information on pandemic phases; and recommended actions for before, during, and after a pandemic. "[E]fforts by the federal government to prepare for pandemic influenza at the national level include a $100 million DHHS initiative in 2003 to build U.S. vaccine production. Several agencies within Department of Health and Human Services (DHHS)—including the Office of the Secretary, the Food and Drug Administration (FDA), CDC , and the National Institute of Allergy and Infectious Diseases (NIAID)—are in the process of working with vaccine manufacturers to facilitate production of pilot vaccine lots for both H5N1 and H9N2 strains as well as contracting for the manufacturing of 2 million doses of an H5N1 vaccine. This H5N1 vaccine production will provide a critical pilot test of the pandemic vaccine system; it will also be used for clinical trials to evaluate dose and immunogenicity and can provide initial vaccine for early use in the event of an emerging pandemic." Each state and territory of the United States has a specific pandemic flu plan which covers avian flu, swine flu (H1N1), and other potential influenza epidemics. The state plans together with a professionally vetted search engine of flu related research, policies, and plans, is available at the current portal: Pandemic Flu Search Archived 18 November 2019 at the Wayback Machine . On 26 August 2004, Secretary of Health and Human Services, Tommy Thompson released a draft Pandemic Influenza Response and Preparedness Plan, which outlined a coordinated national strategy to prepare for and respond to an influenza pandemic. Public comments were accepted for 60 days. In a speech before the United Nations General Assembly on 14 September 2005, President George W. Bush announced the creation of the International Partnership on Avian and Pandemic Influenza . The Partnership brings together nations and international organizations to improve global readiness by: elevating the issue on national agendas; coordinating efforts among donor and affected nations; mobilizing and leveraging resources; increasing transparency in disease reporting and surveillance; and building capacity to identify, contain and respond to a pandemic influenza. On 5 October 2005, Democratic Senators Harry Reid , Evan Bayh , Dick Durbin , Ted Kennedy , Barack Obama , and Tom Harkin introduced the Pandemic Preparedness and Response Act as a proposal to deal with a possible outbreak. On 27 October 2005, the Department of Health and Human Services awarded a $62.5 million contract to Chiron Corporation to manufacture an avian influenza vaccine designed to protect against the H5N1 influenza virus strain. This followed a previous awarded $100 million contract to Sanofi Pasteur , the vaccines business of Sanofi , for avian flu vaccine. In October 2005, Bush urged bird flu vaccine manufacturers to increase their production. On 1 November 2005, Bush unveiled the National Strategy To Safeguard Against The Danger of Pandemic Influenza. He also submitted a request to Congress for $7.1 billion to begin implementing the plan. The request includes $251 million to detect and contain outbreaks before they spread around the world; $2.8 billion to accelerate development of cell-culture technology; $800 million for development of new treatments and vaccines; $1.519 billion for the Departments of Health and Human Services ( HHS ) and Defense to purchase influenza vaccines; $1.029 billion to stockpile antiviral medications; and $644 million to ensure that all levels of government are prepared to respond to a pandemic outbreak. On 6 March 2006, Mike Leavitt , Secretary of Health and Human Services, said U.S. health agencies are continuing to develop vaccine alternatives that will protect against the evolving avian influenza virus. The U.S. government, bracing for the possibility that migrating birds could carry a deadly strain of bird flu to North America, plans to test nearly eight times as many wild birds starting in April 2006 as have been tested in the past decade. On 8 March 2006, Dr. David Nabarro , senior UN coordinator for avian and human influenza, said that given the flight patterns of wild birds that have been spreading avian influenza (bird flu) from Asia to Europe and Africa, birds infected with the H5N1 virus could reach the Americas within the next six to 12 months. July 5, 2006, ( CIDRAP News) – "In an update on pandemic influenza preparedness efforts, the federal government said last week it had stockpiled enough vaccine against H5N1 avian influenza virus to inoculate about 4 million people and enough antiviral medication to treat about 6.3 million." The Public Health Agency of Canada follows the WHO's categories, but has expanded them. The avian flu scare of 2006 prompted The Canadian Public Health Agency to release an updated Pandemic Influenza Plan for Health Officials. This document was created to address the growing concern over the hazards faced by public health officials when exposed to sick or dying patients. [ citation needed ]Since the Nipah virus outbreak in 1999, the Malaysian Health Ministry have put in place processes to be better prepared to protect the Malaysian population from the threat of infectious diseases. Malaysia was fully prepared during the severe acute respiratory syndrome (SARS) situation (Malaysia was not a SARS-affected country) and the episode of the H5N1 outbreak in 2004. The Malaysian government has developed a National Influenza Pandemic Preparedness Plan (NIPPP) which serves as a time bound guide for preparedness and response plan for influenza pandemic. It provides a policy and strategic framework for a multisectoral response and contains specific advice and actions to be undertaken by the Ministry of Health at the different levels, other governmental departments and agencies and non-governmental organizations to ensure that resources are mobilized and used most efficiently before, during and after a pandemic episode.

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Avian influenza

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Influenza A virus subtype H7N9

Influenza A virus subtype H7N9 (A/H7N9) is a bird flu strain of the species Influenza virus A ( avian influenza virus or bird flu virus). Avian influenza A H7 viruses normally circulate amongst avian populations with some variants known to occasionally infect humans. An H7N9 virus was first reported to have infected humans in March 2013, in China. Cases continued to be reported throughout April and then dropped to only a few cases during the summer months. At the closing of the year, 144 cases had been reported of which 46 had died. It is known that influenza tends to strike during the winter months, and the second wave, which began in October, was fanned by a surge in poultry production timed for Lunar New Year feasts that began at the end of January. January 2014 brought a spike in reports of illness with 96 confirmed reports of disease and 19 deaths. As of April 11, 2014, the outbreak's overall total was 419, including 7 in Hong Kong, and the unofficial number of deaths was 127. A 5th epidemic of the H7N9 virus began in October 2016 in China. The epidemic is the largest since the first epidemic in 2013 and accounts for about one-third of human cases ever reported. The cumulative total of laboratory-confirmed cases since the first epidemic is 1,223. About 40 percent have died. The CDC estimates that the H7N9 virus has the greatest potential compared with other influenza A viruses to cause a pandemic, although the risk is low because, like other type A viruses, it is not easily transmitted between people in its current form. The World Health Organization (WHO) has identified H7N9 as "...an unusually dangerous virus for humans." Most of the cases resulted in severe respiratory illness, with a mortality rate of roughly 30 percent. Researchers have commented on the unusual prevalence of older males among H7N9-infected patients. While several environmental, behavioral, and biological explanations for this pattern have been proposed, the reason remains unknown. It has been established that many of the human cases of H7N9 appear to have a link to live bird markets. As of January 2014, there has been no evidence of sustained human-to-human transmission; however, a study group headed by one of the world's leading experts on avian flu reported that several instances of human-to-human infection are suspected. The H7N9 virus does not kill poultry, which makes surveillance much more difficult. [ citation needed ] Chinese scientists announced the development of a vaccine on October 26, 2013, but said that H7N9 had not spread far enough to merit widespread vaccination. Research regarding background and transmission is ongoing. Influenza A viruses are divided into subtypes based on two proteins on the surface of the virus: hemagglutinin (HA) and neuraminidase (NA). The avian influenza A(H7N9) virus designation of H7N9 identifies it as having HA of the H7 subtype and NA of the N9 subtype. Avian influenza A H7 viruses are a group of influenza viruses that normally circulate among birds. H7 influenza infections in humans are uncommon, but have been confirmed worldwide in people who have direct contact with infected birds. Most infections have been mild involving only conjunctivitis and mild upper respiratory symptoms. The avian influenza A(H7N9) virus is a subgroup among this larger group of H7 viruses. Although some H7 viruses (e.g. H7N2 , H7N3 and H7N7 ) have occasionally been found to infect humans, H7N9 has previously been isolated only in birds, with outbreaks reported in the Netherlands , Japan , and the United States . Until the 2013 outbreak in China , no human infections with H7N9 viruses had ever been reported. Genetic characterisation of avian influenza A(H7N9) shows that the H7N9 virus that infects human beings resulted from the recombination of genes between several parent viruses noted in poultry and wild birds in Asia. It is most closely related to sequences found in samples from ducks in Zhejiang province in 2011. Evidence so far suggests that the new H7N9 virus might have evolved from at least four origins. It is hypothesized that the gene that codes for HA has its origin in ducks and the gene that codes for NA has its origin with ducks and probably also wild birds. Six internal genes originated with at least two H9N2 chicken viruses. The HA genes were circulating in the East Asian flyway in both wild birds and ducks, while the NA genes were introduced from European lineages and transferred to ducks in China by wild birds through migration along the East Asian flyway. Dr. Keiji Fukuda , WHO's assistant director-general for health security and environment, remarked at a Toronto interview that "I think we are genuinely in new territory here in which the situation of having something that is low path in birds (yet) appears to be so pathogenic in people... And then to have those genetic changes ... I simply don't know what that combination is going to lead to." "Almost everything you can imagine is possible. And then what's likely to happen are the things which you can't imagine," he also remarked. According to the deputy director of CDC's influenza division, the genetic makeup of H7N9 is "disturbingly different" from that of the H5N1 virus that has infected more than 600 people over the past 10 years and killed more than half of them. "The thing that's different between them is the H5 virus still maintains a lot of the avian or bird flu characteristics, whereas this H7N9 shows some adaptation to mammals. And that's what makes it different and concerning for us. It still has a ways to go before it becomes like a human virus, but the fact is, it's somewhere in that middle ground between purely avian and purely human." In August 2013, it was announced that scientists plan to create mutant forms of the virus so they can gauge the risk of it becoming a lethal human pandemic. The genetic modification work will result in highly transmissible and deadly forms of H7N9, and is being carried out in several high security laboratories around the world. Most human infections with avian influenza viruses, including Asian H7N9 virus, occur after exposure to infected poultry or contaminated environments. Asian H7N9 viruses continue to circulate in poultry in China. Most reported patients with H7N9 virus infection have had severe respiratory illness (e.g., pneumonia). Rare instances of limited person-to-person spread of this virus have been identified in China, but there is no evidence of sustained person-to-person spread. Some human infections with Asian H7N9 virus have been reported outside of mainland China, Hong Kong or Macao but all of these infections have occurred among people who had traveled to China before becoming ill. Asian H7N9 viruses have not been detected in people or birds in the United States. Most human infections with avian influenza viruses, including Asian H7N9 virus, occur after exposure to infected poultry or contaminated environments. Asian H7N9 viruses continue to circulate in poultry in China. Most reported patients with H7N9 virus infection have had severe respiratory illness (e.g., pneumonia). Rare instances of limited person-to-person spread of this virus have been identified in China, but there is no evidence of sustained person-to-person spread. Some human infections with Asian H7N9 virus have been reported outside of mainland China, Hong Kong or Macao but all of these infections have occurred among people who had traveled to China before becoming ill. Asian H7N9 viruses have not been detected in people or birds in the United States. On March 31, 2013, the Centre for Health Protection (CHP) of the Department of Health of Hong Kong and the Chinese National Health and Family Planning Commission notified the World Health Organization of three confirmed human cases of influenza A (H7N9) in Shanghai and Anhui (illness onset between February 19 and March 15, 2013). On April 2, the CHP confirmed four more cases in Jiangsu province , all considered in critical condition in hospitals in Nanjing , Suzhou , and Wuxi . In a statement, the CHP said that no epidemiologic links had been found between the four patients and so far no other H7N9 infections have been identified in 167 of their close contacts. The first reported death associated with H7N9 was an 87-year-old man who died on March 4. A second man, aged 27, died on March 10. On April 3, Chinese authorities reported another death, bringing the number to three. On April 4, the number of reported cases was 14, with 5 deaths. The two victims were a 48-year-old man and a 52-year-old woman, both from Shanghai. On April 5, a farmer, aged 64, living in Huzhou ( Zhejiang province), died, raising the death toll to 6. On April 6, the Chinese Ministry of Health reported 18 positive cases, death toll still at 6. Two days later, positive cases rose to 24 and one death case from Shanghai brought the death toll to 7. On April 9, the Chinese National Health and Family Planning Commission announced "an additional three laboratory-confirmed cases of human infection with influenza A(H7N9) virus." The new patients "are two patients from Jiangsu – an 85-year-old man who became ill on 28 March 2013" and a "25-year-old pregnant woman who became ill on 30 March 2013" and "a 64-year-old man from Shanghai who became ill on 1 April 2013, and died on 7 April 2013". As of April 9, a "total of 24 cases have been laboratory confirmed with influenza A(H7N9) virus in China, including seven deaths, 14 severe cases and three mild cases." In Jiangsu, more than "600 close contacts of the confirmed cases are being closely monitored." In an update on April 11, Xinhua reported 38 identified cases and 10 deaths. According to the WHO , of the 28 patients who had survived their infections, 19 illnesses were severe and 9 were mild. The WHO said they were monitoring 760 close contacts and so far had no evidence of ongoing human-to-human transmission. On April 13, a seven-year-old girl from Beijing was the first confirmed case of H7N9 bird flu outside eastern China. On April 14, Xinhua Chinese state media reported two human cases in central Henan just west of the area where the disease had been centered. Totals included 61 infected and 13 dead. On April 14, Chinese officials also reported the first asymptomatic case in Beijing. A health department notice suggested that a 4-year-old boy had no clinical symptoms and was tested during surveillance of high-risk groups. On April 17, a total of 82 cases had been confirmed, with 17 deaths. On April 18, China reported 87 confirmed cases. On April 20, there were 96 confirmed cases, of which 18 were fatal. On the next day, confirmed cases rose to 102 and fatal cases to 20. On April 22, there were 104 cases with 21 deaths. On April 23, 3 more cases were reported in an update from the WHO . All of the newly reported cases were in older men from eastern China. Two cases came from the Zhejiang province and the third was from the Anhui province. Total cases count reached 108 with 22 deaths. On April 24, a case was confirmed by the Taiwanese Government, marking the first case outside of Mainland China. On April 25, the National Health and Family Planning Commission said that a total of 109 H7N9 cases had been reported within mainland China, including 23 deaths. However, Anne Kelso , director of the WHO Collaborating Centre for Reference and Research on Influenza, VIDRL, Australia, reported that researchers had seen a "dramatic slowdown" in human cases in Shanghai after the city's live poultry markets were closed on April 6. On the following day, cases in mainland China rose to 118. On April 28, four provinces, Zhejiang , Shandong , Jiangxi , and Fujian , reported new cases, raising the total number of cases in mainland China to 125 with 24 deaths. On May 2, there were 127 confirmed cases in mainland China, of which 27 were fatal, and including the case in Taiwan there were a total of 128 cases worldwide. On May 6, in a weekly update, China's Ministry of Health announced there were 129 confirmed cases in mainland China with 31 deaths, for a total of 130 cases worldwide. On May 7, Hong Kong's Centre for Health Protection reported that there were 130 confirmed cases of H7N9 avian flu in mainland China following the hospitalization of a 79-year-old woman from China's Jiangxi province, bringing the count to 131 cases. The Ministry of Health of People's Republic of China reported on July 10 that in the month of June, there was only 1 confirmed case, and there were a total of 132 confirmed cases in Mainland China as of June 30, 2013 (43 fatal, 85 patient recovery cases). Though there is a slow increase in the number of cases, China recently warned that the transmission of H7N9 virus might be active again by autumn and winter seasons. In August, Guangdong province confirmed its first case of H7N9 bird flu, a 51-year-old woman in critical condition after having been admitted to a hospital on August 3. As of November 1, 2013 [ update ] , China reported to the WHO that "rare and sporadic human infections with H7N9" have been reported with "the total number of cases reported to 137, including 45 deaths" in China. The CDC and U.S. government H7N9 preparedness efforts have continued over the summer and are "continuing to watch this situation closely". As of December 14, 2013 [ update ] , two cases of H7N9 were reported in Hong Kong. Hong Kong reported its first death from H7N9 on 26 December 2013. On December 31, Taiwan's CDC released a press statement indicating that an 86-year-old man from Jiangsu Province, China, who was visiting Taiwan, became ill and tested positive for H7N9 flu. This is the second case in Taiwan, the first being in April. On January 21, 2014, it was reported that a 31-year-old thoracic surgeon had died four days previously, the first medical professional to die from H7N9 flu. There was no evidence that he had been in contact with live poultry recently. Yuen Kwok-yung, a University of Hong Kong microbiologist, said, "If the diagnosis is confirmed and no [bird] exposure history is elicited, this does point slightly more to the possibility that H7N9 may be more transmissible between humans than H5N1". On January 28, 2014, it was reported by the Chinese Center for Disease Control and Prevention that the virus had killed 20 people in China in 2014, with the total number of human infections at 102. That is comparable to 144 confirmed cases, including 46 deaths, in the whole of 2013. At the end of January, more than half of the cases in 2014 had been in Zhejiang, with another 24 in Guangdong, and eight in Shanghai. The director of the Chinese National Influenza Center, Shu Yuelong, said a large-scale H7N9 epidemic still remains unlikely because the virus has not yet mutated in such a way that would allow person to person transmission. On February 13, 2014, it was reported that a 67-year-old female tourist from China had been diagnosed with the H7N9 virus while visiting Malaysia. In January 2015, A Canadian visitor to China was diagnosed with H7N9 after she returned home to British Columbia . After returning to Canada on January 12, she felt ill on January 14. In June 2015, 15 cases of H7N9 infection were reported in China . Beginning in October 2016 China began experiencing a 5th epidemic of H7N9, the largest since the first epidemic in 2013. For the 5th epidemic, the WHO reported 460 human infections as of early March 2017, which accounts for about one-third of cases ever reported since this strain of influenza virus first appeared in 2013. The cumulative total of laboratory-confirmed cases since the first epidemic is 1,223. About 40 percent have died. As of September 8, 2017, the World Health Organization and CDC reported a total number to 759 infections with 281 deaths for the fifth epidemic. On March 31, 2013, the Centre for Health Protection (CHP) of the Department of Health of Hong Kong and the Chinese National Health and Family Planning Commission notified the World Health Organization of three confirmed human cases of influenza A (H7N9) in Shanghai and Anhui (illness onset between February 19 and March 15, 2013). On April 2, the CHP confirmed four more cases in Jiangsu province , all considered in critical condition in hospitals in Nanjing , Suzhou , and Wuxi . In a statement, the CHP said that no epidemiologic links had been found between the four patients and so far no other H7N9 infections have been identified in 167 of their close contacts. The first reported death associated with H7N9 was an 87-year-old man who died on March 4. A second man, aged 27, died on March 10. On April 3, Chinese authorities reported another death, bringing the number to three. On April 4, the number of reported cases was 14, with 5 deaths. The two victims were a 48-year-old man and a 52-year-old woman, both from Shanghai. On April 5, a farmer, aged 64, living in Huzhou ( Zhejiang province), died, raising the death toll to 6. On April 6, the Chinese Ministry of Health reported 18 positive cases, death toll still at 6. Two days later, positive cases rose to 24 and one death case from Shanghai brought the death toll to 7. On April 9, the Chinese National Health and Family Planning Commission announced "an additional three laboratory-confirmed cases of human infection with influenza A(H7N9) virus." The new patients "are two patients from Jiangsu – an 85-year-old man who became ill on 28 March 2013" and a "25-year-old pregnant woman who became ill on 30 March 2013" and "a 64-year-old man from Shanghai who became ill on 1 April 2013, and died on 7 April 2013". As of April 9, a "total of 24 cases have been laboratory confirmed with influenza A(H7N9) virus in China, including seven deaths, 14 severe cases and three mild cases." In Jiangsu, more than "600 close contacts of the confirmed cases are being closely monitored." In an update on April 11, Xinhua reported 38 identified cases and 10 deaths. According to the WHO , of the 28 patients who had survived their infections, 19 illnesses were severe and 9 were mild. The WHO said they were monitoring 760 close contacts and so far had no evidence of ongoing human-to-human transmission. On April 13, a seven-year-old girl from Beijing was the first confirmed case of H7N9 bird flu outside eastern China. On April 14, Xinhua Chinese state media reported two human cases in central Henan just west of the area where the disease had been centered. Totals included 61 infected and 13 dead. On April 14, Chinese officials also reported the first asymptomatic case in Beijing. A health department notice suggested that a 4-year-old boy had no clinical symptoms and was tested during surveillance of high-risk groups. On April 17, a total of 82 cases had been confirmed, with 17 deaths. On April 18, China reported 87 confirmed cases. On April 20, there were 96 confirmed cases, of which 18 were fatal. On the next day, confirmed cases rose to 102 and fatal cases to 20. On April 22, there were 104 cases with 21 deaths. On April 23, 3 more cases were reported in an update from the WHO . All of the newly reported cases were in older men from eastern China. Two cases came from the Zhejiang province and the third was from the Anhui province. Total cases count reached 108 with 22 deaths. On April 24, a case was confirmed by the Taiwanese Government, marking the first case outside of Mainland China. On April 25, the National Health and Family Planning Commission said that a total of 109 H7N9 cases had been reported within mainland China, including 23 deaths. However, Anne Kelso , director of the WHO Collaborating Centre for Reference and Research on Influenza, VIDRL, Australia, reported that researchers had seen a "dramatic slowdown" in human cases in Shanghai after the city's live poultry markets were closed on April 6. On the following day, cases in mainland China rose to 118. On April 28, four provinces, Zhejiang , Shandong , Jiangxi , and Fujian , reported new cases, raising the total number of cases in mainland China to 125 with 24 deaths. On May 2, there were 127 confirmed cases in mainland China, of which 27 were fatal, and including the case in Taiwan there were a total of 128 cases worldwide. On May 6, in a weekly update, China's Ministry of Health announced there were 129 confirmed cases in mainland China with 31 deaths, for a total of 130 cases worldwide. On May 7, Hong Kong's Centre for Health Protection reported that there were 130 confirmed cases of H7N9 avian flu in mainland China following the hospitalization of a 79-year-old woman from China's Jiangxi province, bringing the count to 131 cases. The Ministry of Health of People's Republic of China reported on July 10 that in the month of June, there was only 1 confirmed case, and there were a total of 132 confirmed cases in Mainland China as of June 30, 2013 (43 fatal, 85 patient recovery cases). Though there is a slow increase in the number of cases, China recently warned that the transmission of H7N9 virus might be active again by autumn and winter seasons. In August, Guangdong province confirmed its first case of H7N9 bird flu, a 51-year-old woman in critical condition after having been admitted to a hospital on August 3. As of November 1, 2013 [ update ] , China reported to the WHO that "rare and sporadic human infections with H7N9" have been reported with "the total number of cases reported to 137, including 45 deaths" in China. The CDC and U.S. government H7N9 preparedness efforts have continued over the summer and are "continuing to watch this situation closely". As of December 14, 2013 [ update ] , two cases of H7N9 were reported in Hong Kong. Hong Kong reported its first death from H7N9 on 26 December 2013. On December 31, Taiwan's CDC released a press statement indicating that an 86-year-old man from Jiangsu Province, China, who was visiting Taiwan, became ill and tested positive for H7N9 flu. This is the second case in Taiwan, the first being in April. On January 21, 2014, it was reported that a 31-year-old thoracic surgeon had died four days previously, the first medical professional to die from H7N9 flu. There was no evidence that he had been in contact with live poultry recently. Yuen Kwok-yung, a University of Hong Kong microbiologist, said, "If the diagnosis is confirmed and no [bird] exposure history is elicited, this does point slightly more to the possibility that H7N9 may be more transmissible between humans than H5N1". On January 28, 2014, it was reported by the Chinese Center for Disease Control and Prevention that the virus had killed 20 people in China in 2014, with the total number of human infections at 102. That is comparable to 144 confirmed cases, including 46 deaths, in the whole of 2013. At the end of January, more than half of the cases in 2014 had been in Zhejiang, with another 24 in Guangdong, and eight in Shanghai. The director of the Chinese National Influenza Center, Shu Yuelong, said a large-scale H7N9 epidemic still remains unlikely because the virus has not yet mutated in such a way that would allow person to person transmission. On February 13, 2014, it was reported that a 67-year-old female tourist from China had been diagnosed with the H7N9 virus while visiting Malaysia. In January 2015, A Canadian visitor to China was diagnosed with H7N9 after she returned home to British Columbia . After returning to Canada on January 12, she felt ill on January 14. In June 2015, 15 cases of H7N9 infection were reported in China . Beginning in October 2016 China began experiencing a 5th epidemic of H7N9, the largest since the first epidemic in 2013. For the 5th epidemic, the WHO reported 460 human infections as of early March 2017, which accounts for about one-third of cases ever reported since this strain of influenza virus first appeared in 2013. The cumulative total of laboratory-confirmed cases since the first epidemic is 1,223. About 40 percent have died. As of September 8, 2017, the World Health Organization and CDC reported a total number to 759 infections with 281 deaths for the fifth epidemic. According to the World Health Organization, symptoms include fever, cough, and shortness of breath, which may progress to severe pneumonia . The virus can also overload the immune system, causing what is known as a cytokine storm . Blood poisoning and organ failure are also possible. In an article in the New England Journal of Medicine , doctors reported that most of the patients with confirmed cases of H7N9 virus infection were critically ill and that approximately 20% had died of acute respiratory distress syndrome (ARDS) or multiorgan failure . Antigenic and genome sequencing suggests that H7N9 is sensitive to neuraminidase inhibitors , such as oseltamivir and zanamivir . The use of these neuraminidase inhibitors in cases of early infection may be effective, although the benefits of oseltamivir treatment have been questioned. Information released in 2014 indicated that 75% of those that came down with H7N9 influenza had previously been exposed to domestic poultry. In April, 2013, the World Health Organization (WHO) said H7N9 was "unlikely" to become a pandemic and that there was no evidence of human-to-human transmission. In late July, 2013, however, Chinese scientists found evidence that person-to-person transmission was possible, but would not transmit easily. In April 2013, it was also reported that the virus had been found only in chickens, ducks, and pigeons at live poultry markets and that no migratory birds had tested positive for the virus, easing concerns about that route of transmission. However, later investigation demonstrated that H7N9 may infect wild songbirds and caged parakeets, which then shed the virus into their environment. This finding implies that these birds may potentially serve as intermediate hosts with the ability to facilitate transmission and dissemination of H7N9. At an April 26 news conference, the WHO assistant director-general for health stated, "This is an unusually dangerous virus for humans. We think this virus is more easily transmitted from poultry to humans than H5N1 ." Furthermore, there is great concern because unlike the H5N1 virus, H7N9 does not cause visible disease in poultry, which makes surveillance, prevention, and control of the virus in poultry extremely difficult. On April 30, it was announced that the Ministry of Agriculture of the People's Republic of China had asked the Director General of the World Organisation for Animal Health (OIE) to send OIE experts to assess the situation and provide advice. According to the information and data collected, it was confirmed that many of the human cases of H7N9 appeared to have a link with live bird markets, but to that date no human cases or animal infections of H7N9 had been detected on poultry farms. The OIE experts made the hypothesis that people could be infected through exposure to infected birds in markets or to a contaminated environment such as live poultry markets where the virus is present. They believe that live bird markets may play a key role in human and animal infections with H7N9 and that, even if the overall level of infection is relatively low (having not been detected yet in poultry farms), live bird markets provide an environment for amplification and maintenance of the H7N9 virus. The OIE mission also confirmed that currently infection with H7N9 does not cause visible disease in poultry and therefore veterinary services must be especially involved in preventing its further spread. According to the April 30 report, there is no evidence to suggest that the consumption of poultry or eggs could transmit the virus to humans. More assessment is needed to know whether poultry vaccination could be considered as a control option for H7N9. It will also be important to verify whether the H7N9 virus is transmissible from humans to animals because if established, it could be a potential channel for the global spread of the virus. The number of cases detected after April fell abruptly. The decrease in the number of new human H7N9 cases may have resulted from containment measures taken by Chinese authorities, including closing live bird markets, or from a change in seasons, or a possibly a combination of both factors. Studies indicate that avian influenza viruses have a seasonal pattern, much like human seasonal influenza viruses. If this is the case, H7N9 infections – in birds and people – may pick up again when the weather turns cooler in China. Limited person-to-person spread of bird flu is thought to have occurred rarely in the past, most notably with avian influenza A (H5N1). According to the US CDC, based on previous experience, some limited human-to-human spread of this H7N9 virus would not be surprising if the virus reemerges in the fall. Furthermore, according to the WHO, since migratory birds were first implicated in H7N9 transmission, the possibility that the virus may spread into other regions or countries with colder weather cannot be excluded, given the widespread bird migratory patterns. In a study published in July 2013, an international team led by Yoshihiro Kawaoka , one of the world's leading experts on avian flu, reported that while avian flu viruses typically lack the ability to transfer through respiratory droplets, studies using ferrets , who like humans infect one another through coughing and sneezing, showed that one of the H7N9 strains isolated from humans can transmit through respiratory droplets. Kawaoka says, "H7N9 viruses combine several features of pandemic influenza viruses, that is their ability to bind to and replicate in human cells and the ability to transmit via respiratory droplets." Further, because several instances of human-to-human infection are suspected, Kawaoka stated that "If H7N9 viruses acquire the ability to transmit efficiently from person to person, a worldwide outbreak is almost certain since humans lack protective immune responses to these types of viruses." On August 6, 2013, the British Medical Journal released the results of epidemiological investigations conducted after a family cluster of two patients were infected with avian H7N9 in March 2013 and later died in April and May. A 60-year-old man became infected after an exposure to poultry and his daughter, who had not been exposed to poultry but had cared for her ill father, became infected as well. Genome sequence and analyses of phylogenetic trees showed that both viruses were almost genetically identical. Forty-three close contacts of the infected patients did not become ill and they all tested negative for haemagglutination inhibition antibodies specific for avian H7N9. It was concluded that the infection of the daughter probably resulted from close contact with her father during unprotected exposure, suggesting that the virus was able to transmit from person to person. However, the researchers consider the transmissibility of the virus to have remained limited and non-sustainable. In a study published in July 2013, an international team led by Yoshihiro Kawaoka , one of the world's leading experts on avian flu, reported that while avian flu viruses typically lack the ability to transfer through respiratory droplets, studies using ferrets , who like humans infect one another through coughing and sneezing, showed that one of the H7N9 strains isolated from humans can transmit through respiratory droplets. Kawaoka says, "H7N9 viruses combine several features of pandemic influenza viruses, that is their ability to bind to and replicate in human cells and the ability to transmit via respiratory droplets." Further, because several instances of human-to-human infection are suspected, Kawaoka stated that "If H7N9 viruses acquire the ability to transmit efficiently from person to person, a worldwide outbreak is almost certain since humans lack protective immune responses to these types of viruses." On August 6, 2013, the British Medical Journal released the results of epidemiological investigations conducted after a family cluster of two patients were infected with avian H7N9 in March 2013 and later died in April and May. A 60-year-old man became infected after an exposure to poultry and his daughter, who had not been exposed to poultry but had cared for her ill father, became infected as well. Genome sequence and analyses of phylogenetic trees showed that both viruses were almost genetically identical. Forty-three close contacts of the infected patients did not become ill and they all tested negative for haemagglutination inhibition antibodies specific for avian H7N9. It was concluded that the infection of the daughter probably resulted from close contact with her father during unprotected exposure, suggesting that the virus was able to transmit from person to person. However, the researchers consider the transmissibility of the virus to have remained limited and non-sustainable. In the month following the report of the first patient, more than 100 people had been infected, an unusually high rate for a new infection; a fifth of those patients had died, a fifth had recovered, and the rest remained critically ill. Keiji Fukuda , the World Health Organization 's (WHO) assistant director-general for health, security and the environment, identified H7N9 as "...an unusually dangerous virus for humans." By early May 2013, the number of new cases sharply declined and the mortality rate remained at about 20%. As of 2019, the laboratory-confirmed patient fatality risk of H7N9 infection is 39%. However, laboratory-confirmation is biased towards detecting the severest patients. People with H7N9 can have a wide range of symptoms, including asymptomatic and mild infections, but the rate of such infections is less understood. Based on the influenza-like illness surveillance system in China, the number of symptomatic H7N9 infections is likely substantially higher than the number of laboratory-confirmed cases. The estimated symptomatic case fatality risk is 0.16% in the 2013 wave and 0.10% in the 2013/14 wave. A serological study conducted in Guangzhou from December 2013 to April 2014 estimated 3,200 times the number of laboratory-confirmed cases during the same period of time and, for the first time, estimated the infection fatality risk for H7N9 to be 0.036% in the 2013/2014 wave. Researchers have commented on the unusual prevalence of older males among H7N9-infected patients. Two-thirds of persons who are ill from H7N9 are 50 years of age or older, which is an older age curve than that for H5N1 . In addition, two-thirds of persons infected by H7N9 are male. Possible reasons for the prevalence of older males among H7N9-infected patients include: a difference in exposure between males and females due to gender-associated practices; biological differences between males and females; and the differences in healthcare-seeking behavior and healthcare access between males and females. Both the median age and male to female relationship appear to have remained stable: The February 2014, WHO report stated "...37 cases, the median age was 60 years, ranging from 5-84 years, with a male to female ratio of 3.6:1." Dr. Yuzo Arima and his colleagues at WHO report "While poultry exposure appears to be a common risk factor, the age distribution among reported cases also raises the question why so few young adults (i.e. those of working age exposed to poultry as vendors/LBM [ live bird market ] workers/breeders/transporters) have been reported. This not only suggests greater exposure among elderly men but also a possible greater biological susceptibility to more severe outcomes." Danuta M. Skowronski, MD, of the British Columbia Centre for Disease Control and three colleagues put forward the hypothesis that older Chinese men have more lifetime exposure to H7 avian flu viruses and thus have immune responses which are weakly cross-reactive but not protective. This immune phenomenon is called antibody-dependent enhancement (ADE), and is perhaps best known in cases of Dengue fever when a person who has previously been infected with one serotype of Dengue fever becomes infected many months or years later with a different serotype. It is thought to occur when weakly cross-reactive antibodies form bridging complexes to facilitate uptake and replication of related but non-identical variants. Although China has been praised for its quick response, some experts believe that there would be great difficulty providing adequate supplies of a vaccine if the virus were to develop into a pandemic. According to an article in the Journal of the American Medical Association (JAMA) in May 2013, "Even with additional vaccine manufacturing capacity... the global public health community remains woefully underprepared for an effective vaccine response to a pandemic...There is no reason to believe that a yet-to-be-developed pandemic A(H7N9) vaccine will perform any better than existing seasonal vaccines or the A(H1N1)pdm09 vaccines [about 60% to 70% effectiveness], particularly with regard to vaccine efficacy in persons older than 65 years." On October 26, 2013, Chinese scientists announced that they had successfully produced an H7N9 vaccine , the first influenza vaccine to be developed entirely in China. It was developed jointly by researchers from Zhejiang University , Hong Kong University , the Chinese Center for Disease Control and Prevention , China's National Institute for Food and Drug Control, and the Chinese Academy of Medical Sciences . Chinese National Influenza Center director Shu Yuelong said the vaccine passed tests on ferrets and had been approved for humans, but H7N9 has not spread far enough to merit widespread vaccination. The vaccine was developed from a throat swab of an infected patient taken April 3. On November 12, 2013, US scientists at Novavax, Inc. announced their successful clinical testing of an H7N9 vaccine in the New England Journal of Medicine. They had previously described the development, manufacture, and efficacy in mice of an A/Anhui/1/13 (H7N9) viruslike particle (VLP) vaccine produced in insect cells with the use of recombinant baculovirus. The vaccine combined the HA and neuraminidase (NA) of A/Anhui/1/13 with the matrix 1 protein (M1) of A/Indonesia/5/05. The study enrolled 284 adults (≥18 years of age) in a randomized, observer-blinded, placebo-controlled clinical trial of this vaccine. The Centers for Disease Control and Prevention (CDC) began sequencing and development of a vaccine as routine procedure for any new transgenic virus. The CDC and vaccine manufacturers are developing a candidate virus to be used in vaccine manufacturing if there is widespread transmission. On September 18, 2013, NIH announced that researchers have begun testing an investigational H7N9 influenza vaccine in humans. Two Phase II trials are collecting data about the safety of the vaccine, immune system responses to different vaccine dosages, both with and without adjuvants. Healthy adults 19 to 64 years of age will be enrolled in the two studies. The inactivated-virus vaccine was made with H7N9 virus that was isolated in Shanghai, China. Adjuvants are being tested with the vaccine to determine if an adequate immune response can be produced. In addition, during a pandemic, adjuvants may be used as part of a "dose-sparing strategy". In response to a request from the CDC and the Biomedical Advanced Research and Development Authority , following the unprecedented immediate release of the H7N9 flu virus gene sequences from the first human cases, by scientists at the China CDC through the GISAID Initiative, the J. Craig Venter Institute , and Synthetic Genomics Vaccines, Inc. began working with Novartis to synthesize the genes of the new viral strain, and supplied these synthesized genes to the CDC. The scientific community has praised China for its transparency and rapid response to the outbreak of H7N9. In an editorial on April 24, 2013, the journal Nature said "China deserves credit for its rapid response to the outbreaks of H7N9 avian influenza, and its early openness in the reporting and sharing of data." This, in spite of initial worries by Chinese scientists and officials that they might lose credit for their work in isolating and sequencing the novel H7N9 virus, after learning that pharmaceutical company Novartis and the J. Craig Venter Institute had used their sequences to develop US-funded H7N9 vaccine without offering to collaborate with the Chinese team, according to Nature. They believed, the usage of their data was initially not handled in the spirit of the GISAID sharing mechanism, which requires scientists who use the sequences to credit and propose collaboration with those who deposited the data in GISAID. Nature cited a Chinese official who concluded that this situation was quickly mitigated once communication channels were opened and the parties agreed to collaborate, thanks to GISAID president Peter Bogner . Despite concerns that vaccination of poultry against the H5N1 avian influenza virus over the last decade might have made it harder for Chinese veterinary technicians to spot the recent spread of the H7N9 virus, China's Agriculture Ministry defended its policy of large-scale vaccination of poultry against the earlier bird flu strain, saying that it was not interfering with its efforts now to identify the emerging H7N9 virus. On April 15, 2013, the RIWI Corporation, led by researcher Neil Seeman of the University of Toronto released data on 7,016 Chinese "fresh" (i.e. non-panel based) Internet users – with a 24.08% response rate – over 20 hours. The level of contagion awareness was 31% in Beijing, 38% in Hangzhou, 33% in Nanjing, 40% in Shanghai, 52% in Ürümqi, and 28% in Zhengzhou (Chi Square; P = 0.05). The result far exceeds that of other internet surveys, suggesting an intense relevancy of interest and sense of urgency related to the current disease outbreak in the minds of average Chinese citizens. In April 2013, Shanghai's health ministry ordered culling of birds after pigeon samples collected at the Huhuai wholesale agricultural products market in Songjiang District of Shanghai showed H7N9 On April 4, 2013, Shanghai authorities closed a live-poultry-trading zone and began slaughtering all birds. Poultry trading areas in two other areas of the Minhang district were also closed. On April 6, 2013, all Shanghai live poultry markets closed temporarily in response to the H7N9 found in the pigeon samples. The same day, Hangzhou also closed its live poultry markets. After gene sequence analysis, the national avian flu reference laboratory concluded that the strain of the H7N9 virus found on pigeons was highly congenic with those found on persons infected with H7N9 virus, the ministry said. On April 22, 2013, Forbes quoted Chinese state media reporting $2.7 billion in poultry industry losses. When January 2014 brought a dramatic increase in reports of disease, the Chinese government responded by halting live poultry trading in three cities in Zhejiang province where 49 cases and 12 deaths had been reported. In addition, live poultry trading in Shanghai was halted for three months. In Hong Kong, authorities reacted to the discovery of H7N9 in live chickens from the province of Guangdong by suspending imports of fresh poultry from mainland China for 21 days, culling 20,000 chickens, and other measures in an effort to control the spread of the virus. On February 18, 2014, it was announced that the Chinese government would extend the ban for four months. The health minister also said that they plan to prevent diseased birds from entering the market by setting up a facility where imported poultry can be quarantined to ensure they are disease-free. In April 2013, Shanghai's health ministry ordered culling of birds after pigeon samples collected at the Huhuai wholesale agricultural products market in Songjiang District of Shanghai showed H7N9 On April 4, 2013, Shanghai authorities closed a live-poultry-trading zone and began slaughtering all birds. Poultry trading areas in two other areas of the Minhang district were also closed. On April 6, 2013, all Shanghai live poultry markets closed temporarily in response to the H7N9 found in the pigeon samples. The same day, Hangzhou also closed its live poultry markets. After gene sequence analysis, the national avian flu reference laboratory concluded that the strain of the H7N9 virus found on pigeons was highly congenic with those found on persons infected with H7N9 virus, the ministry said. On April 22, 2013, Forbes quoted Chinese state media reporting $2.7 billion in poultry industry losses. When January 2014 brought a dramatic increase in reports of disease, the Chinese government responded by halting live poultry trading in three cities in Zhejiang province where 49 cases and 12 deaths had been reported. In addition, live poultry trading in Shanghai was halted for three months. In Hong Kong, authorities reacted to the discovery of H7N9 in live chickens from the province of Guangdong by suspending imports of fresh poultry from mainland China for 21 days, culling 20,000 chickens, and other measures in an effort to control the spread of the virus. On February 18, 2014, it was announced that the Chinese government would extend the ban for four months. The health minister also said that they plan to prevent diseased birds from entering the market by setting up a facility where imported poultry can be quarantined to ensure they are disease-free. The WHO did not advise against travel to China at that point in time, as there was no evidence of human-to-human transmission of the virus. On April 9, 2013, the Centers for Disease Control and Prevention (CDC) activated its Emergency Operations Center (EOC) in Atlanta at Level II, the second-highest level of alert. Activation was prompted because the novel H7N9 avian influenza virus has never been seen before in animals or humans and because reports from China have linked it to severe human disease. EOC activation will "ensure that internal connections are developed and maintained and that CDC staff are kept informed and up to date with regard to the changing situation." On April 10, 2013, the Public Health Agency of Canada (PHAC) and the Canadian Food Inspection Agency (CFIA) spelled out bio-safety guidance for handling the H7N9 virus. They stated that work with live cultures must be conducted in biosafety level 3 (BSL-3) containment. They also said that studies growing H7N9 virus should not be done in labs that culture human influenza viruses and that personnel should not have contact with susceptible animals for 5 days after handling H7N9 samples. Malaysia announced that it would temporarily ban Chinese chicken imports. Vietnam announced that it would temporarily ban Chinese poultry imports. All hospitals were informed to remain vigilant, and to notify Singapore's Ministry of Health (MOH) immediately of any suspected cases of avian influenza in individuals who have recently returned from affected areas in China. MOH advised returning travellers from affected areas in China (Shanghai, Anhui, Jiangsu, and Zhejiang) to look out for signs and symptoms of respiratory illness, such as fever and cough, and seek early medical attention if they are ill with such symptoms. MOH also advised individuals to inform their doctors of their travel history, should they develop these symptoms after returning to Singapore. On 3 April 2013, the Executive Yuan activated Taiwan's Central Epidemic Command Center (CECC) in response to the epidemic in mainland China. The Executive Yuan deactivated the CECC for H7N9 influenza on 11 April 2014. During this period, 24 meetings were convened with representatives from 24 central government agencies including the Council of Agriculture, the Ministry of Transportation and Communications, and the Ministry of Education, along with 22 city and county governments. Meetings were attended by regional commanding officers and deputy commanding officers of the Communicable Disease Control Network. On 17 May 2013, a ban became effective on the slaughtering of live poultry at traditional wet markets, which eliminated the risk of animal-to-human transmission of avian influenza.

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Avian influenza

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Avian influenza in cats

Cats with avian influenza exhibit symptoms that can result in death. They are one of the few species that can get avian influenza . The specific virus that they get is H5N1, which is a subtype of avian influenza. In order to get the virus, cats need to be in contact with waterfowl, poultry, or uncooked poultry that are infected. Two of the main organs that the virus affects are the lungs and liver. The H5N1 virus has been found in China, Thailand, Vietnam, Indonesia, Iraq, Austria, Germany, and Poland. Besides being found in domestic cats, the virus has infected a variety of wild cats such as the Asiatic golden cat , the clouded leopard , tigers , and leopards . H5N1 was first discovered in domestic and wild cats in Asia, specifically in 2003 in the Thai zoo where two tigers and two leopards died. In 2004, the Thai zoo had 147 tigers that died or were euthanized. This was then followed by an outbreak in Germany in 2006, where three stray cats were found to be either dying or dead during the peak time of the virus outbreak. Currently, as of June 2023, there is an ongoing outbreak in Poland with at least 9 confirmed cases and multiple deaths. Because the virus infects the lungs of cats, it is one of the preferred model animals to study the effects of H5N1 in humans. The most common way a cat can obtain H5N1 is by consuming an infected bird. This has been studied in the 2006 and 2007 cases in Germany and Austria where the strains between the cat and the infected birds were not different between the species. A cat is able to then transfer the virus via the respiratory tract and the digestive tract to other cats. However, studies suggest that a cat cannot transfer the virus to a dog, and vice versa, while sharing a food bowl. Though there is no concrete evidence, there is a potential link between the transfer of the virus between poultry, wild birds, and humans. Once the cat is infected, after an incubation period of 2 to 3 days, the virus can be found in the respiratory tissues, attached to the type II pneumocytes and alveolar macrophages , as well as the intestinal tissues. There have also been some cases where the virus has been found in the brain and other systems in the body. As of right now the H5N1 virus has not adapted to transfer in between mammals, but there is a fear that this can occur. One epidemiological study that was performed in Germany and Austria on 171 cats found that less than 1.8% of this population had H5N1. In this same sample population of cats, less than 2.6% had antibodies to H5N1. Even though Germany and Austria are among the countries that have had naturally occurring cases, this study shows that very few cats have contracted the disease. There have also been studies looking at the T cells , specifically CD4 and CD8, in the cat after viral infection. Though the mechanism is not fully known, there seems to be an inverse relationship with the amount of T cells present and the amount of infected cells. Another study to test whether the ALVAC recombinant canarypox virus could prime the immune system in cats was performed. This vaccine has the same hemagglutinin as the H5N1 virus, and therefore worked on preventing death from two different strains of the virus, HPAIV A/Vietnam/1194/2004 and HPAIV A/Indonesia/05/2005. However, some of the cats that were vaccinated did exhibit hyperthermia and weight loss, and all of the cats did have some disease change (assuming lesions) in their lungs. All of the cats, except one, still excreted the virus even after being vaccinated. One epidemiological study that was performed in Germany and Austria on 171 cats found that less than 1.8% of this population had H5N1. In this same sample population of cats, less than 2.6% had antibodies to H5N1. Even though Germany and Austria are among the countries that have had naturally occurring cases, this study shows that very few cats have contracted the disease. There have also been studies looking at the T cells , specifically CD4 and CD8, in the cat after viral infection. Though the mechanism is not fully known, there seems to be an inverse relationship with the amount of T cells present and the amount of infected cells. Another study to test whether the ALVAC recombinant canarypox virus could prime the immune system in cats was performed. This vaccine has the same hemagglutinin as the H5N1 virus, and therefore worked on preventing death from two different strains of the virus, HPAIV A/Vietnam/1194/2004 and HPAIV A/Indonesia/05/2005. However, some of the cats that were vaccinated did exhibit hyperthermia and weight loss, and all of the cats did have some disease change (assuming lesions) in their lungs. All of the cats, except one, still excreted the virus even after being vaccinated. A cat that is infected with a high dose of the virus can show signs of fever , lethargy , and dyspnea . There have even been recorded cases where a cat has neurological symptoms such as circling or ataxia . In a case in February 2004, a 2-year-old male cat was panting and convulsing on top of having a fever two days prior to death. This cat also had lesions that were identified as renal congestion, pulmonary congestion, edema , and pneumonia . Upon inspection, the cat also had cerebral congestion, conjunctivitis , and hemorrhaging in the serosae of the intestines . However, a cat that is infected with a low dose of the virus may not necessarily show symptoms. Though they may be asymptomatic, they can still transfer small amounts of the virus. Cats can be protected from H5N1 if they are given a vaccination, as mentioned above. However, it was also found that cats can still shed some of the virus but in low numbers. If a cat is exhibiting symptoms, they should be put into isolation and kept indoors. Then they should be taken to a vet to get tested for the presence of H5N1. If there is a possibility that the cat has Avian Influenza, then there should be extra care when handling the cat. Some of the precautions include avoiding all direct contact with the cat by wearing gloves, masks, and goggles. Whatever surfaces the cat comes in contact with should be disinfected with standard household cleaners. Researchers have given tigers an antiviral treatment of Oseltamivir with a dose of 75 mg/60 kg two times a day. The specific dosage was extrapolated from human data, but there hasn't been any data to suggest protection. As with many antiviral treatments, the dosage depends on the species.

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Avian influenza

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Influenza

Influenza , commonly known as " the flu " or just " flu ", is an infectious disease caused by influenza viruses . Symptoms range from mild to severe and often include fever , runny nose , sore throat , muscle pain , headache , coughing , and fatigue . These symptoms begin one to four days after exposure to the virus (typically two days) and last for about 2–8 days. Diarrhea and vomiting can occur, particularly in children. Influenza may progress to pneumonia from the virus or a subsequent bacterial infection. Other complications include acute respiratory distress syndrome , meningitis , encephalitis , and worsening of pre-existing health problems such as asthma and cardiovascular disease . There are four types of influenza virus: A, B, C, and D. Aquatic birds are the primary source of Influenza A virus (IAV), which is also widespread in various mammals, including humans and pigs. Influenza B virus (IBV) and Influenza C virus (ICV) primarily infect humans, and Influenza D virus (IDV) is found in cattle and pigs. IAV and IBV circulate in humans and cause seasonal epidemics, and ICV causes a mild infection, primarily in children. IDV can infect humans but is not known to cause illness. In humans, influenza viruses are primarily transmitted through respiratory droplets from coughing and sneezing. Transmission through aerosols and surfaces contaminated by the virus also occur. Frequent hand washing and covering one's mouth and nose when coughing and sneezing reduce transmission. Annual vaccination can help to provide protection against influenza. Influenza viruses, particularly IAV, evolve quickly, so flu vaccines are updated regularly to match which influenza strains are in circulation. Vaccines provide protection against IAV subtypes H1N1 and H3N2 and one or two IBV subtypes. Influenza infection is diagnosed with laboratory methods such as antibody or antigen tests and a polymerase chain reaction ( PCR ) to identify viral nucleic acid. The disease can be treated with supportive measures and, in severe cases, with antiviral drugs such as oseltamivir . In healthy individuals, influenza is typically self-limiting and rarely fatal, but it can be deadly in high-risk groups. In a typical year, 5–15% of the population contracts influenza. There are 3–5 million severe cases annually, with up to 650,000 respiratory-related deaths globally each year. Deaths most commonly occur in high-risk groups, including young children, the elderly, and people with chronic health conditions. In temperate regions of the world, the number of influenza cases peaks during winter, whereas in the tropics influenza can occur year-round. Since the late 1800s, large outbreaks of novel influenza strains that spread globally, called pandemics, have occurred every 10–50 years. Five flu pandemics have occurred since 1900: the Spanish flu in 1918–1920, which was the most severe flu pandemic, the Asian flu in 1957, the Hong Kong flu in 1968, the Russian flu in 1977, and the swine flu pandemic in 2009.The symptoms of influenza are similar to those of a cold, although usually more severe and less likely to include a runny nose . The time between exposure to the virus and development of symptoms, called the incubation period , is 1–4 days, most commonly 1–2 days. Many infections, however, are asymptomatic. The onset of symptoms is sudden, and initial symptoms are predominately non-specific, including fever, chills, headaches, muscle pain or aching , a feeling of discomfort , loss of appetite , lack of energy/fatigue, and confusion. These symptoms are usually accompanied by respiratory symptoms such as a dry cough, sore or dry throat, hoarse voice, and a stuffy or runny nose. Coughing is the most common symptom. Gastrointestinal symptoms may also occur, including nausea, vomiting, diarrhea, and gastroenteritis, especially in children. The standard influenza symptoms typically last for 2–8 days. A 2021 study suggests influenza can cause long lasting symptoms in a similar way to long COVID . Symptomatic infections are usually mild and limited to the upper respiratory tract, but progression to pneumonia is relatively common. Pneumonia may be caused by the primary viral infection or by a secondary bacterial infection. Primary pneumonia is characterized by rapid progression of fever, cough, labored breathing, and low oxygen levels that cause bluish skin. It is especially common among those who have an underlying cardiovascular disease such as rheumatic heart disease. Secondary pneumonia typically has a period of improvement in symptoms for 1–3 weeks followed by recurrent fever, sputum production, and fluid buildup in the lungs, but can also occur just a few days after influenza symptoms appear. About a third of primary pneumonia cases are followed by secondary pneumonia, which is most frequently caused by the bacteria Streptococcus pneumoniae and Staphylococcus aureus . Influenza viruses comprise four species. Each of the four species is the sole member of its own genus, and the four influenza genera comprise four of the seven genera in the family Orthomyxoviridae . They are: IAV is responsible for most cases of severe illness as well as seasonal epidemics and occasional pandemics. It infects people of all ages but tends to disproportionately cause severe illness in the elderly, the very young, and those who have chronic health issues. Birds are the primary reservoir of IAV, especially aquatic birds such as ducks, geese, shorebirds, and gulls, but the virus also circulates among mammals, including pigs, horses, and marine mammals. IAV is classified into subtypes based on the viral proteins haemagglutinin (H) and neuraminidase (N). As of 2019, 18 H subtypes and 11 N subtypes have been identified. Most potential combinations have been reported in birds, but H17-18 and N10-11 have only been found in bats. Only H subtypes H1-3 and N subtypes N1-2 are known to have circulated in humans. The IAV subtypes in circulation as of 2018 [ update ] are H1N1 and H3N2. IAVs can be classified more specifically by natural host species, geographical origin, year of isolation, and strain number, such as H1N1/A/duck/Alberta/35/76. IBV mainly infects humans but has been identified in seals, horses, dogs, and pigs. IBV does not have subtypes like IAV but has two antigenically distinct lineages, termed the B/Victoria/2/1987-like and B/Yamagata/16/1988-like lineages, or simply (B/)Victoria(-like) and (B/)Yamagata(-like). Both lineages are in circulation in humans, disproportionately affecting children. IBVs contribute to seasonal epidemics alongside IAVs but have never been associated with a pandemic. ICV, like IBV, is primarily found in humans, though it also has been detected in pigs, feral dogs, dromedary camels, cattle, and dogs. ICV infection primarily affects children and is usually asymptomatic or has mild cold-like symptoms, though more severe symptoms such as gastroenteritis and pneumonia can occur. Unlike IAV and IBV, ICV has not been a major focus of research pertaining to antiviral drugs, vaccines, and other measures against influenza. ICV is subclassified into six genetic/antigenic lineages. IDV has been isolated from pigs and cattle, the latter being the natural reservoir. Infection has also been observed in humans, horses, dromedary camels, and small ruminants such as goats and sheep. IDV is distantly related to ICV. While cattle workers have occasionally tested positive to prior IDV infection, it is not known to cause disease in humans. ICV and IDV experience a slower rate of antigenic evolution than IAV and IBV. Because of this antigenic stability, relatively few novel lineages emerge. Influenza viruses have a negative-sense , single-stranded RNA genome that is segmented. The negative sense of the genome means it can be used as a template to synthesize messenger RNA (mRNA). IAV and IBV have eight genome segments that encode 10 major proteins. ICV and IDV have seven genome segments that encode nine major proteins. Three segments encode three subunits of an RNA-dependent RNA polymerase (RdRp) complex: PB1, a transcriptase, PB2, which recognizes 5' caps, and PA (P3 for ICV and IDV), an endonuclease. The matrix protein (M1) and membrane protein (M2) share a segment, as do the non-structural protein (NS1) and the nuclear export protein (NEP). For IAV and IBV, hemagglutinin (HA) and neuraminidase (NA) are encoded on one segment each, whereas ICV and IDV encode a hemagglutinin-esterase fusion (HEF) protein on one segment that merges the functions of HA and NA. The final genome segment encodes the viral nucleoprotein (NP). Influenza viruses also encode various accessory proteins, such as PB1-F2 and PA-X, that are expressed through alternative open reading frames and which are important in host defense suppression, virulence, and pathogenicity. The virus particle, called a virion, is pleomorphic and varies between being filamentous, bacilliform, or spherical in shape. Clinical isolates tend to be pleomorphic, whereas strains adapted to laboratory growth typically produce spherical virions. Filamentous virions are about 250 nanometers (nm) by 80 nm, bacilliform 120–250 by 95 nm, and spherical 120 nm in diameter. The virion consists of each segment of the genome bound to nucleoproteins in separate ribonucleoprotein (RNP) complexes for each segment, all of which are surrounded by a lipid bilayer membrane called the viral envelope . There is a copy of the RdRp, all subunits included, bound to each RNP. The envelope is reinforced structurally by matrix proteins on the interior that enclose the RNPs, and the envelope contains HA and NA (or HEF ) proteins extending outward from the exterior surface of the envelope. HA and HEF proteins have a distinct "head" and "stalk" structure. M2 proteins form proton ion channels through the viral envelope that are required for viral entry and exit. IBVs contain a surface protein named NB that is anchored in the envelope, but its function is unknown. The viral life cycle begins by binding to a target cell. Binding is mediated by the viral HA proteins on the surface of the envelope, which bind to cells that contain sialic acid receptors on the surface of the cell membrane. For N1 subtypes with the "G147R" mutation and N2 subtypes, the NA protein can initiate entry. Prior to binding, NA proteins promote access to target cells by degrading mucus, which helps to remove extracellular decoy receptors that would impede access to target cells. After binding, the virus is internalized into the cell by an endosome that contains the virion inside it. The endosome is acidified by cellular vATPase to have lower pH, which triggers a conformational change in HA that allows fusion of the viral envelope with the endosomal membrane. At the same time, hydrogen ions diffuse into the virion through M2 ion channels, disrupting internal protein-protein interactions to release RNPs into the host cell's cytosol . The M1 protein shell surrounding RNPs is degraded, fully uncoating RNPs in the cytosol. RNPs are then imported into the nucleus with the help of viral localization signals. There, the viral RNA polymerase transcribes mRNA using the genomic negative-sense strand as a template. The polymerase snatches 5' caps for viral mRNA from cellular RNA to prime mRNA synthesis and the 3'-end of mRNA is polyadenylated at the end of transcription. Once viral mRNA is transcribed, it is exported out of the nucleus and translated by host ribosomes in a cap-dependent manner to synthesize viral proteins. RdRp also synthesizes complementary positive-sense strands of the viral genome in a complementary RNP complex which are then used as templates by viral polymerases to synthesize copies of the negative-sense genome. During these processes, RdRps of avian influenza viruses (AIVs) function optimally at a higher temperature than mammalian influenza viruses. Newly synthesized viral polymerase subunits and NP proteins are imported to the nucleus to further increase the rate of viral replication and form RNPs. HA, NA, and M2 proteins are trafficked with the aid of M1 and NEP proteins to the cell membrane through the Golgi apparatus and inserted into the cell's membrane. Viral non-structural proteins including NS1, PB1-F2, and PA-X regulate host cellular processes to disable antiviral responses. PB1-F2 also interacts with PB1 to keep polymerases in the nucleus longer. M1 and NEP proteins localize to the nucleus during the later stages of infection, bind to viral RNPs and mediate their export to the cytoplasm where they migrate to the cell membrane with the aid of recycled endosomes and are bundled into the segments of the genome. Progeny viruses leave the cell by budding from the cell membrane, which is initiated by the accumulation of M1 proteins at the cytoplasmic side of the membrane. The viral genome is incorporated inside a viral envelope derived from portions of the cell membrane that have HA, NA, and M2 proteins. At the end of budding, HA proteins remain attached to cellular sialic acid until they are cleaved by the sialidase activity of NA proteins. The virion is then released from the cell. The sialidase activity of NA also cleaves any sialic acid residues from the viral surface, which helps prevent newly assembled viruses from aggregating near the cell surface and improving infectivity. Similar to other aspects of influenza replication, optimal NA activity is temperature- and pH-dependent. Ultimately, presence of large quantities of viral RNA in the cell triggers apoptosis, i.e. programmed cell death, which is initiated by cellular factors to restrict viral replication. Two key processes that influenza viruses evolve through are antigenic drift and antigenic shift . Antigenic drift is when an influenza virus' antigens change due to the gradual accumulation of mutations in the antigen's (HA or NA) gene. This can occur in response to evolutionary pressure exerted by the host immune response. Antigenic drift is especially common for the HA protein, in which just a few amino acid changes in the head region can constitute antigenic drift. The result is the production of novel strains that can evade pre-existing antibody-mediated immunity. Antigenic drift occurs in all influenza species but is slower in B than A and slowest in C and D. Antigenic drift is a major cause of seasonal influenza, and requires that flu vaccines be updated annually. HA is the main component of inactivated vaccines, so surveillance monitors antigenic drift of this antigen among circulating strains. Antigenic evolution of influenza viruses of humans appears to be faster than influenza viruses in swine and equines. In wild birds, within-subtype antigenic variation appears to be limited but has been observed in poultry. Antigenic shift is a sudden, drastic change in an influenza virus' antigen, usually HA. During antigenic shift, antigenically different strains that infect the same cell can reassort genome segments with each other, producing hybrid progeny. Since all influenza viruses have segmented genomes, all are capable of reassortment. Antigenic shift, however, only occurs among influenza viruses of the same genus and most commonly occurs among IAVs. In particular, reassortment is very common in AIVs, creating a large diversity of influenza viruses in birds, but is uncommon in human, equine, and canine lineages. Pigs, bats, and quails have receptors for both mammalian and avian IAVs, so they are potential "mixing vessels" for reassortment. If an animal strain reassorts with a human strain, then a novel strain can emerge that is capable of human-to-human transmission. This has caused pandemics, but only a limited number have occurred, so it is difficult to predict when the next will happen. Influenza viruses comprise four species. Each of the four species is the sole member of its own genus, and the four influenza genera comprise four of the seven genera in the family Orthomyxoviridae . They are: IAV is responsible for most cases of severe illness as well as seasonal epidemics and occasional pandemics. It infects people of all ages but tends to disproportionately cause severe illness in the elderly, the very young, and those who have chronic health issues. Birds are the primary reservoir of IAV, especially aquatic birds such as ducks, geese, shorebirds, and gulls, but the virus also circulates among mammals, including pigs, horses, and marine mammals. IAV is classified into subtypes based on the viral proteins haemagglutinin (H) and neuraminidase (N). As of 2019, 18 H subtypes and 11 N subtypes have been identified. Most potential combinations have been reported in birds, but H17-18 and N10-11 have only been found in bats. Only H subtypes H1-3 and N subtypes N1-2 are known to have circulated in humans. The IAV subtypes in circulation as of 2018 [ update ] are H1N1 and H3N2. IAVs can be classified more specifically by natural host species, geographical origin, year of isolation, and strain number, such as H1N1/A/duck/Alberta/35/76. IBV mainly infects humans but has been identified in seals, horses, dogs, and pigs. IBV does not have subtypes like IAV but has two antigenically distinct lineages, termed the B/Victoria/2/1987-like and B/Yamagata/16/1988-like lineages, or simply (B/)Victoria(-like) and (B/)Yamagata(-like). Both lineages are in circulation in humans, disproportionately affecting children. IBVs contribute to seasonal epidemics alongside IAVs but have never been associated with a pandemic. ICV, like IBV, is primarily found in humans, though it also has been detected in pigs, feral dogs, dromedary camels, cattle, and dogs. ICV infection primarily affects children and is usually asymptomatic or has mild cold-like symptoms, though more severe symptoms such as gastroenteritis and pneumonia can occur. Unlike IAV and IBV, ICV has not been a major focus of research pertaining to antiviral drugs, vaccines, and other measures against influenza. ICV is subclassified into six genetic/antigenic lineages. IDV has been isolated from pigs and cattle, the latter being the natural reservoir. Infection has also been observed in humans, horses, dromedary camels, and small ruminants such as goats and sheep. IDV is distantly related to ICV. While cattle workers have occasionally tested positive to prior IDV infection, it is not known to cause disease in humans. ICV and IDV experience a slower rate of antigenic evolution than IAV and IBV. Because of this antigenic stability, relatively few novel lineages emerge. Influenza viruses have a negative-sense , single-stranded RNA genome that is segmented. The negative sense of the genome means it can be used as a template to synthesize messenger RNA (mRNA). IAV and IBV have eight genome segments that encode 10 major proteins. ICV and IDV have seven genome segments that encode nine major proteins. Three segments encode three subunits of an RNA-dependent RNA polymerase (RdRp) complex: PB1, a transcriptase, PB2, which recognizes 5' caps, and PA (P3 for ICV and IDV), an endonuclease. The matrix protein (M1) and membrane protein (M2) share a segment, as do the non-structural protein (NS1) and the nuclear export protein (NEP). For IAV and IBV, hemagglutinin (HA) and neuraminidase (NA) are encoded on one segment each, whereas ICV and IDV encode a hemagglutinin-esterase fusion (HEF) protein on one segment that merges the functions of HA and NA. The final genome segment encodes the viral nucleoprotein (NP). Influenza viruses also encode various accessory proteins, such as PB1-F2 and PA-X, that are expressed through alternative open reading frames and which are important in host defense suppression, virulence, and pathogenicity. The virus particle, called a virion, is pleomorphic and varies between being filamentous, bacilliform, or spherical in shape. Clinical isolates tend to be pleomorphic, whereas strains adapted to laboratory growth typically produce spherical virions. Filamentous virions are about 250 nanometers (nm) by 80 nm, bacilliform 120–250 by 95 nm, and spherical 120 nm in diameter. The virion consists of each segment of the genome bound to nucleoproteins in separate ribonucleoprotein (RNP) complexes for each segment, all of which are surrounded by a lipid bilayer membrane called the viral envelope . There is a copy of the RdRp, all subunits included, bound to each RNP. The envelope is reinforced structurally by matrix proteins on the interior that enclose the RNPs, and the envelope contains HA and NA (or HEF ) proteins extending outward from the exterior surface of the envelope. HA and HEF proteins have a distinct "head" and "stalk" structure. M2 proteins form proton ion channels through the viral envelope that are required for viral entry and exit. IBVs contain a surface protein named NB that is anchored in the envelope, but its function is unknown. The viral life cycle begins by binding to a target cell. Binding is mediated by the viral HA proteins on the surface of the envelope, which bind to cells that contain sialic acid receptors on the surface of the cell membrane. For N1 subtypes with the "G147R" mutation and N2 subtypes, the NA protein can initiate entry. Prior to binding, NA proteins promote access to target cells by degrading mucus, which helps to remove extracellular decoy receptors that would impede access to target cells. After binding, the virus is internalized into the cell by an endosome that contains the virion inside it. The endosome is acidified by cellular vATPase to have lower pH, which triggers a conformational change in HA that allows fusion of the viral envelope with the endosomal membrane. At the same time, hydrogen ions diffuse into the virion through M2 ion channels, disrupting internal protein-protein interactions to release RNPs into the host cell's cytosol . The M1 protein shell surrounding RNPs is degraded, fully uncoating RNPs in the cytosol. RNPs are then imported into the nucleus with the help of viral localization signals. There, the viral RNA polymerase transcribes mRNA using the genomic negative-sense strand as a template. The polymerase snatches 5' caps for viral mRNA from cellular RNA to prime mRNA synthesis and the 3'-end of mRNA is polyadenylated at the end of transcription. Once viral mRNA is transcribed, it is exported out of the nucleus and translated by host ribosomes in a cap-dependent manner to synthesize viral proteins. RdRp also synthesizes complementary positive-sense strands of the viral genome in a complementary RNP complex which are then used as templates by viral polymerases to synthesize copies of the negative-sense genome. During these processes, RdRps of avian influenza viruses (AIVs) function optimally at a higher temperature than mammalian influenza viruses. Newly synthesized viral polymerase subunits and NP proteins are imported to the nucleus to further increase the rate of viral replication and form RNPs. HA, NA, and M2 proteins are trafficked with the aid of M1 and NEP proteins to the cell membrane through the Golgi apparatus and inserted into the cell's membrane. Viral non-structural proteins including NS1, PB1-F2, and PA-X regulate host cellular processes to disable antiviral responses. PB1-F2 also interacts with PB1 to keep polymerases in the nucleus longer. M1 and NEP proteins localize to the nucleus during the later stages of infection, bind to viral RNPs and mediate their export to the cytoplasm where they migrate to the cell membrane with the aid of recycled endosomes and are bundled into the segments of the genome. Progeny viruses leave the cell by budding from the cell membrane, which is initiated by the accumulation of M1 proteins at the cytoplasmic side of the membrane. The viral genome is incorporated inside a viral envelope derived from portions of the cell membrane that have HA, NA, and M2 proteins. At the end of budding, HA proteins remain attached to cellular sialic acid until they are cleaved by the sialidase activity of NA proteins. The virion is then released from the cell. The sialidase activity of NA also cleaves any sialic acid residues from the viral surface, which helps prevent newly assembled viruses from aggregating near the cell surface and improving infectivity. Similar to other aspects of influenza replication, optimal NA activity is temperature- and pH-dependent. Ultimately, presence of large quantities of viral RNA in the cell triggers apoptosis, i.e. programmed cell death, which is initiated by cellular factors to restrict viral replication. Two key processes that influenza viruses evolve through are antigenic drift and antigenic shift . Antigenic drift is when an influenza virus' antigens change due to the gradual accumulation of mutations in the antigen's (HA or NA) gene. This can occur in response to evolutionary pressure exerted by the host immune response. Antigenic drift is especially common for the HA protein, in which just a few amino acid changes in the head region can constitute antigenic drift. The result is the production of novel strains that can evade pre-existing antibody-mediated immunity. Antigenic drift occurs in all influenza species but is slower in B than A and slowest in C and D. Antigenic drift is a major cause of seasonal influenza, and requires that flu vaccines be updated annually. HA is the main component of inactivated vaccines, so surveillance monitors antigenic drift of this antigen among circulating strains. Antigenic evolution of influenza viruses of humans appears to be faster than influenza viruses in swine and equines. In wild birds, within-subtype antigenic variation appears to be limited but has been observed in poultry. Antigenic shift is a sudden, drastic change in an influenza virus' antigen, usually HA. During antigenic shift, antigenically different strains that infect the same cell can reassort genome segments with each other, producing hybrid progeny. Since all influenza viruses have segmented genomes, all are capable of reassortment. Antigenic shift, however, only occurs among influenza viruses of the same genus and most commonly occurs among IAVs. In particular, reassortment is very common in AIVs, creating a large diversity of influenza viruses in birds, but is uncommon in human, equine, and canine lineages. Pigs, bats, and quails have receptors for both mammalian and avian IAVs, so they are potential "mixing vessels" for reassortment. If an animal strain reassorts with a human strain, then a novel strain can emerge that is capable of human-to-human transmission. This has caused pandemics, but only a limited number have occurred, so it is difficult to predict when the next will happen. People who are infected can transmit influenza viruses through breathing, talking, coughing, and sneezing, which spread respiratory droplets and aerosols that contain virus particles into the air. A person susceptible to infection can then contract influenza by coming into contact with these particles. Respiratory droplets are relatively large and travel less than two meters before falling onto nearby surfaces. Aerosols are smaller and remain suspended in the air longer, so they take longer to settle and can travel further than respiratory droplets. Inhalation of aerosols can lead to infection, but most transmission is in the area about two meters around an infected person via respiratory droplets that come into contact with mucosa of the upper respiratory tract. Transmission through contact with a person, bodily fluids, or intermediate objects ( fomites ) can also occur, such as through contaminated hands and surfaces since influenza viruses can survive for hours on non-porous surfaces. If one's hands are contaminated, then touching one's face can cause infection. Influenza is usually transmissible from one day before the onset of symptoms to 5–7 days after. In healthy adults, the virus is shed for up to 3–5 days. In children and the immunocompromised, the virus may be transmissible for several weeks. Children ages 2–17 are considered to be the primary and most efficient spreaders of influenza. Children who have not had multiple prior exposures to influenza viruses shed the virus at greater quantities and for a longer duration than other children. People who are at risk of exposure to influenza include health care workers, social care workers, and those who live with or care for people vulnerable to influenza. In long-term care facilities, the flu can spread rapidly after it is introduced. A variety of factors likely encourage influenza transmission, including lower temperature, lower absolute and relative humidity , less ultraviolet radiation from the Sun, and crowding. Influenza viruses that infect the upper respiratory tract like H1N1 tend to be more mild but more transmissible, whereas those that infect the lower respiratory tract like H5N1 tend to cause more severe illness but are less contagious. In humans, influenza viruses first cause infection by infecting epithelial cells in the respiratory tract. Illness during infection is primarily the result of lung inflammation and compromise caused by epithelial cell infection and death, combined with inflammation caused by the immune system's response to infection. Non-respiratory organs can become involved, but the mechanisms by which influenza is involved in these cases are unknown. Severe respiratory illness can be caused by multiple, non-exclusive mechanisms, including obstruction of the airways, loss of alveolar structure, loss of lung epithelial integrity due to epithelial cell infection and death, and degradation of the extracellular matrix that maintains lung structure. In particular, alveolar cell infection appears to drive severe symptoms since this results in impaired gas exchange and enables viruses to infect endothelial cells, which produce large quantities of pro-inflammatory cytokines . Pneumonia caused by influenza viruses is characterized by high levels of viral replication in the lower respiratory tract, accompanied by a strong pro-inflammatory response called a cytokine storm . Infection with H5N1 or H7N9 especially produces high levels of pro-inflammatory cytokines. In bacterial infections, early depletion of macrophages during influenza creates a favorable environment in the lungs for bacterial growth since these white blood cells are important in responding to bacterial infection. Host mechanisms to encourage tissue repair may inadvertently allow bacterial infection. Infection also induces production of systemic glucocorticoids that can reduce inflammation to preserve tissue integrity but allow increased bacterial growth. The pathophysiology of influenza is significantly influenced by which receptors influenza viruses bind to during entry into cells. Mammalian influenza viruses preferentially bind to sialic acids connected to the rest of the oligosaccharide by an α-2,6 link, most commonly found in various respiratory cells, such as respiratory and retinal epithelial cells. AIVs prefer sialic acids with an α-2,3 linkage, which are most common in birds in gastrointestinal epithelial cells and in humans in the lower respiratory tract. Furthermore, cleavage of the HA protein into HA 1 , the binding subunit, and HA 2 , the fusion subunit, is performed by different proteases, affecting which cells can be infected. For mammalian influenza viruses and low pathogenic AIVs, cleavage is extracellular, which limits infection to cells that have the appropriate proteases, whereas for highly pathogenic AIVs, cleavage is intracellular and performed by ubiquitous proteases, which allows for infection of a greater variety of cells, thereby contributing to more severe disease. Cells possess sensors to detect viral RNA, which can then induce interferon production. Interferons mediate expression of antiviral proteins and proteins that recruit immune cells to the infection site, and they also notify nearby uninfected cells of infection. Some infected cells release pro-inflammatory cytokines that recruit immune cells to the site of infection. Immune cells control viral infection by killing infected cells and phagocytizing viral particles and apoptotic cells. An exacerbated immune response, however, can harm the host organism through a cytokine storm. To counter the immune response, influenza viruses encode various non-structural proteins, including NS1, NEP, PB1-F2, and PA-X, that are involved in curtailing the host immune response by suppressing interferon production and host gene expression. B cells , a type of white blood cell, produce antibodies that bind to influenza antigens HA and NA (or HEF ) and other proteins to a lesser degree. Once bound to these proteins, antibodies block virions from binding to cellular receptors, neutralizing the virus. In humans, a sizeable antibody response occurs ~1 week after viral exposure. This antibody response is typically robust and long-lasting, especially for ICV and IDV. In other words, people exposed to a certain strain in childhood still possess antibodies to that strain at a reasonable level later in life, which can provide some protection to related strains. There is, however, an " original antigenic sin ", in which the first HA subtype a person is exposed to influences the antibody-based immune response to future infections and vaccines. People who are infected can transmit influenza viruses through breathing, talking, coughing, and sneezing, which spread respiratory droplets and aerosols that contain virus particles into the air. A person susceptible to infection can then contract influenza by coming into contact with these particles. Respiratory droplets are relatively large and travel less than two meters before falling onto nearby surfaces. Aerosols are smaller and remain suspended in the air longer, so they take longer to settle and can travel further than respiratory droplets. Inhalation of aerosols can lead to infection, but most transmission is in the area about two meters around an infected person via respiratory droplets that come into contact with mucosa of the upper respiratory tract. Transmission through contact with a person, bodily fluids, or intermediate objects ( fomites ) can also occur, such as through contaminated hands and surfaces since influenza viruses can survive for hours on non-porous surfaces. If one's hands are contaminated, then touching one's face can cause infection. Influenza is usually transmissible from one day before the onset of symptoms to 5–7 days after. In healthy adults, the virus is shed for up to 3–5 days. In children and the immunocompromised, the virus may be transmissible for several weeks. Children ages 2–17 are considered to be the primary and most efficient spreaders of influenza. Children who have not had multiple prior exposures to influenza viruses shed the virus at greater quantities and for a longer duration than other children. People who are at risk of exposure to influenza include health care workers, social care workers, and those who live with or care for people vulnerable to influenza. In long-term care facilities, the flu can spread rapidly after it is introduced. A variety of factors likely encourage influenza transmission, including lower temperature, lower absolute and relative humidity , less ultraviolet radiation from the Sun, and crowding. Influenza viruses that infect the upper respiratory tract like H1N1 tend to be more mild but more transmissible, whereas those that infect the lower respiratory tract like H5N1 tend to cause more severe illness but are less contagious. In humans, influenza viruses first cause infection by infecting epithelial cells in the respiratory tract. Illness during infection is primarily the result of lung inflammation and compromise caused by epithelial cell infection and death, combined with inflammation caused by the immune system's response to infection. Non-respiratory organs can become involved, but the mechanisms by which influenza is involved in these cases are unknown. Severe respiratory illness can be caused by multiple, non-exclusive mechanisms, including obstruction of the airways, loss of alveolar structure, loss of lung epithelial integrity due to epithelial cell infection and death, and degradation of the extracellular matrix that maintains lung structure. In particular, alveolar cell infection appears to drive severe symptoms since this results in impaired gas exchange and enables viruses to infect endothelial cells, which produce large quantities of pro-inflammatory cytokines . Pneumonia caused by influenza viruses is characterized by high levels of viral replication in the lower respiratory tract, accompanied by a strong pro-inflammatory response called a cytokine storm . Infection with H5N1 or H7N9 especially produces high levels of pro-inflammatory cytokines. In bacterial infections, early depletion of macrophages during influenza creates a favorable environment in the lungs for bacterial growth since these white blood cells are important in responding to bacterial infection. Host mechanisms to encourage tissue repair may inadvertently allow bacterial infection. Infection also induces production of systemic glucocorticoids that can reduce inflammation to preserve tissue integrity but allow increased bacterial growth. The pathophysiology of influenza is significantly influenced by which receptors influenza viruses bind to during entry into cells. Mammalian influenza viruses preferentially bind to sialic acids connected to the rest of the oligosaccharide by an α-2,6 link, most commonly found in various respiratory cells, such as respiratory and retinal epithelial cells. AIVs prefer sialic acids with an α-2,3 linkage, which are most common in birds in gastrointestinal epithelial cells and in humans in the lower respiratory tract. Furthermore, cleavage of the HA protein into HA 1 , the binding subunit, and HA 2 , the fusion subunit, is performed by different proteases, affecting which cells can be infected. For mammalian influenza viruses and low pathogenic AIVs, cleavage is extracellular, which limits infection to cells that have the appropriate proteases, whereas for highly pathogenic AIVs, cleavage is intracellular and performed by ubiquitous proteases, which allows for infection of a greater variety of cells, thereby contributing to more severe disease. Cells possess sensors to detect viral RNA, which can then induce interferon production. Interferons mediate expression of antiviral proteins and proteins that recruit immune cells to the infection site, and they also notify nearby uninfected cells of infection. Some infected cells release pro-inflammatory cytokines that recruit immune cells to the site of infection. Immune cells control viral infection by killing infected cells and phagocytizing viral particles and apoptotic cells. An exacerbated immune response, however, can harm the host organism through a cytokine storm. To counter the immune response, influenza viruses encode various non-structural proteins, including NS1, NEP, PB1-F2, and PA-X, that are involved in curtailing the host immune response by suppressing interferon production and host gene expression. B cells , a type of white blood cell, produce antibodies that bind to influenza antigens HA and NA (or HEF ) and other proteins to a lesser degree. Once bound to these proteins, antibodies block virions from binding to cellular receptors, neutralizing the virus. In humans, a sizeable antibody response occurs ~1 week after viral exposure. This antibody response is typically robust and long-lasting, especially for ICV and IDV. In other words, people exposed to a certain strain in childhood still possess antibodies to that strain at a reasonable level later in life, which can provide some protection to related strains. There is, however, an " original antigenic sin ", in which the first HA subtype a person is exposed to influences the antibody-based immune response to future infections and vaccines. Annual vaccination is the primary and most effective way to prevent influenza and influenza-associated complications, especially for high-risk groups. Vaccines against the flu are trivalent or quadrivalent, providing protection against an H1N1 strain, an H3N2 strain, and one or two IBV strains corresponding to the two IBV lineages. Two types of vaccines are in use: inactivated vaccines that contain "killed" (i.e. inactivated) viruses and live attenuated influenza vaccines (LAIVs) that contain weakened viruses. There are three types of inactivated vaccines: whole virus, split virus, in which the virus is disrupted by a detergent, and subunit, which only contains the viral antigens HA and NA. Most flu vaccines are inactivated and administered via intramuscular injection. LAIVs are sprayed into the nasal cavity. Vaccination recommendations vary by country. Some recommend vaccination for all people above a certain age, such as 6 months, whereas other countries limit recommendations to high-risk groups. Young infants cannot receive flu vaccines for safety reasons, but they can inherit passive immunity from their mother if inactivated vaccines are administered to the mother during pregnancy. Influenza vaccination helps to reduce the probability of reassortment. In general, influenza vaccines are only effective if there is an antigenic match between vaccine strains and circulating strains. Additionally, most commercially available flu vaccines are manufactured by propagation of influenza viruses in embryonated chicken eggs, taking 6–8 months. Flu seasons are different in the northern and southern hemisphere, so the WHO meets twice a year, one for each hemisphere, to discuss which strains should be included in flu vaccines based on observation from HA inhibition assays. Other manufacturing methods include an MDCK cell culture-based inactivated vaccine and a recombinant subunit vaccine manufactured from baculovirus overexpression in insect cells. Influenza can be prevented or reduced in severity by post-exposure prophylaxis with the antiviral drugs oseltamivir , which can be taken orally by those at least three months old, and zanamivir , which can be inhaled by those above seven years of age. Chemoprophylaxis is most useful for individuals at high-risk of developing complications and those who cannot receive the flu vaccine due to contraindications or lack of effectiveness. Post-exposure chemoprophylaxis is only recommended if oseltamivir is taken within 48 hours of contact with a confirmed or suspected influenza case and zanamivir within 36 hours. It is recommended that it be offered to people who have yet to receive a vaccine for the current flu season, who have been vaccinated less than two week since contact, if there is a significant mismatch between vaccine and circulating strains, or during an outbreak in a closed setting regardless of vaccination history. Hand hygiene is important in reducing the spread of influenza. This includes frequent hand washing with soap and water, using alcohol -based hand sanitizers , and not touching one's eyes, nose, and mouth with one's hands. Covering one's nose and mouth when coughing or sneezing is important. Other methods to limit influenza transmission include staying home when sick, avoiding contact with others until one day after symptoms end, and disinfecting surfaces likely to be contaminated by the virus. Health education through media and posters is often used to remind people of hygiene. There is uncertainty about the use of masks since research thus far has not shown a significant reduction in seasonal influenza with mask usage. Likewise, the effectiveness of screening at points of entry into countries is not well researched. Social distancing measures such as school closures, avoiding contact with infected people via isolation or quarantine, and limiting mass gatherings may reduce transmission, but these measures are often expensive, unpopular, and difficult to implement. Consequently, the commonly recommended methods of infection control are respiratory etiquette, hand hygiene, and mask wearing, which are inexpensive and easy to perform. Pharmaceutical measures are effective but may not be available in the early stages of an outbreak. In health care settings, infected individuals may be cohorted or assigned to individual rooms. Protective clothing such as masks, gloves, and gowns is recommended when coming into contact with infected individuals if there is a risk of exposure to infected bodily fluids. Keeping patients in negative pressure rooms and avoiding aerosol-producing activities may help, but special air handling and ventilation systems are not considered necessary to prevent the spread of influenza in the air. In residential homes, new admissions may need to be closed until the spread of influenza is controlled. When discharging patients to care homes, it is important to take care if there is a known influenza outbreak. Since influenza viruses circulate in animals such as birds and pigs, prevention of transmission from these animals is important. Water treatment , indoor raising of animals, quarantining sick animals, vaccination, and biosecurity are the primary measures used. Placing poultry houses and piggeries on high ground away from high-density farms, backyard farms, live poultry markets, and bodies of water helps to minimize contact with wild birds. Closure of live poultry markets appears to the most effective measure and has shown to be effective at controlling the spread of H5N1, H7N9, and H9N2 . Other biosecurity measures include cleaning and disinfecting facilities and vehicles, banning visits to poultry farms, not bringing birds intended for slaughter back to farms, changing clothes, disinfecting foot baths, and treating food and water. If live poultry markets are not closed, then "clean days" when unsold poultry is removed and facilities are disinfected and "no carry-over" policies to eliminate infectious material before new poultry arrive can be used to reduce the spread of influenza viruses. If a novel influenza viruses has breached the aforementioned biosecurity measures, then rapid detection to stamp it out via quarantining, decontamination, and culling may be necessary to prevent the virus from becoming endemic. Vaccines exist for avian H5, H7, and H9 subtypes that are used in some countries. In China, for example, vaccination of domestic birds against H7N9 successfully limited its spread, indicating that vaccination may be an effective strategy if used in combination with other measures to limit transmission. In pigs and horses, management of influenza is dependent on vaccination with biosecurity. Annual vaccination is the primary and most effective way to prevent influenza and influenza-associated complications, especially for high-risk groups. Vaccines against the flu are trivalent or quadrivalent, providing protection against an H1N1 strain, an H3N2 strain, and one or two IBV strains corresponding to the two IBV lineages. Two types of vaccines are in use: inactivated vaccines that contain "killed" (i.e. inactivated) viruses and live attenuated influenza vaccines (LAIVs) that contain weakened viruses. There are three types of inactivated vaccines: whole virus, split virus, in which the virus is disrupted by a detergent, and subunit, which only contains the viral antigens HA and NA. Most flu vaccines are inactivated and administered via intramuscular injection. LAIVs are sprayed into the nasal cavity. Vaccination recommendations vary by country. Some recommend vaccination for all people above a certain age, such as 6 months, whereas other countries limit recommendations to high-risk groups. Young infants cannot receive flu vaccines for safety reasons, but they can inherit passive immunity from their mother if inactivated vaccines are administered to the mother during pregnancy. Influenza vaccination helps to reduce the probability of reassortment. In general, influenza vaccines are only effective if there is an antigenic match between vaccine strains and circulating strains. Additionally, most commercially available flu vaccines are manufactured by propagation of influenza viruses in embryonated chicken eggs, taking 6–8 months. Flu seasons are different in the northern and southern hemisphere, so the WHO meets twice a year, one for each hemisphere, to discuss which strains should be included in flu vaccines based on observation from HA inhibition assays. Other manufacturing methods include an MDCK cell culture-based inactivated vaccine and a recombinant subunit vaccine manufactured from baculovirus overexpression in insect cells. Influenza can be prevented or reduced in severity by post-exposure prophylaxis with the antiviral drugs oseltamivir , which can be taken orally by those at least three months old, and zanamivir , which can be inhaled by those above seven years of age. Chemoprophylaxis is most useful for individuals at high-risk of developing complications and those who cannot receive the flu vaccine due to contraindications or lack of effectiveness. Post-exposure chemoprophylaxis is only recommended if oseltamivir is taken within 48 hours of contact with a confirmed or suspected influenza case and zanamivir within 36 hours. It is recommended that it be offered to people who have yet to receive a vaccine for the current flu season, who have been vaccinated less than two week since contact, if there is a significant mismatch between vaccine and circulating strains, or during an outbreak in a closed setting regardless of vaccination history. Hand hygiene is important in reducing the spread of influenza. This includes frequent hand washing with soap and water, using alcohol -based hand sanitizers , and not touching one's eyes, nose, and mouth with one's hands. Covering one's nose and mouth when coughing or sneezing is important. Other methods to limit influenza transmission include staying home when sick, avoiding contact with others until one day after symptoms end, and disinfecting surfaces likely to be contaminated by the virus. Health education through media and posters is often used to remind people of hygiene. There is uncertainty about the use of masks since research thus far has not shown a significant reduction in seasonal influenza with mask usage. Likewise, the effectiveness of screening at points of entry into countries is not well researched. Social distancing measures such as school closures, avoiding contact with infected people via isolation or quarantine, and limiting mass gatherings may reduce transmission, but these measures are often expensive, unpopular, and difficult to implement. Consequently, the commonly recommended methods of infection control are respiratory etiquette, hand hygiene, and mask wearing, which are inexpensive and easy to perform. Pharmaceutical measures are effective but may not be available in the early stages of an outbreak. In health care settings, infected individuals may be cohorted or assigned to individual rooms. Protective clothing such as masks, gloves, and gowns is recommended when coming into contact with infected individuals if there is a risk of exposure to infected bodily fluids. Keeping patients in negative pressure rooms and avoiding aerosol-producing activities may help, but special air handling and ventilation systems are not considered necessary to prevent the spread of influenza in the air. In residential homes, new admissions may need to be closed until the spread of influenza is controlled. When discharging patients to care homes, it is important to take care if there is a known influenza outbreak. Since influenza viruses circulate in animals such as birds and pigs, prevention of transmission from these animals is important. Water treatment , indoor raising of animals, quarantining sick animals, vaccination, and biosecurity are the primary measures used. Placing poultry houses and piggeries on high ground away from high-density farms, backyard farms, live poultry markets, and bodies of water helps to minimize contact with wild birds. Closure of live poultry markets appears to the most effective measure and has shown to be effective at controlling the spread of H5N1, H7N9, and H9N2 . Other biosecurity measures include cleaning and disinfecting facilities and vehicles, banning visits to poultry farms, not bringing birds intended for slaughter back to farms, changing clothes, disinfecting foot baths, and treating food and water. If live poultry markets are not closed, then "clean days" when unsold poultry is removed and facilities are disinfected and "no carry-over" policies to eliminate infectious material before new poultry arrive can be used to reduce the spread of influenza viruses. If a novel influenza viruses has breached the aforementioned biosecurity measures, then rapid detection to stamp it out via quarantining, decontamination, and culling may be necessary to prevent the virus from becoming endemic. Vaccines exist for avian H5, H7, and H9 subtypes that are used in some countries. In China, for example, vaccination of domestic birds against H7N9 successfully limited its spread, indicating that vaccination may be an effective strategy if used in combination with other measures to limit transmission. In pigs and horses, management of influenza is dependent on vaccination with biosecurity. Diagnosis based on symptoms is fairly accurate in otherwise healthy people during seasonal epidemics and should be suspected in cases of pneumonia, acute respiratory distress syndrome (ARDS), sepsis , or if encephalitis, myocarditis , or breaking down of muscle tissue occur. Because influenza is similar to other viral respiratory tract illnesses, laboratory diagnosis is necessary for confirmation. Common ways of collecting samples for testing include nasal and throat swabs. Samples may be taken from the lower respiratory tract if infection has cleared the upper but not lower respiratory tract. Influenza testing is recommended for anyone hospitalized with symptoms resembling influenza during flu season or who is connected to an influenza case. For severe cases, earlier diagnosis improves patient outcome. Diagnostic methods that can identify influenza include viral cultures , antibody- and antigen-detecting tests, and nucleic acid-based tests. Viruses can be grown in a culture of mammalian cells or embryonated eggs for 3–10 days to monitor cytopathic effect. Final confirmation can then be done via antibody staining, hemadsorption using red blood cells , or immunofluorescence microscopy. Shell vial cultures, which can identify infection via immunostaining before a cytopathic effect appears, are more sensitive than traditional cultures with results in 1–3 days. Cultures can be used to characterize novel viruses, observe sensitivity to antiviral drugs, and monitor antigenic drift, but they are relatively slow and require specialized skills and equipment. Serological assays can be used to detect an antibody response to influenza after natural infection or vaccination. Common serological assays include hemagglutination inhibition assays that detect HA-specific antibodies, virus neutralization assays that check whether antibodies have neutralized the virus, and enzyme-linked immunoabsorbant assays. These methods tend to be relatively inexpensive and fast but are less reliable than nucleic-acid based tests. Direct fluorescent or immunofluorescent antibody (DFA/IFA) tests involve staining respiratory epithelial cells in samples with fluorescently-labeled influenza-specific antibodies, followed by examination under a fluorescent microscope. They can differentiate between IAV and IBV but can not subtype IAV. Rapid influenza diagnostic tests (RIDTs) are a simple way of obtaining assay results, are low cost, and produce results quickly, at less than 30 minutes, so they are commonly used, but they can not distinguish between IAV and IBV or between IAV subtypes and are not as sensitive as nucleic-acid based tests. Nucleic acid-based tests (NATs) amplify and detect viral nucleic acid. Most of these tests take a few hours, but rapid molecular assays are as fast as RIDTs. Among NATs, reverse transcription polymerase chain reaction (RT-PCR) is the most traditional and considered the gold standard for diagnosing influenza because it is fast and can subtype IAV, but it is relatively expensive and more prone to false-positives than cultures. Other NATs that have been used include loop-mediated isothermal amplification -based assays, simple amplification-based assays, and nucleic acid sequence-based amplification. Nucleic acid sequencing methods can identify infection by obtaining the nucleic acid sequence of viral samples to identify the virus and antiviral drug resistance. The traditional method is Sanger sequencing , but it has been largely replaced by next-generation methods that have greater sequencing speed and throughput. Treatment of influenza in cases of mild or moderate illness is supportive and includes anti-fever medications such as acetaminophen and ibuprofen , adequate fluid intake to avoid dehydration, and resting at home. Cough drops and throat sprays may be beneficial for sore throat. It is recommended to avoid alcohol and tobacco use while sick with the flu. Aspirin is not recommended to treat influenza in children due to an elevated risk of developing Reye syndrome. Corticosteroids likewise are not recommended except when treating septic shock or an underlying medical condition, such as chronic obstructive pulmonary disease or asthma exacerbation, since they are associated with increased mortality. If a secondary bacterial infection occurs, then treatment with antibiotics may be necessary. Antiviral drugs are primarily used to treat severely ill patients, especially those with compromised immune systems. Antivirals are most effective when started in the first 48 hours after symptoms appear. Later administration may still be beneficial for those who have underlying immune defects, those with more severe symptoms, or those who have a higher risk of developing complications if these individuals are still shedding the virus. Antiviral treatment is also recommended if a person is hospitalized with suspected influenza instead of waiting for test results to return and if symptoms are worsening. Most antiviral drugs against influenza fall into two categories: neuraminidase (NA) inhibitors and M2 inhibitors. Baloxavir marboxil is a notable exception, which targets the endonuclease activity of the viral RNA polymerase and can be used as an alternative to NA and M2 inhibitors for IAV and IBV. NA inhibitors target the enzymatic activity of NA receptors, mimicking the binding of sialic acid in the active site of NA on IAV and IBV virions so that viral release from infected cells and the rate of viral replication are impaired. NA inhibitors include oseltamivir, which is consumed orally in a prodrug form and converted to its active form in the liver, and zanamivir, which is a powder that is inhaled nasally. Oseltamivir and zanamivir are effective for prophylaxis and post-exposure prophylaxis, and research overall indicates that NA inhibitors are effective at reducing rates of complications, hospitalization, and mortality and the duration of illness. Additionally, the earlier NA inhibitors are provided, the better the outcome, though late administration can still be beneficial in severe cases. Other NA inhibitors include laninamivir and peramivir, the latter of which can be used as an alternative to oseltamivir for people who cannot tolerate or absorb it. The adamantanes amantadine and rimantadine are orally administered drugs that block the influenza virus' M2 ion channel, preventing viral uncoating. These drugs are only functional against IAV but are no longer recommended for use because of widespread resistance to them among IAVs. Adamantane resistance first emerged in H3N2 in 2003, becoming worldwide by 2008. Oseltamivir resistance is no longer widespread because the 2009 pandemic H1N1 strain (H1N1 pdm09), which is resistant to adamantanes, seemingly replaced resistant strains in circulation. Since the 2009 pandemic, oseltamivir resistance has mainly been observed in patients undergoing therapy, especially the immunocompromised and young children. Oseltamivir resistance is usually reported in H1N1, but has been reported in H3N2 and IBVs less commonly. Because of this, oseltamivir is recommended as the first drug of choice for immunocompetent people, whereas for the immunocompromised, oseltamivir is recommended against H3N2 and IBV and zanamivir against H1N1 pdm09. Zanamivir resistance is observed less frequently, and resistance to peramivir and baloxavir marboxil is possible. Antiviral drugs are primarily used to treat severely ill patients, especially those with compromised immune systems. Antivirals are most effective when started in the first 48 hours after symptoms appear. Later administration may still be beneficial for those who have underlying immune defects, those with more severe symptoms, or those who have a higher risk of developing complications if these individuals are still shedding the virus. Antiviral treatment is also recommended if a person is hospitalized with suspected influenza instead of waiting for test results to return and if symptoms are worsening. Most antiviral drugs against influenza fall into two categories: neuraminidase (NA) inhibitors and M2 inhibitors. Baloxavir marboxil is a notable exception, which targets the endonuclease activity of the viral RNA polymerase and can be used as an alternative to NA and M2 inhibitors for IAV and IBV. NA inhibitors target the enzymatic activity of NA receptors, mimicking the binding of sialic acid in the active site of NA on IAV and IBV virions so that viral release from infected cells and the rate of viral replication are impaired. NA inhibitors include oseltamivir, which is consumed orally in a prodrug form and converted to its active form in the liver, and zanamivir, which is a powder that is inhaled nasally. Oseltamivir and zanamivir are effective for prophylaxis and post-exposure prophylaxis, and research overall indicates that NA inhibitors are effective at reducing rates of complications, hospitalization, and mortality and the duration of illness. Additionally, the earlier NA inhibitors are provided, the better the outcome, though late administration can still be beneficial in severe cases. Other NA inhibitors include laninamivir and peramivir, the latter of which can be used as an alternative to oseltamivir for people who cannot tolerate or absorb it. The adamantanes amantadine and rimantadine are orally administered drugs that block the influenza virus' M2 ion channel, preventing viral uncoating. These drugs are only functional against IAV but are no longer recommended for use because of widespread resistance to them among IAVs. Adamantane resistance first emerged in H3N2 in 2003, becoming worldwide by 2008. Oseltamivir resistance is no longer widespread because the 2009 pandemic H1N1 strain (H1N1 pdm09), which is resistant to adamantanes, seemingly replaced resistant strains in circulation. Since the 2009 pandemic, oseltamivir resistance has mainly been observed in patients undergoing therapy, especially the immunocompromised and young children. Oseltamivir resistance is usually reported in H1N1, but has been reported in H3N2 and IBVs less commonly. Because of this, oseltamivir is recommended as the first drug of choice for immunocompetent people, whereas for the immunocompromised, oseltamivir is recommended against H3N2 and IBV and zanamivir against H1N1 pdm09. Zanamivir resistance is observed less frequently, and resistance to peramivir and baloxavir marboxil is possible. In healthy individuals, influenza infection is usually self-limiting and rarely fatal. Symptoms usually last for 2–8 days. Influenza can cause people to miss work or school, and it is associated with decreased job performance and, in older adults, reduced independence. Fatigue and malaise may last for several weeks after recovery, and healthy adults may experience pulmonary abnormalities that can take several weeks to resolve. Complications and mortality primarily occur in high-risk populations and those who are hospitalized. Severe disease and mortality are usually attributable to pneumonia from the primary viral infection or a secondary bacterial infection, which can progress to ARDS. Other respiratory complications that may occur include sinusitis , bronchitis , bronchiolitis , excess fluid buildup in the lungs, and exacerbation of chronic bronchitis and asthma. Middle ear infection and croup may occur, most commonly in children. Secondary S. aureus infection has been observed, primarily in children, to cause toxic shock syndrome after influenza, with hypotension, fever, and reddening and peeling of the skin. Complications affecting the cardiovascular system are rare and include pericarditis, fulminant myocarditis with a fast, slow, or irregular heartbeat , and exacerbation of pre-existing cardiovascular disease. Inflammation or swelling of muscles accompanied by muscle tissue breaking down occurs rarely, usually in children, which presents as extreme tenderness and muscle pain in the legs and a reluctance to walk for 2–3 days. Influenza can affect pregnancy, including causing smaller neonatal size, increased risk of premature birth, and an increased risk of child death shortly before or after birth. Neurological complications have been associated with influenza on rare occasions, including aseptic meningitis, encephalitis, disseminated encephalomyelitis, transverse myelitis, and Guillain–Barré syndrome . Additionally, febrile seizures and Reye syndrome can occur, most commonly in children. Influenza-associated encephalopathy can occur directly from central nervous system infection from the presence of the virus in blood and presents as sudden onset of fever with convulsions, followed by rapid progression to coma. An atypical form of encephalitis called encephalitis lethargica, characterized by headache, drowsiness, and coma, may rarely occur sometime after infection. In survivors of influenza-associated encephalopathy, neurological defects may occur. Primarily in children, in severe cases the immune system may rarely dramatically overproduce white blood cells that release cytokines, causing severe inflammation. People who are at least 65 years of age, due to a weakened immune system from aging or a chronic illness, are a high-risk group for developing complications, as are children less than one year of age and children who have not been previously exposed to influenza viruses multiple times. Pregnant women are at an elevated risk, which increases by trimester and lasts up to two weeks after childbirth. Obesity, in particular a body mass index greater than 35–40, is associated with greater amounts of viral replication, increased severity of secondary bacterial infection, and reduced vaccination efficacy. People who have underlying health conditions are also considered at-risk, including those who have congenital or chronic heart problems or lung (e.g. asthma), kidney, liver, blood, neurological, or metabolic (e.g. diabetes ) disorders, as are people who are immunocompromised from chemotherapy, asplenia , prolonged steroid treatment, splenic dysfunction, or HIV infection. Tobacco use, including past use, places a person at risk. The role of genetics in influenza is not well researched, but it may be a factor in influenza mortality. Influenza is typically characterized by seasonal epidemics and sporadic pandemics. Most of the burden of influenza is a result of flu seasons caused by IAV and IBV. Among IAV subtypes, H1N1 and H3N2 circulate in humans and are responsible for seasonal influenza. Cases disproportionately occur in children, but most severe causes are among the elderly, the very young, and the immunocompromised. In a typical year, influenza viruses infect 5–15% of the global population, causing 3–5 million cases of severe illness annually and accounting for 290,000–650,000 deaths each year due to respiratory illness. 5–10% of adults and 20–30% of children contract influenza each year. The reported number of influenza cases is usually much lower than the actual number of cases. During seasonal epidemics, it is estimated that about 80% of otherwise healthy people who have a cough or sore throat have the flu. Approximately 30–40% of people hospitalized for influenza develop pneumonia, and about 5% of all severe pneumonia cases in hospitals are due to influenza, which is also the most common cause of ARDS in adults. In children, influenza is one of the two most common causes of ARDS, the other being the respiratory syncytial virus . About 3–5% of children each year develop otitis media due to influenza. Adults who develop organ failure from influenza and children who have PIM scores and acute renal failure have higher rates of mortality. During seasonal influenza, mortality is concentrated in the very young and the elderly, whereas during flu pandemics, young adults are often affected at a high rate. In temperate regions, the number of influenza cases varies from season to season. Lower vitamin D levels, presumably due to less sunlight, lower humidity, lower temperature, and minor changes in virus proteins caused by antigenic drift contribute to annual epidemics that peak during the winter season. In the northern hemisphere, this is from October to May (more narrowly December to April ), and in the southern hemisphere, this is from May to October (more narrowly June to September ). There are therefore two distinct influenza seasons every year in temperate regions, one in the northern hemisphere and one in the southern hemisphere. In tropical and subtropical regions, seasonality is more complex and appears to be affected by various climatic factors such as minimum temperature, hours of sunshine, maximum rainfall, and high humidity. Influenza may therefore occur year-round in these regions. Influenza epidemics in modern times have the tendency to start in the eastern or southern hemisphere, with Asia being a key reservoir of influenza viruses. IAV and IBV co-circulate, so the two have the same patterns of transmission. The seasonality of ICV, however, is poorly understood. ICV infection is most common in children under the age of two, and by adulthood most people have been exposed to it. ICV-associated hospitalization most commonly occurs in children under the age of three and is frequently accompanied by co-infection with another virus or a bacterium, which may increase the severity of disease. When considering all hospitalizations for respiratory illness among young children, ICV appears to account for only a small percentage of such cases. Large outbreaks of ICV infection can occur, so incidence varies significantly. Outbreaks of influenza caused by novel influenza viruses are common. Depending on the level of pre-existing immunity in the population, novel influenza viruses can spread rapidly and cause pandemics with millions of deaths. These pandemics, in contrast to seasonal influenza, are caused by antigenic shifts involving animal influenza viruses. To date, all known flu pandemics have been caused by IAVs, and they follow the same pattern of spreading from an origin point to the rest of the world over the course of multiple waves in a year. Pandemic strains tend to be associated with higher rates of pneumonia in otherwise healthy individuals. Generally after each influenza pandemic, the pandemic strain continues to circulate as the cause of seasonal influenza, replacing prior strains. From 1700 to 1889, influenza pandemics occurred about once every 50–60 years. Since then, pandemics have occurred about once every 10–50 years, so they may be getting more frequent over time. The first influenza epidemic may have occurred around 6,000 BC in China, and possible descriptions of influenza exist in Greek writings from the 5th century BC. In both 1173–1174 AD and 1387 AD, epidemics occurred across Europe that were named "influenza". Whether these epidemics or others were caused by influenza is unclear since there was then no consistent naming pattern for epidemic respiratory diseases, and "influenza" did not become clearly associated with respiratory disease until centuries later. Influenza may have been brought to the Americas as early as 1493, when an epidemic disease resembling influenza killed most of the population of the Antilles . The first convincing record of an influenza pandemic was in 1510 . It began in East Asia before spreading to North Africa and then Europe. Following the pandemic, seasonal influenza occurred, with subsequent pandemics in 1557 and 1580. The flu pandemic in 1557 was potentially the first time influenza was connected to miscarriage and death of pregnant women. The 1580 influenza pandemic originated in Asia during summer, spread to Africa, then Europe, and finally America. By the end of the 16th century, influenza was beginning to become understood as a specific, recognizable disease with epidemic and endemic forms. In 1648, it was discovered that horses also experience influenza. Influenza data after 1700 is more accurate, so it is easier to identify flu pandemics after this point. The first flu pandemic of the 18th century started in 1729 in Russia in spring, spreading worldwide over the course of three years with distinct waves, the later ones being more lethal. Another flu pandemic occurred in 1781–1782, starting in China in autumn. From this pandemic, influenza became associated with sudden outbreaks of febrile illness. The next flu pandemic was from 1830 to 1833, beginning in China in winter. This pandemic had a high attack rate, but the mortality rate was low. A minor influenza pandemic occurred from 1847 to 1851 at the same time as the third cholera pandemic and was the first flu pandemic to occur with vital statistics being recorded, so influenza mortality was clearly recorded for the first time. Highly pathogenic avian influenza was recognized in 1878 and was soon linked to transmission to humans. By the time of the 1889 pandemic , which may have been caused by an H2N2 strain, the flu had become an easily recognizable disease. The microbial agent responsible for influenza was incorrectly identified in 1892 by R. F. J. Pfeiffer as the bacteria species Haemophilus influenzae , which retains "influenza" in its name. From 1901 to 1903, Italian and Austrian researchers were able to show that avian influenza, then called "fowl plague", was caused by a microscopic agent smaller than bacteria by using filters with pores too small for bacteria to pass through. The fundamental differences between viruses and bacteria, however, were not yet fully understood. From 1918 to 1920, the Spanish flu pandemic became the most devastating influenza pandemic and one of the deadliest pandemics in history. The pandemic, probably caused by H1N1, likely began in the United States before spreading worldwide via soldiers during and after the First World War . The initial wave in the first half of 1918 was relatively minor and resembled past flu pandemics, but the second wave later that year had a much higher mortality rate. A third wave with lower mortality occurred in many places a few months after the second. By the end of 1920, it is estimated that about a third to half of all people in the world had been infected, with tens of millions of deaths, disproportionately young adults. During the 1918 pandemic, the respiratory route of transmission was clearly identified and influenza was shown to be caused by a "filter passer", not a bacterium, but there remained a lack of agreement about influenza's cause for another decade and research on influenza declined. After the pandemic, H1N1 circulated in humans in seasonal form until the next pandemic. In 1931, Richard Shope published three papers identifying a virus as the cause of swine influenza, a then newly recognized disease among pigs that was characterized during the second wave of the 1918 pandemic. Shope's research reinvigorated research on human influenza, and many advances in virology, serology, immunology, experimental animal models, vaccinology, and immunotherapy have since arisen from influenza research. Just two years after influenza viruses were discovered, in 1933, IAV was identified as the agent responsible for human influenza. Subtypes of IAV were discovered throughout the 1930s, and IBV was discovered in 1940. During the Second World War , the US government worked on developing inactivated vaccines for influenza, resulting in the first influenza vaccine being licensed in 1945 in the United States. ICV was discovered two years later in 1947. In 1955, avian influenza was confirmed to be caused by IAV. Four influenza pandemics have occurred since WWII. The first of these was the Asian flu from 1957 to 1958, caused by an H2N2 strain and beginning in China's Yunnan province. The number of deaths probably exceeded one million, mostly among the very young and very old. This was the first flu pandemic to occur in the presence of a global surveillance system and laboratories able to study the novel influenza virus. After the pandemic, H2N2 was the IAV subtype responsible for seasonal influenza. The first antiviral drug against influenza, amantadine , was approved in 1966, with additional antiviral drugs being used since the 1990s. In 1968, H3N2 was introduced into humans through a rearrangement between an avian H3N2 strain and an H2N2 strain that was circulating in humans. The novel H3N2 strain emerged in Hong Kong and spread worldwide, causing the Hong Kong flu pandemic, which resulted in 500,000–2,000,000 deaths. This was the first pandemic to spread significantly by air travel. H2N2 and H3N2 co-circulated after the pandemic until 1971 when H2N2 waned in prevalence and was completely replaced by H3N2. In 1977, H1N1 reemerged in humans, possibly after it was released from a freezer in a laboratory accident, and caused a pseudo-pandemic . This H1N1 strain was antigenically similar to the H1N1 strains that circulated prior to 1957. Since 1977, both H1N1 and H3N2 have circulated in humans as part of seasonal influenza. In 1980, the classification system used to subtype influenza viruses was introduced. At some point, IBV diverged into two strains, named the B/Victoria-like and B/Yamagata-like lineages, both of which have been circulating in humans since 1983. In 1996, HPAI H5N1 was detected in Guangdong , China and a year later emerged in poultry in Hong Kong, gradually spreading worldwide from there. A small H5N1 outbreak in humans in Hong Kong occurred then, and sporadic human cases have occurred since 1997, carrying a high case fatality rate. The most recent flu pandemic was the 2009 swine flu pandemic , which originated in Mexico and resulted in hundreds of thousands of deaths. It was caused by a novel H1N1 strain that was a reassortment of human, swine, and avian influenza viruses. The 2009 pandemic had the effect of replacing prior H1N1 strains in circulation with the novel strain but not any other influenza viruses. Consequently, H1N1, H3N2, and both IBV lineages have been in circulation in seasonal form since the 2009 pandemic. In 2011, IDV was discovered in pigs in Oklahoma, USA, and cattle were later identified as the primary reservoir of IDV. In the same year, avian H7N9 was detected in China and began to cause human infections in 2013, starting in Shanghai and Anhui and remaining mostly in China. HPAI H7N9 emerged sometime in 2016 and has occasionally infected humans incidentally. Other AIVs have less commonly infected humans since the 1990s, including H5N6 , H6N1 , H7N2-4, H7N7 , and H10N7-8, and HPAI H subtypes such as H5N1-3, H5N5-6, and H5N8 have begun to spread throughout much of the world since the 2010s. Future flu pandemics, which may be caused by an influenza virus of avian origin, are viewed as almost inevitable, and increased globalization has made it easier for novel viruses to spread, so there are continual efforts to prepare for future pandemics and improve the prevention and treatment of influenza. The word influenza comes from the Italian word influenza , from medieval Latin influentia , originally meaning 'visitation' or 'influence'. Terms such as influenza di freddo , meaning 'influence of the cold', and influenza di stelle , meaning 'influence of the stars' are attested from the 14th century. The latter referred to the disease's cause, which at the time was ascribed by some to unfavorable astrological conditions. As early as 1504, influenza began to mean a 'visitation' or 'outbreak' of any disease affecting many people in a single place at once. During an outbreak of influenza in 1743 that started in Italy and spread throughout Europe, the word reached the English language and was anglicized in pronunciation. Since the mid-1800s, influenza has also been used to refer to severe colds. The shortened form of the word, "flu", is first attested in 1839 as flue with the spelling flu confirmed in 1893. Other names that have been used for influenza include epidemic catarrh , la grippe from French , sweating sickness , and, especially when referring to the 1918 pandemic strain, Spanish fever . The word influenza comes from the Italian word influenza , from medieval Latin influentia , originally meaning 'visitation' or 'influence'. Terms such as influenza di freddo , meaning 'influence of the cold', and influenza di stelle , meaning 'influence of the stars' are attested from the 14th century. The latter referred to the disease's cause, which at the time was ascribed by some to unfavorable astrological conditions. As early as 1504, influenza began to mean a 'visitation' or 'outbreak' of any disease affecting many people in a single place at once. During an outbreak of influenza in 1743 that started in Italy and spread throughout Europe, the word reached the English language and was anglicized in pronunciation. Since the mid-1800s, influenza has also been used to refer to severe colds. The shortened form of the word, "flu", is first attested in 1839 as flue with the spelling flu confirmed in 1893. Other names that have been used for influenza include epidemic catarrh , la grippe from French , sweating sickness , and, especially when referring to the 1918 pandemic strain, Spanish fever . Influenza research includes efforts to understand how influenza viruses enter hosts, the relationship between influenza viruses and bacteria, how influenza symptoms progress, and why some influenza viruses are deadlier than others. Non-structural proteins encoded by influenza viruses are periodically discovered and their functions are continually under research. Past pandemics, and especially the 1918 pandemic, are the subject of much research to understand flu pandemics. As part of pandemic preparedness, the Global Influenza Surveillance and Response System is a global network of laboratories that monitors influenza transmission and epidemiology. Additional areas of research include ways to improve the diagnosis, treatment, and prevention of influenza. Existing diagnostic methods have a variety of limitations coupled with their advantages. For example, NATs have high sensitivity and specificity but are impractical in under-resourced regions due to their high cost, complexity, maintenance, and training required. Low-cost, portable RIDTs can rapidly diagnose influenza but have highly variable sensitivity and are unable to subtype IAV. As a result of these limitations and others, research into new diagnostic methods revolves around producing new methods that are cost-effective, less labor-intensive, and less complex than existing methods while also being able to differentiate influenza species and IAV subtypes. One approach in development are lab-on-a-chips , which are diagnostic devices that make use of a variety of diagnostic tests, such as RT-PCR and serological assays, in microchip form. These chips have many potential advantages, including high reaction efficiency, low energy consumption, and low waste generation. New antiviral drugs are also in development due to the elimination of adamantines as viable drugs and concerns over oseltamivir resistance. These include: NA inhibitors that can be injected intravenously, such as intravenous formulations of zanamivir; favipiravir , which is a polymerase inhibitor used against several RNA viruses; pimodivir , which prevents cap-binding required during viral transcription; and nitazoxanide , which inhibits HA maturation. Reducing excess inflammation in the respiratory tract is also subject to much research since this is one of the primary mechanisms of influenza pathology. Other forms of therapy in development include monoclonal and polyclonal antibodies that target viral proteins, convalescent plasma, different approaches to modify the host antiviral response, and stem cell -based therapies to repair lung damage. Much research on LAIVs focuses on identifying genome sequences that can be deleted to create harmless influenza viruses in vaccines that still confer immunity. The high variability and rapid evolution of influenza virus antigens, however, is a major obstacle in developing effective vaccines. Furthermore, it is hard to predict which strains will be in circulation during the next flu season, manufacturing a sufficient quantity of flu vaccines for the next season is difficult, LAIVs have limited efficacy, and repeated annual vaccination potentially has diminished efficacy. For these reasons, "broadly-reactive" or "universal" flu vaccines are being researched that can provide protection against many or all influenza viruses. Approaches to develop such a vaccine include HA stalk-based methods such as chimeras that have the same stalk but different heads, HA head-based methods such as computationally optimized broadly neutralizing antigens, anti-idiotypic antibodies , and vaccines to elicit immune responses to highly conserved viral proteins. mRNA vaccines to provide protection against influenza are also under research. In recent years, controversy emerged over the ethical justifications for certain 'gain-of-function' (GOF) studies on influenza. Aquatic birds such as ducks, geese, shorebirds, and gulls are the primary reservoir of IAVs. In birds, AIVs may be either low pathogenic avian influenza (LPAI) viruses that produce little to no symptoms or highly pathogenic avian influenza (HPAI) viruses that cause severe illness. Symptoms of HPAI infection include lack of energy and appetite, decreased egg production, soft-shelled or misshapen eggs, swelling of the head, comb, wattles, and hocks, purple discoloration of wattles, combs, and legs, nasal discharge, coughing, sneezing, incoordination, and diarrhea. Birds infected with an HPAI virus may also die suddenly without any signs of infection. The distinction between LPAI and HPAI can generally be made based on how lethal an AIV is to chickens. At the genetic level, an AIV can be usually be identified as an HPAI virus if it has a multibasic cleavage site in the HA protein, which contains additional residues in the HA gene. Most AIVs are LPAI. Notable HPAI viruses include HPAI H5N1 and HPAI H7N9. HPAI viruses have been a major disease burden in the 21st century, resulting in the death of large numbers of birds. In H7N9's case, some circulating strains were originally LPAI but became HPAI by acquiring the HA multibasic cleavage site. Avian H9N2 is also of concern because although it is LPAI, it is a common donor of genes to H5N1 and H7N9 during reassortment. Migratory birds can spread influenza across long distances. An example of this was when an H5N1 strain in 2005 infected birds at Qinghai Lake , China, which is a stopover and breeding site for many migratory birds, subsequently spreading the virus to more than 20 countries across Asia, Europe, and the Middle East. AIVs can be transmitted from wild birds to domestic free-range ducks and in turn to poultry through contaminated water, aerosols, and fomites. Ducks therefore act as key intermediates between wild and domestic birds. Transmission to poultry typically occurs in backyard farming and live animal markets where multiple species interact with each other. From there, AIVs can spread to poultry farms in the absence of adequate biosecurity. Among poultry, HPAI transmission occurs through aerosols and contaminated feces, cages, feed, and dead animals. Back-transmission of HPAI viruses from poultry to wild birds has occurred and is implicated in mass die-offs and intercontinental spread. AIVs have occasionally infected humans through aerosols, fomites, and contaminated water. Direction transmission from wild birds is rare. Instead, most transmission involves domestic poultry, mainly chickens, ducks, and geese but also a variety of other birds such as guinea fowl, partridge, pheasants, and quails. The primary risk factor for infection with AIVs is exposure to birds in farms and live poultry markets. Typically, infection with an AIV has an incubation period of 3–5 days but can be up to 9 days. H5N1 and H7N9 cause severe lower respiratory tract illness, whereas other AIVs such as H9N2 cause a more mild upper respiratory tract illness, commonly with conjunctivitis. Limited transmission of avian H2, H5-7, H9, and H10 subtypes from one person to another through respiratory droplets, aerosols, and fomites has occurred, but sustained human-to-human transmission of AIVs has not occurred. Before 2013, H5N1 was the most common AIV to infect humans. Since then, H7N9 has been responsible for most human cases. Influenza in pigs is a respiratory disease similar to influenza in humans and is found worldwide. Asymptomatic infections are common. Symptoms typically appear 1–3 days after infection and include fever, lethargy, anorexia, weight loss, labored breathing, coughing, sneezing, and nasal discharge. In sows, pregnancy may be aborted. Complications include secondary infections and potentially fatal bronchopneumonia . Pigs become contagious within a day of infection and typically spread the virus for 7–10 days, which can spread rapidly within a herd. Pigs usually recover from infection within 3–7 days after symptoms appear. Prevention and control measures include inactivated vaccines and culling infected herds. The influenza viruses usually responsible for swine flu are IAV subtypes H1N1, H1N2 , and H3N2. Some IAVs can be transmitted via aerosols from pigs to humans and vice versa. Furthermore, pigs, along with bats and quails, are recognized as a mixing vessel of influenza viruses because they have both α-2,3 and α-2,6 sialic acid receptors in their respiratory tract. Because of that, both avian and mammalian influenza viruses can infect pigs. If co-infection occurs, then reassortment is possible. A notable example of this was the reassortment of a swine, avian, and human influenza virus in 2009, resulting in a novel H1N1 strain that caused the 2009 flu pandemic. Spillover events from humans to pigs, however, appear to be more common than from pigs to humans. Influenza viruses have been found in many other animals, including cattle, horses, dogs, cats, and marine mammals. Nearly all IAVs are apparently descended from ancestral viruses in birds. The exception are bat influenza-like viruses, which have an uncertain origin. These bat viruses have HA and NA subtypes H17, H18, N10, and N11. H17N10 and H18N11 are unable to reassort with other IAVs, but they are still able to replicate in other mammals. AIVs sometimes crossover into mammals. For example, in late 2016 to early 2017, an avian H7N2 strain was found to be infecting cats in New York. Equine IAVs include H7N7 and two lineages of H3N8 . H7N7, however, has not been detected in horses since the late 1970s, so it may have become extinct in horses. H3N8 in equines spreads via aerosols and causes respiratory illness. Equine H3N8 perferentially binds to α-2,3 sialic acids, so horses are usually considered dead-end hosts, but transmission to dogs and camels has occurred, raising concerns that horses may be mixing vessels for reassortment. In canines, the only IAVs in circulation are equine-derived H3N8 and avian-derived H3N2. Canine H3N8 has not been observed to reassort with other subtypes. H3N2 has a much broader host range and can reassort with H1N1 and H5N1. An isolated case of H6N1 likely from a chicken was found infecting a dog, so other AIVs may emerge in canines. Other mammals to be infected by IAVs include H7N7 and H4N5 in seals, H1N3 in whales, and H10N4 and H3N2 in minks. Various mutations have been identified that are associated with AIVs adapting to mammals. Since HA proteins vary in which sialic acids they bind to, mutations in the HA receptor binding site can allow AIVs to infect mammals. Other mutations include mutations affecting which sialic acids NA proteins cleave and a mutation in the PB2 polymerase subunit that improves tolerance of lower temperatures in mammalian respiratory tracts and enhances RNP assembly by stabilizing NP and PB2 binding. IBV is mainly found in humans but has also been detected in pigs, dogs, horses, and seals. Likewise, ICV primarily infects humans but has been observed in pigs, dogs, cattle, and dromedary camels. IDV causes an influenza-like illness in pigs but its impact in its natural reservoir, cattle, is relatively unknown. It may cause respiratory disease resembling human influenza on its own, or it may be part of a bovine respiratory disease (BRD) complex with other pathogens during co-infection. BRD is a concern for the cattle industry, so IDV's possible involvement in BRD has led to research on vaccines for cattle that can provide protection against IDV. Two antigenic lineages are in circulation: D/swine/Oklahoma/1334/2011 (D/OK) and D/bovine/Oklahoma/660/2013 (D/660). Aquatic birds such as ducks, geese, shorebirds, and gulls are the primary reservoir of IAVs. In birds, AIVs may be either low pathogenic avian influenza (LPAI) viruses that produce little to no symptoms or highly pathogenic avian influenza (HPAI) viruses that cause severe illness. Symptoms of HPAI infection include lack of energy and appetite, decreased egg production, soft-shelled or misshapen eggs, swelling of the head, comb, wattles, and hocks, purple discoloration of wattles, combs, and legs, nasal discharge, coughing, sneezing, incoordination, and diarrhea. Birds infected with an HPAI virus may also die suddenly without any signs of infection. The distinction between LPAI and HPAI can generally be made based on how lethal an AIV is to chickens. At the genetic level, an AIV can be usually be identified as an HPAI virus if it has a multibasic cleavage site in the HA protein, which contains additional residues in the HA gene. Most AIVs are LPAI. Notable HPAI viruses include HPAI H5N1 and HPAI H7N9. HPAI viruses have been a major disease burden in the 21st century, resulting in the death of large numbers of birds. In H7N9's case, some circulating strains were originally LPAI but became HPAI by acquiring the HA multibasic cleavage site. Avian H9N2 is also of concern because although it is LPAI, it is a common donor of genes to H5N1 and H7N9 during reassortment. Migratory birds can spread influenza across long distances. An example of this was when an H5N1 strain in 2005 infected birds at Qinghai Lake , China, which is a stopover and breeding site for many migratory birds, subsequently spreading the virus to more than 20 countries across Asia, Europe, and the Middle East. AIVs can be transmitted from wild birds to domestic free-range ducks and in turn to poultry through contaminated water, aerosols, and fomites. Ducks therefore act as key intermediates between wild and domestic birds. Transmission to poultry typically occurs in backyard farming and live animal markets where multiple species interact with each other. From there, AIVs can spread to poultry farms in the absence of adequate biosecurity. Among poultry, HPAI transmission occurs through aerosols and contaminated feces, cages, feed, and dead animals. Back-transmission of HPAI viruses from poultry to wild birds has occurred and is implicated in mass die-offs and intercontinental spread. AIVs have occasionally infected humans through aerosols, fomites, and contaminated water. Direction transmission from wild birds is rare. Instead, most transmission involves domestic poultry, mainly chickens, ducks, and geese but also a variety of other birds such as guinea fowl, partridge, pheasants, and quails. The primary risk factor for infection with AIVs is exposure to birds in farms and live poultry markets. Typically, infection with an AIV has an incubation period of 3–5 days but can be up to 9 days. H5N1 and H7N9 cause severe lower respiratory tract illness, whereas other AIVs such as H9N2 cause a more mild upper respiratory tract illness, commonly with conjunctivitis. Limited transmission of avian H2, H5-7, H9, and H10 subtypes from one person to another through respiratory droplets, aerosols, and fomites has occurred, but sustained human-to-human transmission of AIVs has not occurred. Before 2013, H5N1 was the most common AIV to infect humans. Since then, H7N9 has been responsible for most human cases. Influenza in pigs is a respiratory disease similar to influenza in humans and is found worldwide. Asymptomatic infections are common. Symptoms typically appear 1–3 days after infection and include fever, lethargy, anorexia, weight loss, labored breathing, coughing, sneezing, and nasal discharge. In sows, pregnancy may be aborted. Complications include secondary infections and potentially fatal bronchopneumonia . Pigs become contagious within a day of infection and typically spread the virus for 7–10 days, which can spread rapidly within a herd. Pigs usually recover from infection within 3–7 days after symptoms appear. Prevention and control measures include inactivated vaccines and culling infected herds. The influenza viruses usually responsible for swine flu are IAV subtypes H1N1, H1N2 , and H3N2. Some IAVs can be transmitted via aerosols from pigs to humans and vice versa. Furthermore, pigs, along with bats and quails, are recognized as a mixing vessel of influenza viruses because they have both α-2,3 and α-2,6 sialic acid receptors in their respiratory tract. Because of that, both avian and mammalian influenza viruses can infect pigs. If co-infection occurs, then reassortment is possible. A notable example of this was the reassortment of a swine, avian, and human influenza virus in 2009, resulting in a novel H1N1 strain that caused the 2009 flu pandemic. Spillover events from humans to pigs, however, appear to be more common than from pigs to humans. Influenza viruses have been found in many other animals, including cattle, horses, dogs, cats, and marine mammals. Nearly all IAVs are apparently descended from ancestral viruses in birds. The exception are bat influenza-like viruses, which have an uncertain origin. These bat viruses have HA and NA subtypes H17, H18, N10, and N11. H17N10 and H18N11 are unable to reassort with other IAVs, but they are still able to replicate in other mammals. AIVs sometimes crossover into mammals. For example, in late 2016 to early 2017, an avian H7N2 strain was found to be infecting cats in New York. Equine IAVs include H7N7 and two lineages of H3N8 . H7N7, however, has not been detected in horses since the late 1970s, so it may have become extinct in horses. H3N8 in equines spreads via aerosols and causes respiratory illness. Equine H3N8 perferentially binds to α-2,3 sialic acids, so horses are usually considered dead-end hosts, but transmission to dogs and camels has occurred, raising concerns that horses may be mixing vessels for reassortment. In canines, the only IAVs in circulation are equine-derived H3N8 and avian-derived H3N2. Canine H3N8 has not been observed to reassort with other subtypes. H3N2 has a much broader host range and can reassort with H1N1 and H5N1. An isolated case of H6N1 likely from a chicken was found infecting a dog, so other AIVs may emerge in canines. Other mammals to be infected by IAVs include H7N7 and H4N5 in seals, H1N3 in whales, and H10N4 and H3N2 in minks. Various mutations have been identified that are associated with AIVs adapting to mammals. Since HA proteins vary in which sialic acids they bind to, mutations in the HA receptor binding site can allow AIVs to infect mammals. Other mutations include mutations affecting which sialic acids NA proteins cleave and a mutation in the PB2 polymerase subunit that improves tolerance of lower temperatures in mammalian respiratory tracts and enhances RNP assembly by stabilizing NP and PB2 binding. IBV is mainly found in humans but has also been detected in pigs, dogs, horses, and seals. Likewise, ICV primarily infects humans but has been observed in pigs, dogs, cattle, and dromedary camels. IDV causes an influenza-like illness in pigs but its impact in its natural reservoir, cattle, is relatively unknown. It may cause respiratory disease resembling human influenza on its own, or it may be part of a bovine respiratory disease (BRD) complex with other pathogens during co-infection. BRD is a concern for the cattle industry, so IDV's possible involvement in BRD has led to research on vaccines for cattle that can provide protection against IDV. Two antigenic lineages are in circulation: D/swine/Oklahoma/1334/2011 (D/OK) and D/bovine/Oklahoma/660/2013 (D/660).

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Avian influenza

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Canine influenza

Canine influenza ( dog flu ) is influenza occurring in canine animals. Canine influenza is caused by varieties of influenzavirus A , such as equine influenza virus H3N8 , which was discovered to cause disease in canines in 2004. Because of the lack of previous exposure to this virus, dogs have no natural immunity to it. Therefore, the disease is rapidly transmitted between individual dogs. Canine influenza may be endemic in some regional dog populations of the United States. It is a disease with a high morbidity (incidence of symptoms) but a low incidence of death . A newer form was identified in Asia during the 2000s and has since caused outbreaks in the US as well. It is a mutation of H3N2 that adapted from its avian influenza origins. Vaccines have been developed for both strains. The two strains of Type A influenza virus found in canines are A(H3N2) and A(H3N8). Over time, there has been a discovery of sources of transmissions, identification of specific symptoms and the creation of vaccines. The highly contagious equine influenza A virus subtype H3N8 was found to have been the cause of Greyhound race dog fatalities from a respiratory illness at a Florida racetrack in January 2004. The exposure and transfer apparently occurred at horse-racing tracks, where dog racing had also occurred. This was the first evidence of an influenza A virus causing disease in dogs. However, serum collected from racing Greyhounds between 1984 and 2004 and tested for canine influenza virus (CIV) in 2007 had positive tests going as far back as 1999. CIV possibly caused some of the respiratory disease outbreaks at tracks between 1999 and 2003. H3N8 was also responsible for a major dog-flu outbreak in New York state in all breeds of dogs. From January to May 2005, outbreaks occurred at 20 racetracks in 10 states ( Arizona , Arkansas , Colorado , Florida, Iowa , Kansas , Massachusetts , Rhode Island , Texas , and West Virginia ). As of August 2006, dog flu has been confirmed in 22 U.S. states, including pet dogs in Wyoming, California, Connecticut, Delaware, and Hawaii. Three areas in the United States may now be considered endemic for CIV due to continuous waves of cases: New York, southern Florida, and northern Colorado/southern Wyoming. No evidence shows the virus can be transferred to people, cats, or other species. H5N1 ( avian influenza ) was also shown to cause death in one dog in Thailand , following ingestion of an infected duck . The H3N2 virus made its first appearance in Canada at the start of 2018, following the importation of two unknowingly infected canines from South Korea. In 2006-2007 canine H3N2 first had reports in South Korea and was thought to be transferred to dogs from avian origins ( avian influenza H3N2). It was not until 2015 that the canine H3N2 strain was discovered in the United States after there was an outbreak of dogs having respiratory infections in Chicago. As canine H3N2 influenza began to spread through the United States, in 2016 cats in an Indiana began to show symptoms of the disease as well, it is believed they were infected by coming in to contact with sick dogs. Following this incidence, reports of the virus possibly spreading, with two other canines reporting alarming symptoms, were made public. By March 5th, 25 cases of infection were reportedly spread, although the number is thought to be closer to approximately 100. Influenza A viruses are enveloped , negative sense , single-stranded RNA viruses . Genome analysis has shown that H3N8 was transferred from horses to dogs and then adapted to dogs through point mutations in the genes . The incubation period is two to five days, and viral shedding may occur for seven to ten days following the onset of symptoms. It does not induce a persistent carrier state. [ citation needed ] In late 2022, together with Bordetella bronchiseptica and other respiratory pathogens, the H3N2 canine flu virus experienced a surge in canine infections. This was partially due to increased human travel and reopened offices following the relaxation of COVID-19 pandemic public health measures, leading to large numbers of dogs being placed together in kennels and doggy day care centers. Changing pet ownership behaviors also led to overcrowded animal shelters, which had been emptied at the height of the pandemic. The infection of canine influenza can be transmitted from animal to animal and almost all dogs that come in contact with the virus will contract it. This makes canine influenza most common among dogs but can also be transmitted to cats in a shelter or a household. Canine influenza is an airborne disease , when a dog coughs or sneezes they secrete respiratory droplets that are then inhaled by other animals causing infection. Kennels, dog parks, grooming parlors, and things alike are high risk areas for infections. About 80% of infected dogs with H3N8 show symptoms, usually mild (the other 20% have subclinical infections ), and the fatality rate for Greyhounds in early outbreaks was 5 to 8%, although the overall fatality rate in the general pet and shelter population is probably less than 1%. Most animals infected with canine influenza will show symptoms such as coughing, runny nose, fever, lethargy, eye discharge, and a reduced appetite lasting anywhere from 2-3 weeks. Symptoms of the mild form include a cough that lasts for 10 to 30 days and possibly a greenish nasal discharge. Dogs with the more severe form may have a high fever and pneumonia . Pneumonia in these dogs is not caused by the influenza virus, but by secondary bacterial infections. The fatality rate of dogs that develop pneumonia secondary to canine influenza can reach 50% if not given proper treatment. Necropsies in dogs that die from the disease have revealed severe hemorrhagic pneumonia and evidence of vasculitis . The presence of an upper respiratory tract infection in a dog that has been vaccinated for the other major causes of kennel cough increases suspicion of infection with canine influenza, especially in areas where the disease has been documented. A serum sample from a dog suspected of having canine influenza can be submitted to a laboratory that performs PCR tests for this virus. In June 2009, the United States Department of Agriculture (USDA) Animal and Plant Health Inspection Service (APHIS) approved the first canine influenza vaccine. This veterinarian provided vaccine help fight the infection and are preventative measures for dogs who are constantly facing exposure of the H3N8 and H3N2 strain. This vaccine must be given twice initially with a two-week break, then annually thereafter. A second form of canine influenza was first identified during 2006 in South Korea and southern China. The virus is an H3N2 variant that adapted from its avian influenza origins. An outbreak in the US was first reported in the Chicago area during 2015. Outbreaks were reported in several US states during the spring and summer of 2015 and had been reported in 25 states by late 2015. As of April 2015, the question of whether vaccination against the earlier strain offered protection had not been resolved. The US Department of Agriculture granted conditional approval for a canine H3N2-protective vaccine in December 2015. In March 2016, researchers reported that this strain had infected cats and suggested that it may be transmitted between them. The H3N2 virus as a stand-alone virus is deemed harmless to humans. According to the Windsor-Essex County Health Unit, it is only when the H3N2 virus strain combines with a human strain of flu, "those strains could combine to create a new virus." The possibility of this is unlikely; however, if an infected dog contracts a human flu, there stands a slight chance.

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Avian influenza

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Influenza A virus subtype H5N8

H 5 N 8 is a subtype of the influenza A virus (sometimes called bird flu ) and is highly lethal to wild birds and poultry . H5N8 is typically not associated with humans. However, seven people in Russia were found to be infected in 2021, becoming the first documented human cases. The H5N8 virus manifests itself in various ways, from asymptomatic and sub-clinical to highly lethal in some populations. Many of the findings in wild birds are based on the discovery of dead animals. Its intravenous pathogenicity index (IVPI) is greater than 1.2, giving it a mortality rate of at least 75 percent. H5N8 has previously been used in place of the highly pathogenic H1N1 in studies. Perhaps the most known outbreak of H5N8 occurred in Ireland in 1983. Poultry on two farms showed the usual symptoms, plus diarrhea, nervousness, and depression. Poultry farms within close proximity soon began to show signs of infection, as well, but no contact between the farms could be established. In the end, 8,000 turkeys, 28,020 chickens, and 270,000 ducks were culled. When investigated in the lab, clinical findings demonstrated that turkeys were the most susceptible to infection. The virus could not be clinically reproduced in ducks. An outbreak of H5N8 was reported in breeding ducks in North Jeolla Province , South Korea , on 18 January 2014. The virus spread in duck and chicken farms and at least 12 million poultry were culled. In the second half of 2016, an H5N8 outbreak was first reported in Europe, spreading to Asia by the end of the year. [ citation needed ] On 27 October 2016, an H5N8 case was first reported in a wild swan in Hungary . Further reports were subsequently made from seven additional European countries. There were outbreaks in poultry and wild birds in Austria , Hungary , and Germany . There were reports of infection in wild birds only in Croatia, Denmark, Poland, and Switzerland. [ citation needed ] In the Netherlands, H5N8 was found in wild birds and birds in a zoo and on 26 November 190,000 ducks were destroyed at six farms. Outbreaks have also been reported in India, Israel, South Korea, Taiwan and Russia. On 16 December 2016, it was confirmed that there was an outbreak of the H5N8 virus at a farm near Tetney, Louth — the first outbreak in the United Kingdom. This outbreak has caused the combined death and culling of 5,000 turkeys. At the time of writing (16 December 2016), a 3 km protection zone and a 10 km surveillance zone were enforced by the Department for Environment, Food and Rural Affairs. In the second week of December official delegations from Japan, South Korea and China gathered in Beijing for a symposium on preventing and controlling bird flu and other diseases in East Asia, according to the website of China's ministry of agriculture. By the end of December the outbreak had spread to South Korea, Japan, Germany, and the United Kingdom. Thousands of birds and animals were being culled in Germany to stop the spread. In the United Kingdom the flu was found in a wild duck at a turkey farm in Lincolnshire. In South Korea, a record total of 18.4 million birds had been killed by December since the first outbreak of avian flu was reported at a farm on Nov. 18. Japan has reported five outbreaks since the end of November with 800,000 chickens having been culled in one month. In early January 2017, France culled about 800,000 birds to prevent the spread of H5N8. In Nigeria , it was reported that the virus affected 3.5 million birds. The virus was also detected in Spain and Slovenia . Uganda detected aves flu in two locations, one affecting wild birds and another striking domestic birds. Two cases of the virus were detected in Northern Ireland amongst wild geese. As a response, the Department of Agriculture extended restrictions on poultry flocks until at least 16 March. A case of the virus was detected in Harare , Zimbabwe at one of the major poultry producers, Irvine's Private Limited. The virus saw over 7,000 birds succumbing to the virus. As a result, the company, culled over 140,000 birds to prevent the spread of the virus. Even though a ban on all avian products from Zimbabwe was issued, on 22 June an outbreak was reported at a commercial broiler poultry farm outside Villiers , South Africa after 5,000 chickens died. A few days later, just over 60 km away from the first outbreak, a separate outbreak was reported in Standerton , Mpumalanga , where over 25,000 birds were culled to prevent the virus spreading. The South African Poultry Association reported that wild ducks migrating from Europe are spreading the virus. On 20 December 2017, the Ministry of Environment, Water and Agriculture (MEWA) in Saudi Arabia announced the detection of the highly pathogenic H5N8 virus among birds at a poultry market in Riyadh. A few days later, the virus was detected in other farms in other cities including Al-Ahsa, Al-Kharj, Al-Quaiyat, Dharma, and Mazahmiya. This outbreak in the country led to a cull of more than 100,000 birds at 12 locations across the country to prevent the spread of the virus. On 4 February, Saudi Arabia reported an outbreak of the highly pathogenic H5N8 bird flu virus on a poultry farm. The outbreak, which occurred in the central Sudair region, killed 22,700 birds. In the summer of 2020, H5N8 was detected in wild birds in western Russia and Kazakhstan. Because this included waterbirds that migrate into northern and western Europe, it was considered likely that the virus would be detected there later in the year (as would be confirmed in October–November). On 22 October, the agriculture minister Carola Schouten of the Netherlands confirmed that H5N8 had been found in samples from wild birds in the country. As a countermeasure, it was required that birds in poultry farms were kept indoors and isolated. From late October to mid-November, it had spread to three chicken farms and a duck farm in the country, and the 320,000 birds in the farms had been eradicated to stop the spread. Shortly after the first detection in the Netherlands, it was confirmed in the United Kingdom (October: poultry; November: wild birds and poultry), Germany (October: wild birds; November: wild birds and poultry), Ireland (October and November: wild birds), Belgium (November: wild birds), Denmark (November: wild birds and poultry), France (November: poultry) and Sweden (November: poultry). These outbreaks resulted in countermeasures that were similar to those already taken in the Netherlands. According to official confirmed reports from the Ministry of Agriculture Forestry and Fisheries of Japan, multiple dead chickens were found in 49 chicken poultry farms in Japan, from 5 November 2020 to 25 February 2021, 16 places in Shikoku Island , 15 places in Kyushu Island , ten places in Kantō region , five places in western Honshu and each one place in Awaji Island , Gifu Prefecture , and Toyama Prefecture . According to local official confirmed report, these cases were highly pathogenic H5N8 type flu. [ citation needed ] On 10 November, South Korea's agriculture ministry said it had confirmed the highly pathogenic H5N8 strain of bird flu in samples from wild birds in the central west of the country and issued its bird flu warning. At the end of November 2020, about 10,500 turkeys were killed on a British farm in North Yorkshire in order to limit the spread of H5N8 bird flu after health officials discovered an outbreak. On 16 December several birds were found dead on the Isle of Wight, in the UK, and the cause of death was identified as H5N8. [ citation needed ] India reported the virus first in the migratory birds following which in January 2021 culling of chickens and ducks began on Tuesday 6 Jan in parts of Kerala to contain the H5N8 strain of bird flu, while Jammu and Kashmir sounded an alert and started collecting samples from migratory species after Himachal Pradesh, Rajasthan and Madhya Pradesh reported cases of avian influenza. Kerala officials have said around 40,000 domestic birds, including 34,000 in the Kuttanad region alone, will be culled to check the spread of the H5N8 virus. Till now, 2,700 migratory birds, mostly bar-headed geese, have been found dead in the lake area and samples have been sent for testing, state animal husbandry officials said. According to Japan's Ministry of Agriculture, Forestry and Fisheries official report, several dead edible ducks were found in two poultry farms near Narita , Chiba Prefecture . Both cases were confirmed as H5N8 type bird flu via genetic test by a regional official on 21 January and 24. 5400 ducks were culled in response. As a larger nationwide trend in avian flu, 7 million poultry were culled with aid from the Japan Ground Self-Defense Force as of February 17, 2021. On 20 February 2021, Russia reported the first known cases of H5N8 in humans. Seven people were confirmed to have been infected at a farm in southern Russia where outbreaks had been reported. There was no indication of human-to-human transmission and the seven cases were described as "mild." Anna Popova , head of Rospotrebnadzor , has said the seven poultry workers have since recovered, and that "the situation did not develop further." WHO later confirmed that all cases remained asymptomatic for the whole follow-up. In an interview published in The Moscow Times on 12 March 2021, Popova warned that there was a "high degree of probability" of human-to-human transmission of H5N8. Perhaps the most known outbreak of H5N8 occurred in Ireland in 1983. Poultry on two farms showed the usual symptoms, plus diarrhea, nervousness, and depression. Poultry farms within close proximity soon began to show signs of infection, as well, but no contact between the farms could be established. In the end, 8,000 turkeys, 28,020 chickens, and 270,000 ducks were culled. When investigated in the lab, clinical findings demonstrated that turkeys were the most susceptible to infection. The virus could not be clinically reproduced in ducks. An outbreak of H5N8 was reported in breeding ducks in North Jeolla Province , South Korea , on 18 January 2014. The virus spread in duck and chicken farms and at least 12 million poultry were culled. In the second half of 2016, an H5N8 outbreak was first reported in Europe, spreading to Asia by the end of the year. [ citation needed ] On 27 October 2016, an H5N8 case was first reported in a wild swan in Hungary . Further reports were subsequently made from seven additional European countries. There were outbreaks in poultry and wild birds in Austria , Hungary , and Germany . There were reports of infection in wild birds only in Croatia, Denmark, Poland, and Switzerland. [ citation needed ] In the Netherlands, H5N8 was found in wild birds and birds in a zoo and on 26 November 190,000 ducks were destroyed at six farms. Outbreaks have also been reported in India, Israel, South Korea, Taiwan and Russia. On 16 December 2016, it was confirmed that there was an outbreak of the H5N8 virus at a farm near Tetney, Louth — the first outbreak in the United Kingdom. This outbreak has caused the combined death and culling of 5,000 turkeys. At the time of writing (16 December 2016), a 3 km protection zone and a 10 km surveillance zone were enforced by the Department for Environment, Food and Rural Affairs. In the second week of December official delegations from Japan, South Korea and China gathered in Beijing for a symposium on preventing and controlling bird flu and other diseases in East Asia, according to the website of China's ministry of agriculture. By the end of December the outbreak had spread to South Korea, Japan, Germany, and the United Kingdom. Thousands of birds and animals were being culled in Germany to stop the spread. In the United Kingdom the flu was found in a wild duck at a turkey farm in Lincolnshire. In South Korea, a record total of 18.4 million birds had been killed by December since the first outbreak of avian flu was reported at a farm on Nov. 18. Japan has reported five outbreaks since the end of November with 800,000 chickens having been culled in one month. In early January 2017, France culled about 800,000 birds to prevent the spread of H5N8. In Nigeria , it was reported that the virus affected 3.5 million birds. The virus was also detected in Spain and Slovenia . Uganda detected aves flu in two locations, one affecting wild birds and another striking domestic birds. Two cases of the virus were detected in Northern Ireland amongst wild geese. As a response, the Department of Agriculture extended restrictions on poultry flocks until at least 16 March. A case of the virus was detected in Harare , Zimbabwe at one of the major poultry producers, Irvine's Private Limited. The virus saw over 7,000 birds succumbing to the virus. As a result, the company, culled over 140,000 birds to prevent the spread of the virus. Even though a ban on all avian products from Zimbabwe was issued, on 22 June an outbreak was reported at a commercial broiler poultry farm outside Villiers , South Africa after 5,000 chickens died. A few days later, just over 60 km away from the first outbreak, a separate outbreak was reported in Standerton , Mpumalanga , where over 25,000 birds were culled to prevent the virus spreading. The South African Poultry Association reported that wild ducks migrating from Europe are spreading the virus. On 20 December 2017, the Ministry of Environment, Water and Agriculture (MEWA) in Saudi Arabia announced the detection of the highly pathogenic H5N8 virus among birds at a poultry market in Riyadh. A few days later, the virus was detected in other farms in other cities including Al-Ahsa, Al-Kharj, Al-Quaiyat, Dharma, and Mazahmiya. This outbreak in the country led to a cull of more than 100,000 birds at 12 locations across the country to prevent the spread of the virus. On 27 October 2016, an H5N8 case was first reported in a wild swan in Hungary . Further reports were subsequently made from seven additional European countries. There were outbreaks in poultry and wild birds in Austria , Hungary , and Germany . There were reports of infection in wild birds only in Croatia, Denmark, Poland, and Switzerland. [ citation needed ]In the Netherlands, H5N8 was found in wild birds and birds in a zoo and on 26 November 190,000 ducks were destroyed at six farms. Outbreaks have also been reported in India, Israel, South Korea, Taiwan and Russia. On 16 December 2016, it was confirmed that there was an outbreak of the H5N8 virus at a farm near Tetney, Louth — the first outbreak in the United Kingdom. This outbreak has caused the combined death and culling of 5,000 turkeys. At the time of writing (16 December 2016), a 3 km protection zone and a 10 km surveillance zone were enforced by the Department for Environment, Food and Rural Affairs. In the second week of December official delegations from Japan, South Korea and China gathered in Beijing for a symposium on preventing and controlling bird flu and other diseases in East Asia, according to the website of China's ministry of agriculture. By the end of December the outbreak had spread to South Korea, Japan, Germany, and the United Kingdom. Thousands of birds and animals were being culled in Germany to stop the spread. In the United Kingdom the flu was found in a wild duck at a turkey farm in Lincolnshire. In South Korea, a record total of 18.4 million birds had been killed by December since the first outbreak of avian flu was reported at a farm on Nov. 18. Japan has reported five outbreaks since the end of November with 800,000 chickens having been culled in one month. In early January 2017, France culled about 800,000 birds to prevent the spread of H5N8. In Nigeria , it was reported that the virus affected 3.5 million birds. The virus was also detected in Spain and Slovenia . Uganda detected aves flu in two locations, one affecting wild birds and another striking domestic birds. Two cases of the virus were detected in Northern Ireland amongst wild geese. As a response, the Department of Agriculture extended restrictions on poultry flocks until at least 16 March. A case of the virus was detected in Harare , Zimbabwe at one of the major poultry producers, Irvine's Private Limited. The virus saw over 7,000 birds succumbing to the virus. As a result, the company, culled over 140,000 birds to prevent the spread of the virus. Even though a ban on all avian products from Zimbabwe was issued, on 22 June an outbreak was reported at a commercial broiler poultry farm outside Villiers , South Africa after 5,000 chickens died. A few days later, just over 60 km away from the first outbreak, a separate outbreak was reported in Standerton , Mpumalanga , where over 25,000 birds were culled to prevent the virus spreading. The South African Poultry Association reported that wild ducks migrating from Europe are spreading the virus. On 20 December 2017, the Ministry of Environment, Water and Agriculture (MEWA) in Saudi Arabia announced the detection of the highly pathogenic H5N8 virus among birds at a poultry market in Riyadh. A few days later, the virus was detected in other farms in other cities including Al-Ahsa, Al-Kharj, Al-Quaiyat, Dharma, and Mazahmiya. This outbreak in the country led to a cull of more than 100,000 birds at 12 locations across the country to prevent the spread of the virus. On 4 February, Saudi Arabia reported an outbreak of the highly pathogenic H5N8 bird flu virus on a poultry farm. The outbreak, which occurred in the central Sudair region, killed 22,700 birds. In the summer of 2020, H5N8 was detected in wild birds in western Russia and Kazakhstan. Because this included waterbirds that migrate into northern and western Europe, it was considered likely that the virus would be detected there later in the year (as would be confirmed in October–November). On 22 October, the agriculture minister Carola Schouten of the Netherlands confirmed that H5N8 had been found in samples from wild birds in the country. As a countermeasure, it was required that birds in poultry farms were kept indoors and isolated. From late October to mid-November, it had spread to three chicken farms and a duck farm in the country, and the 320,000 birds in the farms had been eradicated to stop the spread. Shortly after the first detection in the Netherlands, it was confirmed in the United Kingdom (October: poultry; November: wild birds and poultry), Germany (October: wild birds; November: wild birds and poultry), Ireland (October and November: wild birds), Belgium (November: wild birds), Denmark (November: wild birds and poultry), France (November: poultry) and Sweden (November: poultry). These outbreaks resulted in countermeasures that were similar to those already taken in the Netherlands. According to official confirmed reports from the Ministry of Agriculture Forestry and Fisheries of Japan, multiple dead chickens were found in 49 chicken poultry farms in Japan, from 5 November 2020 to 25 February 2021, 16 places in Shikoku Island , 15 places in Kyushu Island , ten places in Kantō region , five places in western Honshu and each one place in Awaji Island , Gifu Prefecture , and Toyama Prefecture . According to local official confirmed report, these cases were highly pathogenic H5N8 type flu. [ citation needed ] On 10 November, South Korea's agriculture ministry said it had confirmed the highly pathogenic H5N8 strain of bird flu in samples from wild birds in the central west of the country and issued its bird flu warning. At the end of November 2020, about 10,500 turkeys were killed on a British farm in North Yorkshire in order to limit the spread of H5N8 bird flu after health officials discovered an outbreak. On 16 December several birds were found dead on the Isle of Wight, in the UK, and the cause of death was identified as H5N8. [ citation needed ]On 4 February, Saudi Arabia reported an outbreak of the highly pathogenic H5N8 bird flu virus on a poultry farm. The outbreak, which occurred in the central Sudair region, killed 22,700 birds. In the summer of 2020, H5N8 was detected in wild birds in western Russia and Kazakhstan. Because this included waterbirds that migrate into northern and western Europe, it was considered likely that the virus would be detected there later in the year (as would be confirmed in October–November). On 22 October, the agriculture minister Carola Schouten of the Netherlands confirmed that H5N8 had been found in samples from wild birds in the country. As a countermeasure, it was required that birds in poultry farms were kept indoors and isolated. From late October to mid-November, it had spread to three chicken farms and a duck farm in the country, and the 320,000 birds in the farms had been eradicated to stop the spread. Shortly after the first detection in the Netherlands, it was confirmed in the United Kingdom (October: poultry; November: wild birds and poultry), Germany (October: wild birds; November: wild birds and poultry), Ireland (October and November: wild birds), Belgium (November: wild birds), Denmark (November: wild birds and poultry), France (November: poultry) and Sweden (November: poultry). These outbreaks resulted in countermeasures that were similar to those already taken in the Netherlands. According to official confirmed reports from the Ministry of Agriculture Forestry and Fisheries of Japan, multiple dead chickens were found in 49 chicken poultry farms in Japan, from 5 November 2020 to 25 February 2021, 16 places in Shikoku Island , 15 places in Kyushu Island , ten places in Kantō region , five places in western Honshu and each one place in Awaji Island , Gifu Prefecture , and Toyama Prefecture . According to local official confirmed report, these cases were highly pathogenic H5N8 type flu. [ citation needed ] On 10 November, South Korea's agriculture ministry said it had confirmed the highly pathogenic H5N8 strain of bird flu in samples from wild birds in the central west of the country and issued its bird flu warning. At the end of November 2020, about 10,500 turkeys were killed on a British farm in North Yorkshire in order to limit the spread of H5N8 bird flu after health officials discovered an outbreak. On 16 December several birds were found dead on the Isle of Wight, in the UK, and the cause of death was identified as H5N8. [ citation needed ]India reported the virus first in the migratory birds following which in January 2021 culling of chickens and ducks began on Tuesday 6 Jan in parts of Kerala to contain the H5N8 strain of bird flu, while Jammu and Kashmir sounded an alert and started collecting samples from migratory species after Himachal Pradesh, Rajasthan and Madhya Pradesh reported cases of avian influenza. Kerala officials have said around 40,000 domestic birds, including 34,000 in the Kuttanad region alone, will be culled to check the spread of the H5N8 virus. Till now, 2,700 migratory birds, mostly bar-headed geese, have been found dead in the lake area and samples have been sent for testing, state animal husbandry officials said. According to Japan's Ministry of Agriculture, Forestry and Fisheries official report, several dead edible ducks were found in two poultry farms near Narita , Chiba Prefecture . Both cases were confirmed as H5N8 type bird flu via genetic test by a regional official on 21 January and 24. 5400 ducks were culled in response. As a larger nationwide trend in avian flu, 7 million poultry were culled with aid from the Japan Ground Self-Defense Force as of February 17, 2021. On 20 February 2021, Russia reported the first known cases of H5N8 in humans. Seven people were confirmed to have been infected at a farm in southern Russia where outbreaks had been reported. There was no indication of human-to-human transmission and the seven cases were described as "mild." Anna Popova , head of Rospotrebnadzor , has said the seven poultry workers have since recovered, and that "the situation did not develop further." WHO later confirmed that all cases remained asymptomatic for the whole follow-up. In an interview published in The Moscow Times on 12 March 2021, Popova warned that there was a "high degree of probability" of human-to-human transmission of H5N8. India reported the virus first in the migratory birds following which in January 2021 culling of chickens and ducks began on Tuesday 6 Jan in parts of Kerala to contain the H5N8 strain of bird flu, while Jammu and Kashmir sounded an alert and started collecting samples from migratory species after Himachal Pradesh, Rajasthan and Madhya Pradesh reported cases of avian influenza. Kerala officials have said around 40,000 domestic birds, including 34,000 in the Kuttanad region alone, will be culled to check the spread of the H5N8 virus. Till now, 2,700 migratory birds, mostly bar-headed geese, have been found dead in the lake area and samples have been sent for testing, state animal husbandry officials said. According to Japan's Ministry of Agriculture, Forestry and Fisheries official report, several dead edible ducks were found in two poultry farms near Narita , Chiba Prefecture . Both cases were confirmed as H5N8 type bird flu via genetic test by a regional official on 21 January and 24. 5400 ducks were culled in response. As a larger nationwide trend in avian flu, 7 million poultry were culled with aid from the Japan Ground Self-Defense Force as of February 17, 2021. On 20 February 2021, Russia reported the first known cases of H5N8 in humans. Seven people were confirmed to have been infected at a farm in southern Russia where outbreaks had been reported. There was no indication of human-to-human transmission and the seven cases were described as "mild." Anna Popova , head of Rospotrebnadzor , has said the seven poultry workers have since recovered, and that "the situation did not develop further." WHO later confirmed that all cases remained asymptomatic for the whole follow-up. In an interview published in The Moscow Times on 12 March 2021, Popova warned that there was a "high degree of probability" of human-to-human transmission of H5N8.

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Avian influenza

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Influenza A virus subtype H5N2

H5 N2 is a subtype of the species Influenzavirus A (avian influenza virus or bird flu virus). The subtype infects a wide variety of birds, including chickens, ducks, turkeys, falcons, and ostriches. Affected birds usually do not appear ill, and the disease is often mild as avian influenza viral subtypes go. Some variants of the subtype are much more pathogenic than others, and outbreaks of "high-path" H5N2 result in the culling of thousands of birds in poultry farms from time to time. It appears that people who work with birds can be infected by the virus, but suffer hardly any noticeable health effects. Even people exposed to the highly pathogenic H5N2 variety that killed ostrich chicks in South Africa only seem to have developed conjunctivitis, or a perhaps a mild respiratory illness. There is no evidence of human-to-human spread of H5N2. On November 12, 2005 it was reported that a falcon was found to have H5N2. In China, inactivated H5N2 has been effectively used as a poultry vaccine for H5N1 . In December 2017, the Paris-based World Organisation for Animal Health (OIE) announced that the Russian ministry of agriculture detected highly pathogenic H5N2 that led to the culling of more than 660,000 birds in Kostroma Oblast , Central Federal District . Owners reported that the chickens stopped breathing and their combs became bluish. The factory was affected by the virus at least twice during the year. The investigation later found that the forage wasn't thermally disinfected before dispersion and water was of low quality. In Korea, ducks have been destroyed at the farm since quarantine officials detected the suspected low pathogenic H5N2 strain of avian influenza on December 1, 2004. In Japan, H5N2 virus was isolated or an anti-H5 antibody was identified from chickens in 40 chicken farms in Ibaraki Prefecture and in one chicken farm in Saitama Prefecture from June through December 2005. The strain was named as A/ chicken /Ibaraki/1/2005(H5N2). About 5.7 million birds were destroyed in Ibaraki following the H5N2 outbreaks. [ citation needed ] In Taiwan , an outbreak of H5N2 was confirmed in December 2008. In March 2012, the first documented occurrence in Taiwan of highly pathogenic avian influenza H5N2 was reported to the World Organization for Animal Health (OIE). The outbreak began in February 2012. In Sri Lanka outbreak of H5N2 in Bingiriya have been confirmed by the Health Ministry in January 2012. Around 5000-6000 chicken were destroyed, after some of them were confirmed having infected with H5N2. In 2006, an H5N2 outbreak on a single farm in South Africa resulted in the destruction of all its sixty ostriches . The strain was similar to the one that caused outbreaks in South Africa 2004/2005. In 2012 a strain of highly pathogenic avian influenza is devastating the South African commercial ostrich industry with 41,000 birds already been reported culled. Low pathogenic avian influenza H5N2 virus in poultry later gained accentuated virulence in the United States and Mexico. A highly pathogenic strain of H5N2 caused flu outbreaks with significant spread to numerous farms, resulting in great economic losses in 1983 in Pennsylvania, USA in chickens and turkeys, in 1994 in Mexico in chickens and a minor outbreak in 1997 in Italy in chickens. In February 2004, an outbreak occurred in Texas and the affected flock was culled without any further transmission. In 2007, a low-pathogenic strain of H5N2 was found in samples collected from 25,000 turkeys in West Virginia in a routine testing prior to their slaughter. The birds showed no sign of illness or mortality. Measures were taken to prevent the virus from mutating and spreading. In 2015, an outbreak of H5N2 was identified in a series of chicken and turkey farming operations in the Midwestern region of the United States . As of 30 May, more than 43 million birds in 15 states had been destroyed as a result of the outbreak, including nearly 30 million in Iowa alone, the nation's largest egg producer. In January 2017, the US Department of Agriculture announced that H5N2 was discovered on a duck in Fergus County, Montana . In February 2009, a commercial turkey farm in Abbottsford , British Columbia (the Fraser Valley ) was struck with a H5N2 outbreak, and 36 sites were quarantined as precautionary measure. In July 2016, a duck farm "near St. Catharines, Ontario " was the site of an outbreak of H5N2. The CFIA directed the biological heat treatment of the compost at the infected premises to ensure that a reservoir for the virus was destroyed. In late 2007 (December 21), an H5N2 outbreak was found in the Dominican Republic. 15 roosters and 2 hens were eliminated even though they had no visible sign of infection. In October 2017, the Dominican Department of Agriculture announced that H5N2 was discovered on several chicken in Moca, Dominican Republic , in a northern province of the country. In May and June 2008, there were three outbreaks of low-pathogenic H5N2 avian flu in birds at three locations in the central, northern, and southern parts of Haiti . In December 2017, the Paris-based World Organisation for Animal Health (OIE) announced that the Russian ministry of agriculture detected highly pathogenic H5N2 that led to the culling of more than 660,000 birds in Kostroma Oblast , Central Federal District . Owners reported that the chickens stopped breathing and their combs became bluish. The factory was affected by the virus at least twice during the year. The investigation later found that the forage wasn't thermally disinfected before dispersion and water was of low quality. In Korea, ducks have been destroyed at the farm since quarantine officials detected the suspected low pathogenic H5N2 strain of avian influenza on December 1, 2004. In Japan, H5N2 virus was isolated or an anti-H5 antibody was identified from chickens in 40 chicken farms in Ibaraki Prefecture and in one chicken farm in Saitama Prefecture from June through December 2005. The strain was named as A/ chicken /Ibaraki/1/2005(H5N2). About 5.7 million birds were destroyed in Ibaraki following the H5N2 outbreaks. [ citation needed ]In Taiwan , an outbreak of H5N2 was confirmed in December 2008. In March 2012, the first documented occurrence in Taiwan of highly pathogenic avian influenza H5N2 was reported to the World Organization for Animal Health (OIE). The outbreak began in February 2012. In Sri Lanka outbreak of H5N2 in Bingiriya have been confirmed by the Health Ministry in January 2012. Around 5000-6000 chicken were destroyed, after some of them were confirmed having infected with H5N2. In 2006, an H5N2 outbreak on a single farm in South Africa resulted in the destruction of all its sixty ostriches . The strain was similar to the one that caused outbreaks in South Africa 2004/2005. In 2012 a strain of highly pathogenic avian influenza is devastating the South African commercial ostrich industry with 41,000 birds already been reported culled. Low pathogenic avian influenza H5N2 virus in poultry later gained accentuated virulence in the United States and Mexico. A highly pathogenic strain of H5N2 caused flu outbreaks with significant spread to numerous farms, resulting in great economic losses in 1983 in Pennsylvania, USA in chickens and turkeys, in 1994 in Mexico in chickens and a minor outbreak in 1997 in Italy in chickens. In February 2004, an outbreak occurred in Texas and the affected flock was culled without any further transmission. In 2007, a low-pathogenic strain of H5N2 was found in samples collected from 25,000 turkeys in West Virginia in a routine testing prior to their slaughter. The birds showed no sign of illness or mortality. Measures were taken to prevent the virus from mutating and spreading. In 2015, an outbreak of H5N2 was identified in a series of chicken and turkey farming operations in the Midwestern region of the United States . As of 30 May, more than 43 million birds in 15 states had been destroyed as a result of the outbreak, including nearly 30 million in Iowa alone, the nation's largest egg producer. In January 2017, the US Department of Agriculture announced that H5N2 was discovered on a duck in Fergus County, Montana . In February 2009, a commercial turkey farm in Abbottsford , British Columbia (the Fraser Valley ) was struck with a H5N2 outbreak, and 36 sites were quarantined as precautionary measure. In July 2016, a duck farm "near St. Catharines, Ontario " was the site of an outbreak of H5N2. The CFIA directed the biological heat treatment of the compost at the infected premises to ensure that a reservoir for the virus was destroyed. In late 2007 (December 21), an H5N2 outbreak was found in the Dominican Republic. 15 roosters and 2 hens were eliminated even though they had no visible sign of infection. In October 2017, the Dominican Department of Agriculture announced that H5N2 was discovered on several chicken in Moca, Dominican Republic , in a northern province of the country. In May and June 2008, there were three outbreaks of low-pathogenic H5N2 avian flu in birds at three locations in the central, northern, and southern parts of Haiti . Japan's Health Ministry said in January, 2006 that poultry farm workers in Ibaraki prefecture may have been exposed to H5N2 (which was not previously known to infect humans) in 2005. Data were collected from 257 workers at 35 chicken farms by Ibaraki prefectural government. It was determined that their H5N2 antibody titers after the outbreak were significantly higher than those collected prior to the outbreak.

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Avian influenza

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Timeline of influenza

This is a timeline of influenza , briefly describing major events such as outbreaks , epidemics , pandemics , discoveries and developments of vaccines . In addition to specific year/period-related events, there is the seasonal flu that kills between 250,000 and 500,000 people every year and has claimed between 340 million and 1 billion human lives throughout history. The 1557 influenza pandemic spread from Asia to the Ottoman Empire , then Europe, the Americas , and Africa. This flu pandemic is the first to be reliably recorded as spreading worldwide, is when flu received its first English names. It is also the first pandemic in which flu is linked to miscarriages. The pandemic lasted for at least two years. : 307–308 The 1580 pandemic is well-documented, with high mortality recorded as influenza spreads across Europe. Influenza has been studied by countless physicians, epidemiologists, and medical historians. Chroniclers distinguished its outbreaks from other diseases by the rapid, indiscriminate way it struck down entire populations. Flu has been called various names including tac , coqueluche , the new disease , gruppie , grippe , castrone , : 17 influenza , and commonly just catarrh by many chroniclers and physicians throughout the ages. The disease seems to have been present in the northeast United States as early as October 1732, after which reports of it came out of Newfoundland , Barbados , Jamaica , Mexico , Peru , and Chile . : 9 : 23 The following month it appeared in Germany, reportedly coming from Russia through Poland . : 23 It spread throughout Germany in November and into December, when it caused outbreaks in Switzerland and Holland through the end of the year. : 23 Notably, it was reported on the Isle of Bourbon , off of Madagascar , in December as well. : 9 It prevailed in London and Paris in January 1733, as well as the Netherlands ; that same month, it was reported in Italy, where it continued into March. : 9 Madrid was visited in February. : 9 Though the name had been used in English before, this was the first time "influenza" was broadly used to refer to the disease. While it prevailed extensively in Italy, the rumor of a "great epidemic" of "influenza" in that country spread faster than the disease itself, and the name came to be used in England, at least for the duration of the outbreak. Once it had passed, the name fell out of common use. : 304 On the whole, the epidemic was notable for seeming to follow no clear path, "being reported now here, now there," : 27 and for missing certain locales altogether, such as Paris. : 358 Morbidity was "great" where the disease did strike. : 27 Mortality was relatively low, though it did vary, with some cities seeing more severe epidemics than others even within the same country. : 27 : 358 Spontaneous abortions and premature births were reported as new complications during this pandemic, which can be taken as a piece of supporting evidence that this was indeed a pandemic of influenza, in addition to its high attack rate and broad distribution across at least two continents. : 27 Other authors, however, consider only the 1781–1782 experience to be a true pandemic. : 18 : 30 : 27 If anything, the outbreaks in Russia and North America in 1780–1781 were possible "herald waves" of the later, greater epidemic. : 27 During this true pandemic period, influenza is said to have first broken out in China and British India in the fall of 1781. : 11 By the winter, it was sweeping through Siberia and Russia, visiting St. Petersburg again in January 1782. : 11 It moved through Germany between February and June. : 11 It struck Finland in February and Denmark, Sweden, and Hungary in April. After reaching England as early as April, influenza broke out in London and other parts in May and was general in England and Scotland in June. : 11 After hitting the Netherlands in May, it spread to France and then to Italy, where it broke out in June. : 30 Finally, it reached Spain by August, prevailing in Madrid and other parts. : 11 This epidemic solidified "influenza" as the name of the disease in English. Although first used generally in 1743 to refer to the affliction epidemic in Italy at the time, it was not until an epidemic in 1775 that the term began to be used again more generally, and by 1782, it was the typical name applied. In the summer of that year, when the disease hit England, the Royal College of Physicians formally adopted the Italian word as the official name. : 362 The influenza was first reported in Russia in March 1788, in St. Petersburg and Kherson and in Poland. : 11 It then spread westward, invading Germany, Hungary, Denmark, England, Scotland, France, and Italy successively throughout the year and being reported finally in Switzerland in October. : 11 Observed influenza activity then remained low for nearly a year before the disease appeared in the Western Hemisphere, breaking out in the US states of Georgia and New York in September 1789. : 11 The epidemic crossed the entire United States in six to eight weeks. : 290 It was reported in Jamaica in October : 11 and Grenada in November, : 256–257 and by the end of the year it was prevalent in Nova Scotia and South America . : 11 After a short reprieve, the influenza resumed epidemic proportions in the spring of 1790 in the northeast United States and perhaps some other parts, : 12 declining about the first week of June. : 259 There is some evidence of increased severity during the spring wave as compared to the fall one. : 291 The disease was prevalent again in Philadelphia and neighboring counties in Pennsylvania , and was observed as well in Virginia and Rhode Island , in the winter of 1790–1791, but it was not nearly as widespread as its first two appearances. : 260

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Avian influenza

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Influenza A virus subtype H7N7

Influenza A virus subtype H7N7 (A/H7N7) is a subtype of Influenza A virus , a genus of Orthomyxovirus , the viruses responsible for influenza . Highly pathogenic strains (HPAI) and low pathogenic strains (LPAI) exist. H7N7 can infect humans, birds, pigs, seals , and horses in the wild; and has infected mice in laboratory studies. This unusual zoonotic potential represents a pandemic threat. In 2003, 89 people in the Netherlands were confirmed to have been infected by H7N7 following an outbreak in poultry on approximately 255 farms. One death was recorded – a veterinarian who had been testing chickens for the virus – and all infected flocks were culled. Most affected people had mild symptoms including conjunctivitis . Antibodies were found in over half of 500 people tested according to the final official report by the Dutch government: As at least 50% of the people exposed to infected poultry had H7 antibodies detectable with the modified assay, it was estimated that avian influenza A/H7N7 virus infection occurred in at least 1000, and perhaps as many as 2000 people. The seroprevalence of H7 antibodies in people without contact with infected poultry, but with close household contact to an infected poultry worker, was 59%. This suggests that the population at risk for avian influenza was not limited to those with direct contact to infected poultry, and that person to person transmission may have occurred on a large scale. Final analysis of Dutch avian influenza outbreaks reveals much higher levels of transmission to humans than previously thought. In August 2006, low pathogenic (LP) H7N7 was found during routine testing at a poultry farm in Voorthuizen in the central Netherlands. As a precautionary measure, 25,000 chickens were culled from Voorthuizen and surrounding farms. In June 2008, high pathogenic (HP) H7N7 was confirmed on a 25,000-bird laying unit at Shenington , England; probably derived from a pre-existing low pathogenic variety. Farmers Guardian reported a 2.5 per cent increased mortality in one shed and a reduction in egg production recorded two weeks before numerous deaths on 2 June that led to the diagnosis of HP H7N7 on 4 June. In October 2009, high pathogenic (HP) H7N7 was confirmed on a farm in Almoguera , Guadalajara , Spain. Hong Kong announced that it would suspend the import of poultry from Spain. In August 2013, high pathogenic (HP) H7N7 was found in markets in Wenzhou , Zhejiang province in China when testing for H7N9. In July 2015, high pathogenic (HP) H7N7 was confirmed on a poultry farm in Lancashire , England . In August 2020, H7N7 was confirmed on a free range farm in Lethbridge, Victoria .

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Avian influenza

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Influenza A virus subtype H1N1

In virology , influenza A virus subtype H1N1 ( A/H1N1 ) is a subtype of influenza A virus . Major outbreaks of H1N1 strains in humans include the 1918 Spanish flu pandemic , the 1977 Russian flu pandemic and the 2009 swine flu pandemic . It is an orthomyxovirus that contains the glycoproteins hemagglutinin (H) and neuraminidase (N), antigens whose subtypes are used to classify the strains of the virus as H1N1, H1N2 etc. Hemagglutinin causes red blood cells to clump together and binds the virus to the infected cell. Neuraminidase is a type of glycoside hydrolase enzyme which helps to move the virus particles through the infected cell and assist in budding from the host cells. Some strains of H1N1 are endemic in humans and cause a small fraction of all influenza-like illness and a small fraction of all seasonal influenza , for instance in 2004–2005. Other strains of H1N1 are endemic in pigs ( swine influenza ) and in birds ( avian influenza ). Its size is 80 to 120 nm (3.1 × 10 −6 to 4.7 × 10 −6 in) in diameter. Genetic analyses of virus from tissue preserved medically or in permafrost suggest that modern seasonal H1N1 strains descended from the 1918 flu pandemic virus, but not conclusively so. Swine influenza (also known as swine flu or pig flu) is a respiratory disease that occurs in pigs that is caused by the Influenza A virus. Influenza viruses that are normally found in swine are known as swine influenza viruses (SIVs). The known SIV strains include influenza C and the subtypes of influenza A known as H1N1, H1N2 , H3N1 , H3N2 and H2N3 . Pigs can also become infected with the H4N6 and H9N2 subtypes. Swine influenza virus is common throughout pig populations worldwide. Transmission of the virus from pigs to humans is not common and does not always lead to human influenza, often resulting only in the production of antibodies in the blood. If transmission does cause human influenza, it is called zoonotic swine flu or a variant virus. People with regular exposure to pigs are at increased risk of swine flu infection. Properly cooking the meat of an infected animal removes the risk of infection. Pigs experimentally infected with the strain of swine flu that caused the human pandemic of 2009–10 showed clinical signs of flu within four days, and the virus spread to other uninfected pigs housed with the infected ones. The 1918 flu was an unusually severe and deadly strain of H1N1 avian influenza , which killed from 17 to 50 or more million people worldwide over about a year in 1918 and 1920. It was one of the deadliest pandemics in human history . The 1918 flu caused an abnormally high number of deaths, possibly due to it provoking a cytokine storm in the body. (The H5N1 bird flu , also an Influenza A virus, has a similar effect.) After the 1918 flu infected lung cells, it frequently led to overstimulation of the immune system via release of immune response-stimulating cytokines (proteins that transmit signals between cells) into the lung tissue. This leads to extensive leukocyte migration towards the lungs, resulting in the destruction of lung cells and secretion of blood and mucus into the alveoli and airways. This makes it difficult for the patient to breathe and can result in suffocation. In contrast to other pandemics, which mostly kill the old and the very young, the 1918 pandemic killed unusual numbers of young adults, which may have been due to their healthy immune systems mounting a too-strong and damaging response to the infection. The term "Spanish" flu was coined because Spain was at the time the only European country where the press were printing reports of the outbreak, which had killed thousands in the armies fighting World War I (1914–1918). Other countries suppressed the news in order to protect morale. In 1976, a novel swine influenza A (H1N1) caused severe respiratory illness in 13 soldiers, with one death at Fort Dix , New Jersey. The virus was detected only from 19 January to 9 February and did not spread beyond Fort Dix. Retrospective serologic testing subsequently demonstrated that up to 230 soldiers had been infected with the novel virus, which was an H1N1 strain. The cause of the outbreak is still unknown and no exposure to pigs was identified. The 1977 Russian flu pandemic was caused by strain Influenza A/USSR/90/77 (H1N1) . It infected mostly children and young adults under 23; because a similar strain was prevalent in 1947–57, most adults had substantial immunity. Later analysis found that the re-emergent strain had been circulating for approximately one year before it was detected in China and Russia. The virus was included in the 1978–79 influenza vaccine . In the 2009 flu pandemic , the virus isolated from patients in the United States was found to be made up of genetic elements from four different flu viruses – North American swine influenza, North American avian influenza, human influenza, and swine influenza virus typically found in Asia and Europe – "an unusually mongrelised mix of genetic sequences." This new strain appears to be a result of reassortment of human influenza and swine influenza viruses, in all four different strains of subtype H1N1. Preliminary genetic characterization found that the hemagglutinin (HA) gene was similar to that of swine flu viruses present in U.S. pigs since 1999, but the neuraminidase (NA) and matrix protein (M) genes resembled versions present in European swine flu isolates. The six genes from American swine flu are themselves mixtures of swine flu, bird flu, and human flu viruses. While viruses with this genetic makeup had not previously been found to be circulating in humans or pigs, there is no formal national surveillance system to determine what viruses are circulating in pigs in the U.S. In April 2009, an outbreak of influenza-like illness (ILI) occurred in Mexico and then in the United States; the CDC reported seven cases of novel A/H1N1 influenza and promptly shared the genetic sequences on the GISAID database. With similar timely sharing of data for Mexican isolates, by 24 April it became clear that the outbreak of ILI in Mexico and the confirmed cases of novel influenza A in the southwest US were related and WHO issued a health advisory on the outbreak of "influenza-like illness in the United States and Mexico". The disease then spread very rapidly, with the number of confirmed cases rising to 2,099 by 7 May, despite aggressive measures taken by the Mexican government to curb the spread of the disease. The outbreak had been predicted a year earlier by noticing the increasing number of replikins , a type of peptide , found in the virus. On 11 June 2009, the WHO declared an H1N1 pandemic, moving the alert level to phase 6, marking the first global pandemic since the 1968 Hong Kong flu . On 25 October 2009, U.S. President Barack Obama officially declared H1N1 a national emergency . The President's declaration caused many U.S. employers to take actions to help stem the spread of the swine flu and to accommodate employees and / or workflow which may have been impacted by an outbreak. A study conducted in coordination with the University of Michigan Health Service – scheduled for publication in the December 2009 American Journal of Roentgenology – warned that H1N1 flu can cause pulmonary embolism , surmised as a leading cause of death in this pandemic. The study authors suggest physician evaluation via contrast enhanced CT scans for the presence of pulmonary emboli when caring for patients diagnosed with respiratory complications from a "severe" case of the H1N1 flu. H1N1 may induce other embolic events, such as myocardial infarction , bilateral massive DVT , arterial thrombus of infrarenal aorta, thrombosis of right external iliac vein and common femoral vein or cerebral gas embolism. The type of embolic events caused by H1N1 infection are summarized in a 2010 review by Dimitroulis Ioannis et al. The 21 March 2010 worldwide update, by the U.N.'s World Health Organization (WHO), states that "213 countries and overseas territories/communities have reported laboratory confirmed cases of pandemic influenza H1N1 2009, including at least 16,931 deaths." As of 30 May 2010 [ update ] , worldwide update by World Health Organization (WHO) more than 214 countries and overseas territories or communities have reported laboratory confirmed cases of pandemic influenza H1N1 2009, including over 18,138 deaths. The research team of Andrew Miller showed pregnant patients are at increased risk. It has been suggested that pregnant women and certain populations such as native North Americans have a greater likelihood of developing a T helper type 2 response to H1N1 influenza which may be responsible for the systemic inflammatory response syndrome that causes pulmonary edema and death. On 26 April 2011, an H1N1 pandemic preparedness alert was issued by the World Health Organization for the Americas. In August 2011, according to the U.S. Geological Survey and the CDC, northern sea otters off the coast of Washington state were infected with the same version of the H1N1 flu virus that caused the 2009 pandemic and "may be a newly identified animal host of influenza viruses". In May 2013, seventeen people died during an H1N1 outbreak in Venezuela , and a further 250 were infected. As of early January 2014, Texas health officials have confirmed at least thirty-three H1N1 deaths and widespread outbreak during the 2013/2014 flu season, while twenty-one more deaths have been reported across the US. Nine people have been reported dead from an outbreak in several Canadian cities, and Mexico reports outbreaks resulting in at least one death. Spanish health authorities have confirmed 35 H1N1 cases in the Aragon region, 18 of whom are in intensive care. On 17 March 2014, three cases were confirmed with a possible fourth awaiting results occurring at the Centre for Addiction and Mental Health in Toronto , Ontario, Canada. With more than 300 infections and over 20 deaths, India's health ministry declared an outbreak "well under control" with "no reason to panic" in April 2012. According to the Indian Health Ministry , 31,974 cases of swine flu had been reported and 1,895 people had died from an outbreak by mid-March. Maldives reported swine flu in early 2017; [ better source needed ] 501 people were tested for the disease and 185 (37%) of those tested were positive for the disease. Four of those who tested positive from these 185 died due to this disease. The total number of people who have died due to the disease is unknown. Patient Zero was never identified. Schools were closed for a week due to the disease, but were ordered by the Ministry of Education to open after the holidays even though the disease was not fully under control. Myanmar reported H1N1 in late July 2017. As of 27 July, there were 30 confirmed cases and six people had died. The Ministry of Health and Sports of Myanmar sent an official request to WHO to provide help to control the virus; and also mentioned that the government would be seeking international assistance, including from the UN , China and the United States. Pakistan reported H1N1 cases mostly arising from the city of Multan , with deaths resulting from the epidemic reaching 42. There have also been confirmed cases in cities of Gujranwala and Lahore . An outbreak of swine flu in the European Union member state was reported in mid-January 2019, with the island's main state hospital overcrowded within a week, with more than 30 cases being treated. In January 2019 an outbreak of H1N1 was recorded in Morocco, with nine confirmed fatalities. In November 2019 an outbreak of H1N1 was recorded in Iran, with 56 fatalities and 4,000 people hospitalized. The G4 virus , also known as the "G4 swine flu virus" (G4) and "G4 EA H1N1", is a swine influenza virus strain discovered in China. The virus is a variant genotype 4 (G4) Eurasian avian-like (EA) H1N1 virus that mainly affects pigs, but there is some evidence of it infecting people. A 2020 peer-reviewed paper from the Proceedings of the National Academy of Sciences ( PNAS ) stated that "G4 EA H1N1 viruses possess all the essential hallmarks of being highly adapted to infect humans ... Controlling the prevailing G4 EA H1N1 viruses in pigs and close monitoring of swine working populations should be promptly implemented." Michael Ryan, executive director of the World Health Organization (WHO) Health Emergencies Program , stated in July 2020 that this strain of influenza virus was not new and had been under surveillance since 2011. The Chinese CDC said it had implemented an influenza surveillance program in 2010, analyzing more than 400,000 tests annually, to facilitate early identification of influenza. Of those, 13 A(H1N1) cases were detected, of which three were of the G4 variant. The study stated that almost 30,000 swine had been monitored via nasal swabs between 2011 and 2018. While other variants of the virus have appeared and diminished, the study claimed the G4 variant had sharply increased since 2016 to become the predominant strain. The Chinese Ministry of Agriculture and Rural Affairs rebutted the study, saying that the number of pigs sampled was too small to demonstrate G4 had become the dominant strain and that the media had interpreted the study "in an exaggerated and nonfactual way". They also said the infected workers "did not show flu symptoms and the test sample is not representative of the pig population in China". The US Centers for Disease Control and Prevention (CDC) said the study suggested that human infection by the G4 virus is more common than it was thought to be. Both the European Centre for Disease Prevention and Control (ECDC) and the US CDC stated that, like all flu viruses with pandemic potential, the variant is a concern that will be monitored. The ECDC stated that "the most important intervention in preparing for the pandemic potential of influenza viruses is the development and use of human vaccines ...". Health officials (including Anthony Fauci ) have said that the virus should be monitored, particularly among those in close contact with pigs, but it is not an immediate threat. While there have been no reported cases or evidence of the virus outside China as of July 2020, Smithsonian Magazine reported in July 2020 that scientists agree that the virus should be closely monitored , but because it "so far cannot jump from person to person", it should not be a cause for alarm yet. The 1918 flu was an unusually severe and deadly strain of H1N1 avian influenza , which killed from 17 to 50 or more million people worldwide over about a year in 1918 and 1920. It was one of the deadliest pandemics in human history . The 1918 flu caused an abnormally high number of deaths, possibly due to it provoking a cytokine storm in the body. (The H5N1 bird flu , also an Influenza A virus, has a similar effect.) After the 1918 flu infected lung cells, it frequently led to overstimulation of the immune system via release of immune response-stimulating cytokines (proteins that transmit signals between cells) into the lung tissue. This leads to extensive leukocyte migration towards the lungs, resulting in the destruction of lung cells and secretion of blood and mucus into the alveoli and airways. This makes it difficult for the patient to breathe and can result in suffocation. In contrast to other pandemics, which mostly kill the old and the very young, the 1918 pandemic killed unusual numbers of young adults, which may have been due to their healthy immune systems mounting a too-strong and damaging response to the infection. The term "Spanish" flu was coined because Spain was at the time the only European country where the press were printing reports of the outbreak, which had killed thousands in the armies fighting World War I (1914–1918). Other countries suppressed the news in order to protect morale. In 1976, a novel swine influenza A (H1N1) caused severe respiratory illness in 13 soldiers, with one death at Fort Dix , New Jersey. The virus was detected only from 19 January to 9 February and did not spread beyond Fort Dix. Retrospective serologic testing subsequently demonstrated that up to 230 soldiers had been infected with the novel virus, which was an H1N1 strain. The cause of the outbreak is still unknown and no exposure to pigs was identified. The 1977 Russian flu pandemic was caused by strain Influenza A/USSR/90/77 (H1N1) . It infected mostly children and young adults under 23; because a similar strain was prevalent in 1947–57, most adults had substantial immunity. Later analysis found that the re-emergent strain had been circulating for approximately one year before it was detected in China and Russia. The virus was included in the 1978–79 influenza vaccine . In the 2009 flu pandemic , the virus isolated from patients in the United States was found to be made up of genetic elements from four different flu viruses – North American swine influenza, North American avian influenza, human influenza, and swine influenza virus typically found in Asia and Europe – "an unusually mongrelised mix of genetic sequences." This new strain appears to be a result of reassortment of human influenza and swine influenza viruses, in all four different strains of subtype H1N1. Preliminary genetic characterization found that the hemagglutinin (HA) gene was similar to that of swine flu viruses present in U.S. pigs since 1999, but the neuraminidase (NA) and matrix protein (M) genes resembled versions present in European swine flu isolates. The six genes from American swine flu are themselves mixtures of swine flu, bird flu, and human flu viruses. While viruses with this genetic makeup had not previously been found to be circulating in humans or pigs, there is no formal national surveillance system to determine what viruses are circulating in pigs in the U.S. In April 2009, an outbreak of influenza-like illness (ILI) occurred in Mexico and then in the United States; the CDC reported seven cases of novel A/H1N1 influenza and promptly shared the genetic sequences on the GISAID database. With similar timely sharing of data for Mexican isolates, by 24 April it became clear that the outbreak of ILI in Mexico and the confirmed cases of novel influenza A in the southwest US were related and WHO issued a health advisory on the outbreak of "influenza-like illness in the United States and Mexico". The disease then spread very rapidly, with the number of confirmed cases rising to 2,099 by 7 May, despite aggressive measures taken by the Mexican government to curb the spread of the disease. The outbreak had been predicted a year earlier by noticing the increasing number of replikins , a type of peptide , found in the virus. On 11 June 2009, the WHO declared an H1N1 pandemic, moving the alert level to phase 6, marking the first global pandemic since the 1968 Hong Kong flu . On 25 October 2009, U.S. President Barack Obama officially declared H1N1 a national emergency . The President's declaration caused many U.S. employers to take actions to help stem the spread of the swine flu and to accommodate employees and / or workflow which may have been impacted by an outbreak. A study conducted in coordination with the University of Michigan Health Service – scheduled for publication in the December 2009 American Journal of Roentgenology – warned that H1N1 flu can cause pulmonary embolism , surmised as a leading cause of death in this pandemic. The study authors suggest physician evaluation via contrast enhanced CT scans for the presence of pulmonary emboli when caring for patients diagnosed with respiratory complications from a "severe" case of the H1N1 flu. H1N1 may induce other embolic events, such as myocardial infarction , bilateral massive DVT , arterial thrombus of infrarenal aorta, thrombosis of right external iliac vein and common femoral vein or cerebral gas embolism. The type of embolic events caused by H1N1 infection are summarized in a 2010 review by Dimitroulis Ioannis et al. The 21 March 2010 worldwide update, by the U.N.'s World Health Organization (WHO), states that "213 countries and overseas territories/communities have reported laboratory confirmed cases of pandemic influenza H1N1 2009, including at least 16,931 deaths." As of 30 May 2010 [ update ] , worldwide update by World Health Organization (WHO) more than 214 countries and overseas territories or communities have reported laboratory confirmed cases of pandemic influenza H1N1 2009, including over 18,138 deaths. The research team of Andrew Miller showed pregnant patients are at increased risk. It has been suggested that pregnant women and certain populations such as native North Americans have a greater likelihood of developing a T helper type 2 response to H1N1 influenza which may be responsible for the systemic inflammatory response syndrome that causes pulmonary edema and death. On 26 April 2011, an H1N1 pandemic preparedness alert was issued by the World Health Organization for the Americas. In August 2011, according to the U.S. Geological Survey and the CDC, northern sea otters off the coast of Washington state were infected with the same version of the H1N1 flu virus that caused the 2009 pandemic and "may be a newly identified animal host of influenza viruses". In May 2013, seventeen people died during an H1N1 outbreak in Venezuela , and a further 250 were infected. As of early January 2014, Texas health officials have confirmed at least thirty-three H1N1 deaths and widespread outbreak during the 2013/2014 flu season, while twenty-one more deaths have been reported across the US. Nine people have been reported dead from an outbreak in several Canadian cities, and Mexico reports outbreaks resulting in at least one death. Spanish health authorities have confirmed 35 H1N1 cases in the Aragon region, 18 of whom are in intensive care. On 17 March 2014, three cases were confirmed with a possible fourth awaiting results occurring at the Centre for Addiction and Mental Health in Toronto , Ontario, Canada. With more than 300 infections and over 20 deaths, India's health ministry declared an outbreak "well under control" with "no reason to panic" in April 2012. According to the Indian Health Ministry , 31,974 cases of swine flu had been reported and 1,895 people had died from an outbreak by mid-March. Maldives reported swine flu in early 2017; [ better source needed ] 501 people were tested for the disease and 185 (37%) of those tested were positive for the disease. Four of those who tested positive from these 185 died due to this disease. The total number of people who have died due to the disease is unknown. Patient Zero was never identified. Schools were closed for a week due to the disease, but were ordered by the Ministry of Education to open after the holidays even though the disease was not fully under control. Myanmar reported H1N1 in late July 2017. As of 27 July, there were 30 confirmed cases and six people had died. The Ministry of Health and Sports of Myanmar sent an official request to WHO to provide help to control the virus; and also mentioned that the government would be seeking international assistance, including from the UN , China and the United States. Pakistan reported H1N1 cases mostly arising from the city of Multan , with deaths resulting from the epidemic reaching 42. There have also been confirmed cases in cities of Gujranwala and Lahore .An outbreak of swine flu in the European Union member state was reported in mid-January 2019, with the island's main state hospital overcrowded within a week, with more than 30 cases being treated. In January 2019 an outbreak of H1N1 was recorded in Morocco, with nine confirmed fatalities. In November 2019 an outbreak of H1N1 was recorded in Iran, with 56 fatalities and 4,000 people hospitalized. The G4 virus , also known as the "G4 swine flu virus" (G4) and "G4 EA H1N1", is a swine influenza virus strain discovered in China. The virus is a variant genotype 4 (G4) Eurasian avian-like (EA) H1N1 virus that mainly affects pigs, but there is some evidence of it infecting people. A 2020 peer-reviewed paper from the Proceedings of the National Academy of Sciences ( PNAS ) stated that "G4 EA H1N1 viruses possess all the essential hallmarks of being highly adapted to infect humans ... Controlling the prevailing G4 EA H1N1 viruses in pigs and close monitoring of swine working populations should be promptly implemented." Michael Ryan, executive director of the World Health Organization (WHO) Health Emergencies Program , stated in July 2020 that this strain of influenza virus was not new and had been under surveillance since 2011. The Chinese CDC said it had implemented an influenza surveillance program in 2010, analyzing more than 400,000 tests annually, to facilitate early identification of influenza. Of those, 13 A(H1N1) cases were detected, of which three were of the G4 variant. The study stated that almost 30,000 swine had been monitored via nasal swabs between 2011 and 2018. While other variants of the virus have appeared and diminished, the study claimed the G4 variant had sharply increased since 2016 to become the predominant strain. The Chinese Ministry of Agriculture and Rural Affairs rebutted the study, saying that the number of pigs sampled was too small to demonstrate G4 had become the dominant strain and that the media had interpreted the study "in an exaggerated and nonfactual way". They also said the infected workers "did not show flu symptoms and the test sample is not representative of the pig population in China". The US Centers for Disease Control and Prevention (CDC) said the study suggested that human infection by the G4 virus is more common than it was thought to be. Both the European Centre for Disease Prevention and Control (ECDC) and the US CDC stated that, like all flu viruses with pandemic potential, the variant is a concern that will be monitored. The ECDC stated that "the most important intervention in preparing for the pandemic potential of influenza viruses is the development and use of human vaccines ...". Health officials (including Anthony Fauci ) have said that the virus should be monitored, particularly among those in close contact with pigs, but it is not an immediate threat. While there have been no reported cases or evidence of the virus outside China as of July 2020, Smithsonian Magazine reported in July 2020 that scientists agree that the virus should be closely monitored , but because it "so far cannot jump from person to person", it should not be a cause for alarm yet. Pregnant women who contract the H1N1 infection are at greater risk of developing complications because of hormonal changes, physical changes and changes to their immune system to accommodate the growing fetus. For this reason the Centers for Disease Control and Prevention recommends that those who are pregnant be vaccinated to prevent the influenza virus. The vaccination should not be taken by people who have had a severe allergic reaction to the influenza vaccination. Those who are moderately to severely ill, with or without a fever should wait until they recover before vaccination. Pregnant women who become infected with the influenza are advised to contact their doctor immediately. Influenza can be treated with prescription antiviral medications. Oseltamivir (trade name Tamiflu) and zanamivir (Relenza) are two neuraminidase inhibitors (antiviral medications) recommended. They are most effective when taken within two days of becoming sick. Since 1 October 2008, the CDC has tested 1,146 seasonal influenza A (H1N1) viruses for resistance against oseltamivir and zanamivir. It was found that 99.6% of the samples were resistant to oseltamivir while none were resistant to zanamivir. After 2009 Influenza A (H1N1) virus samples were tested, only 4% (of 853 samples) showed resistance to oseltamivir (again, no samples showed resistance to zanamivir). A study conducted in Japan during the 2009 H1N1 pandemic concluded that infants exposed to either oseltamivir or zanamivir had no short term adverse effects. Both amantadine and rimantadine have been found to be teratogenic and embryotoxic (malformations and toxic effects on the embryo) when given at high doses in animal studies.

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Avian influenza

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Flu season

Flu season is an annually recurring time period characterized by the prevalence of an outbreak of influenza (flu). The season occurs during the cold half of the year in each hemisphere . It takes approximately two days to show symptoms. Influenza activity can sometimes be predicted and even tracked geographically. While the beginning of major flu activity in each season varies by location, in any specific location these minor epidemics usually take about three weeks to reach its pinnacle, and another three weeks to significantly diminish. Annually, about 3 to 5 million cases of severe illness and 290,000 to 650,000 deaths from seasonal flu occur worldwide. Three virus families, Influenza virus A , B , and C are the main infective agents that cause influenza. During periods of cooler temperature, influenza cases increase roughly tenfold or more. Despite the higher incidence of manifestations of the flu during the season, the viruses are actually transmitted throughout populations all year round. [ citation needed ] Each annual flu season is normally associated with a major influenza virus sub type. The associated sub type changes each year, due to development of immunological resistance to a previous year's strain (through exposure and vaccinations), and mutational changes in previously dormant viruses strains. The exact mechanism behind the seasonal nature of influenza outbreaks is unknown. Some proposed explanations are: Research in guinea pigs has shown that the aerosol transmission of the virus is enhanced when the air is cold and dry. The dependence on aridity appears to be due to degradation of the virus particles in moist air, while the dependence on cold appears to be due to infected hosts shedding the virus for a longer period of time. The researchers did not find that the cold impaired the immune response of the guinea pigs to the virus. [ citation needed ] Research done by the National Institute of Child Health and Human Development (NICHD) in 2008 found that the influenza virus has a butter-like coating. The coating melts when it enters the respiratory tract. In the winter, the coating becomes a hardened shell; therefore, it can survive in the cold weather similar to a spore. In the summer, the coating melts before the virus reaches the respiratory tract. In the United States , the flu season is considered October through May. It typically reaches an apex in February, with a seasonal baseline varying between 6.1% and 7.7% of all deaths. In Australia , the flu season is considered May to October. It usually peaks in August. For other southern hemisphere countries such as Argentina , Chile , South Africa , and Paraguay also tend to start around June. Brazil has a complex seasonality component for its flu season, due to part of its being in a tropical climate, but its further south latitudes have their flu peaks in June–July, during the southern hemisphere winters. Flu seasons also exist in the tropics and subtropics , with variability from region to region. In Hong Kong , which has a humid subtropical climate , the flu season runs from December to March, in the winter and early spring. Flu vaccinations are used to diminish the effects of the flu season and can lower an individual's risk of getting the flu by about half. Since the Northern and Southern Hemisphere have winter at different times of the year, there are actually two flu seasons each year. Therefore, the World Health Organization (assisted by the National Influenza Centers ) recommends two vaccine formulations every year; one for the Northern, and one for the Southern Hemisphere. According to the U.S. Department of Health, a growing number of large companies provide their employees with seasonal flu shots, either at a small cost to the employee or as a free service. The annually updated trivalent influenza vaccine consists of hemagglutinin (HA) surface glycoprotein components from influenza H3N2 , H1N1 , and B influenza viruses. The dominant strain in January 2006 was H3N2. Measured resistance to the standard antiviral drugs amantadine and rimantadine in H3N2 has increased from 1% in 1994 to 12% in 2003 to 91% in 2005. Medical conditions that compromise the immune system increase the risks from flu. [ citation needed ] Millions of people have diabetes . When blood sugars are not well controlled, diabetics can quickly develop a wide range of complications. Diabetes results in elevated blood sugars in the body, and this environment allows viruses and bacteria to thrive. [ citation needed ] If blood sugars are poorly controlled, a mild flu can quickly turn severe, leading to hospitalization and even death . Uncontrolled blood sugars suppresses the immune systems and generally lead to more severe cases of the common cold or influenza. Thus, it has been recommended that diabetics be vaccinated against flu, before the start of the flu season. The CDC recommends that people with asthma and chronic obstructive pulmonary disease (COPD) be vaccinated against flu before the flu season. People with asthma can develop life-threatening complications from influenza and the common cold viruses. Some of these complications include pneumonias , acute bronchitis , and acute respiratory distress syndrome . Each year flu related complications in the USA affect close to 100,000 asthmatics, and millions more are seen in the emergency room because of severe shortness of breath . The CDC recommends that asthmatics are vaccinated between October and November, before the peak of the flu season. Flu vaccines take about two weeks to become effective. People with cancer usually have a suppressed immune system . Moreover, many cancer patients undergo radiation therapy and potent immunosuppressive medications, which further suppresses the body's ability to fight off infections. Everyone with cancer is highly susceptible and is at risk for complications from flu. People with cancer or a history of cancer should receive the seasonal flu shot. Flu vaccination is also strict for lung cancer patients, as cancer leads to complications of pneumonia and bronchitis. People with cancer should not receive the nasal spray vaccine. The flu shot is made up of inactivated (killed) viruses, and the nasal spray vaccines are made up of live viruses. The flu shot is safer for those with a weakened immune system. Those who have received cancer treatment such as chemotherapy and/or radiation therapy within the last month, or have a blood or lymphatic form of cancer should call their doctor immediately if they suspect they may have flu. Individuals who have HIV/AIDS are prone to a variety of infections. HIV weakens the body's immune system, leaving them vulnerable to viral, bacterial, fungal, and protozoa disorders. People with HIV are at an increased risk of serious flu-related complications. Many reports have shown that individuals with HIV can develop serious pneumonias that need hospitalization and aggressive antibiotic therapy. Moreover, people with HIV have a longer flu season and are at a high risk of death. Vaccination with the flu shot has been shown to boost the immune system and protect against the seasonal flu in some patients with HIV. Millions of people have diabetes . When blood sugars are not well controlled, diabetics can quickly develop a wide range of complications. Diabetes results in elevated blood sugars in the body, and this environment allows viruses and bacteria to thrive. [ citation needed ] If blood sugars are poorly controlled, a mild flu can quickly turn severe, leading to hospitalization and even death . Uncontrolled blood sugars suppresses the immune systems and generally lead to more severe cases of the common cold or influenza. Thus, it has been recommended that diabetics be vaccinated against flu, before the start of the flu season. The CDC recommends that people with asthma and chronic obstructive pulmonary disease (COPD) be vaccinated against flu before the flu season. People with asthma can develop life-threatening complications from influenza and the common cold viruses. Some of these complications include pneumonias , acute bronchitis , and acute respiratory distress syndrome . Each year flu related complications in the USA affect close to 100,000 asthmatics, and millions more are seen in the emergency room because of severe shortness of breath . The CDC recommends that asthmatics are vaccinated between October and November, before the peak of the flu season. Flu vaccines take about two weeks to become effective. People with cancer usually have a suppressed immune system . Moreover, many cancer patients undergo radiation therapy and potent immunosuppressive medications, which further suppresses the body's ability to fight off infections. Everyone with cancer is highly susceptible and is at risk for complications from flu. People with cancer or a history of cancer should receive the seasonal flu shot. Flu vaccination is also strict for lung cancer patients, as cancer leads to complications of pneumonia and bronchitis. People with cancer should not receive the nasal spray vaccine. The flu shot is made up of inactivated (killed) viruses, and the nasal spray vaccines are made up of live viruses. The flu shot is safer for those with a weakened immune system. Those who have received cancer treatment such as chemotherapy and/or radiation therapy within the last month, or have a blood or lymphatic form of cancer should call their doctor immediately if they suspect they may have flu. Individuals who have HIV/AIDS are prone to a variety of infections. HIV weakens the body's immune system, leaving them vulnerable to viral, bacterial, fungal, and protozoa disorders. People with HIV are at an increased risk of serious flu-related complications. Many reports have shown that individuals with HIV can develop serious pneumonias that need hospitalization and aggressive antibiotic therapy. Moreover, people with HIV have a longer flu season and are at a high risk of death. Vaccination with the flu shot has been shown to boost the immune system and protect against the seasonal flu in some patients with HIV. The cost of a flu season in lives lost, medical expenses and economic impact can be severe. In 2017, the World Health Organization (WHO) estimated that the seasonal flu causes 290,000 to 650,000 annual deaths worldwide. In 2003, the WHO estimated that the cost of flu epidemics in the United States was US$71–167 billion per year. A 2007 study found that annual influenza epidemics in the US result in approximately 600,000 life-years lost , 3 million hospitalized days, and 30 million outpatient visits, resulting in medical costs of $10 billion annually. According to this study, lost earnings due to illness and loss of life amounted to over $15 billion annually and the total economic burden of annual influenza epidemics amounts to over $80 billion. Also, in the US the flu season usually accounts for 200,000 hospitalizations and 41,000 deaths. [ citation needed ] Because the mortality rate of the H1N1 swine flu is lower than that of common flu strains, this [ clarification needed ] number was actually lower in 2009. According to an article in Clinical Infectious Diseases , published in 2011, the estimated health burden of 2009 Pandemic Influenza A (H1N1), between April 2009 to April 2010, was "approximately 60.8 million cases (range: 43.3–89.3 million), 274,304 hospitalizations (195,086–402,719), and 12,469 deaths (8,868–18,306)" "in the United States due to pH1N1." Seasonal epidemics of influenza can be severe. Some can even rival pandemics in terms of excess mortality. In fact, it is not so much mortality that distinguishes seasonal epidemics from pandemics but rather the extent to which the disease has spread, though the reasons behind this distinction between epidemic and pandemic, as well as the geographic variability observed within individual flu seasons, remain poorly understood. As such, some flu seasons are particularly notable in terms of severity. Others are notable due to other unique or unusual factors, as described below. According to the United States Public Health Service , "The epidemic of 1928–1929 was the most important since that of 1920", itself considered to be the final wave, at least in the US, of the 1918 pandemic . There were approximately 50,000 excess influenza and pneumonia deaths in the country, or about half of the mortality attributed to the 1920 epidemic. The 1946–1947 flu season was characterized by a previously unheard of phenomenon. The first influenza vaccine came into use in the 1940s. At this time, the vaccine contained a strain of H1N1 isolated in 1943, and this had been effective during the 1943–1944 and 1944–1945 seasons. During the 1946–1947 season, however, this once-effective vaccine totally failed to protect the military personnel who had received it. A worldwide epidemic occurred, which for a time was considered to have been a pandemic due to its vast spread, albeit a mild one, with relatively low mortality. Antigenetic analysis later revealed that the influenza A virus had undergone intrasubtypic reassortment, in which genes were swapped between two viruses of the same subtype (H1N1), resulting in an extreme drift variant but not an entirely new subtype. The new strains were so different, however, that they were for a time classified into a distinct category, though this distinction has since been lost due to more recent analysis, which supports classifying both the older and the newer strains as influenza A/H1N1. Nevertheless, this experience informed public health experts of the need to update vaccine composition periodically to account for variations in the influenza virus, even if there has been no complete shift in subtype. The 1950–1951 flu season was particularly severe in England and Wales and in Canada. Influenza A predominated. The rates of excess pneumonia and influenza mortality in these places was higher than those which would later be experienced in both the 1957 and 1968 pandemics. Liverpool in particular experienced a peak in weekly mortality even higher than that of the 1918 pandemic. Northern Europe also experienced severe epidemics this season. By contrast, the United States experienced a relatively milder epidemic. There was no observed shift in the viruses in circulation this flu season. During the 1952–1953 flu season, the Americas and Europe experienced widespread outbreaks of influenza A. Beginning the first week of January, 1953, influenza in epidemic proportions emerged in various states in the US. Outbreaks soon developed around the country, with Texas experiencing particularly high activity, though the northeast mostly saw smaller, more localized outbreaks. Schools were shuttered in many places due to the high incidence of disease among students and teachers. After an initial attempt to minimize the threat of the outbreak and a resistance to describe it as an "epidemic", the US Public Health Service eventually acknowledged it as such when deaths began to rise around the country. By the end of January, activity was decreasing around the country. Around the time that the epidemic was peaking in the US, outbreaks developed in France, Germany, and southern England and later in Scandinavia, Switzerland, and Austria; sporadic activity was reported in other parts of Europe. In the US, influenza and pneumonia mortality peaked in early February, earlier than in the three preceding flu seasons, in which mortality did not begin to rise until late February, and was the greatest out of the three preceding seasons, including 1951. It was subsequently found that strains isolated during this season were influenza A but had shifted antigenically relative to previously isolated strains, further demonstrating the significance of antigenic variation in influenza viruses. The 1967–1968 flu season was the last to be dominated by H2N2 before the emergence of H3N2 in 1968 and the consequent " Hong Kong flu " pandemic that lasted until 1970. This season was particularly severe in England and France, in which pneumonia and influenza excess mortality was two to three times greater than in other countries. By contrast, North America (the US and Canada) experienced a relatively milder epidemic than other places, with lower all-cause excess mortality and a lower increase in both pneumonia-influenza and all-cause excess mortality, both indicating that this season had a lesser impact in North America relative to other countries. In Britain, this epidemic was the "largest" it had experienced in seven years, with an estimated two million cases occurring in the population as a whole. The 2012–2013 flu season was particularly harsh in the United States , where the majority of states were reporting high rates of influenza-like illness . The Centers for Disease Control and Prevention reported that the available flu vaccine was 60% effective. It further recommended that all persons over age 6 months get the vaccine. According to one source, the season 2014-2015 saw a particularly heavy prevalence of influenza in the United Kingdom .

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Avian influenza

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Influenza A virus subtype H7N2

Influenza A virus subtype H7N2 (A/H7N2) is a subtype of the species Influenza A virus . This subtype is one of several sometimes called bird flu virus. H7N2 is considered a low pathogenicity avian influenza (LPAI) virus. With this in mind, H5 & H7 influenza viruses can re-assort into the Highly Pathogenic variant if conditions are favorable. A CDC study following outbreaks of H7N2 in commercial poultry farms in western Virginia in 2002 concluded: One person in Virginia , United States in 2002, one person in New York , United States, in 2003, and one person in New York , United States, in 2016 were found to have serologic evidence of infection from H7N2; all fully recovered. An analysis of the New York 2003 case concluded that the H7N2 virus responsible could be evolving toward the same strong sugar-binding properties of the three worldwide viral pandemics in 1918, 1957 and 1968. ( Human flus and bird flus differ in the molecules they are good at binding with because mammals and birds differ in the molecules on the cell surface to be bound with. Humans have very few cells with the bird sugar on its cell surface.) A study with ferrets showed that this H7N2 strain could be passed from mammal to mammal. In February 2004, an outbreak of low pathogenic avian influenza (LPAI) A (H7N2) was reported on 2 chicken farms in Delaware and in four live bird markets in New Jersey supplied by the same farms. In March 2004, surveillance samples from a flock of chickens in Maryland tested positive for LPAI H7N2. It is likely that this was the same strain. On 24 May 2007, an outbreak of H7N2 was confirmed at a poultry farm near Corwen , in Wales from tests on chickens that died from H7N2. The owners of the Conwy farm bought 15 Rhode Island Red chickens two weeks prior but all died from H7N2. The 32 other poultry at the site were slaughtered. A one kilometer exclusion zone was put in force around the property in which birds and bird products cannot be moved and bird gathering can only take place under licence. Nine people who were associated with the infected or dead poultry and reported flu-like symptoms were tested. Four tested positive for evidence of infection from H7N2 and were successfully treated for mild flu. In early June it was discovered that the virus had spread to a poultry farm 70 miles (113 km) away near St. Helens in north-west England. All the poultry at the farm were slaughtered and a 1 km exclusion zone imposed. In December 2016, an outbreak of low pathogenic avian influenza H7N2 occurred in a feline population in the New York City Animal Care Center (ACC) shelters after testing by the University of Wisconsin-Madison School of Veterinary Medicine and confirmed by USDA's National Veterinary Diagnostic Services Laboratory. Over 100 cats were found to be infected and subsequently quarantined, but only one human, a veterinarian involved in obtaining respiratory specimens, was found to be infected. The veterinarian had a brief illness with mild symptoms and recovered completely. All other humans exposed to the infected cats tested negative.

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Avian influenza

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Influenza A virus subtype H9N2

Influenza A virus subtype H9N2 (A/H9N2) is a subtype of the species Influenza A virus ( bird flu virus). Since 1998 a total of 86 cases of human infection with H9N2 viruses have been reported. H9N2 is the most common subtype of influenza viruses in Chinese chickens and thus causes great economic loss for the poultry industry, even under the long-term vaccination programs. Recent human infections with avian influenza virus revealed that H9N2 is the gene donor for H7N9 and H10N8 viruses that are infecting humans too. The crucial role of H9N2 viruses due to the wide host range, adaptation to both poultry and mammals and extensive gene reassortment. In China, which is regarded as a breeding ground of avian influenza viruses, the H9N2 virus has been detected in multiple avian species, including chicken , duck , quail , pheasant , partridge , pigeon , silky chicken, chukar and egret . Epidemiological and genetic studies revealed that the hemagglutinin (HA) gene of the H9N2 influenza viruses could be divided into Eurasian avian and American avian lineages. The Eurasian avian lineage involved three distinct lineages, including A/chicken/Beijing/1/94-like (BJ/94-like), A/quail/Hong Kong/G1/97-like (G1-like), and A/duck/Hong Kong/Y439/97 (Y439-like). The H9N2 influenza virus can be transmitted by air droplet, dust, feed, or water. Chickens usually seemed to be healthy after the infection but some of them do show depression and ruffled feathers. The virus replicates itself in the trachea. It makes chickens more susceptible to secondary infections, especially Escherichia coli infections with a mortality rate of at least 10%. Also, the trachea or bronchi are easily embolized by mucus when the ventilation is poor, leading to severe respiratory disease and death. H9N2 viruses isolated from chickens in China showed antigenic drift that evolved into distinct antigenic groups. This antigenic drift may have led to immunization failure and may explain the current prevalence of the H9N2 influenza virus in China. The identification of amino acids in H9 antigenic sites revealed different distribution of antigenic areas among other subtypes. Multiple amino acid positions in HA protein related to the antigenicity of H9N2 viruses were identified, most of which located in the distal head of the HA trimer. H9N2 influenza virus has been recognized to reassort with multiple other subtypes, including H6N1 , H6N2 , and H5N1 viruses. Moreover, H7N9 influenza viruses continued to reassort with circulating H9N2 viruses, resulting in multiple genotypes of H7N9 viruses. The contribution of H9N2 genes, especially ribonucleoprotein (RNP) genes, to the infection in human needs to be determined.

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Avian influenza

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Avian

Avian may refer to:

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Avian influenza

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Influenza A virus subtype H10N3

Influenza A virus subtype H10N3 is a subtype of viruses that causes influenza (flu). It is mostly present in wild avian species. The first human case was reported in 2021.Only around 160 cases of the virus have been reported in the 40 years before 2018, mostly in various waterfowl or wild birds. Existing studies show that H10 influenza viruses are present in a wide range of domestic and wild avian species, as well as in mammals, showing potential for adaptation. H10N3 has been isolated across a wide geographic distribution, including in species such as domestic poultry (chickens), ducks, other waterfowl, and terrestrial birds. In animals, the viruses display a complex pathology, with complex reassortments and mutations contributing to pathobiology patterns in chickens, ducks and mice indicative of a possible threat to humans, although H10N3 is usually a less severe strain and is unlikely to cause a significant outbreak. The first human case of H10N3 was reported in Zhenjiang , in China 's eastern province of Jiangsu. This index case was a patient admitted to the hospital with a fever and worsening respiratory symptoms on April 28, 2021, with a diagnosis of H10N3 confirmed in May 2021. None of the individual's close contacts developed any symptoms or signs of infection. The virus identified from this individual contains an HA cleavage site that is consistent with a "low pathogenicity avian influenza" ( LPAI ), and is also a reassortant strain , combining the HA and NA genes from H10N3 with internal genes from H9N2 viruses. According to China's National Health Commission (NHC), human cases of H10N3 have not been reported elsewhere in China. There are no indications that the virus is easily transmissible among humans, with no confirmed cases of human-to-human transmission. Other types of avian-origin H10 influenza have been reported in human beings, including in Egypt, Australia and China, highlighting a potential public health hazard, although none of the strains so far detected have shown signs of human transmission.

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Avian influenza

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Influenza A virus subtype H3N2

Influenza A virus subtype H3N2 ( A/H3N2 ) is a subtype of viruses that causes influenza (flu). H3N2 viruses can infect birds and mammals. In birds, humans, and pigs, the virus has mutated into many strains. In years in which H3N2 is the predominant strain, there are more hospitalizations. H3N2 is a subtype of the viral genus Influenzavirus A , which is an important cause of human influenza . Its name derives from the forms of the two kinds of proteins on the surface of its coat, hemagglutinin (H) and neuraminidase (N). By reassortment , H3N2 exchanges genes for internal proteins with other influenza subtypes. Seasonal influenza kills an estimated 36,000 people in the United States each year. Flu vaccines are based on predicting which "mutants" of H1N1 , H3N2, H1N2 , and influenza B will proliferate in the next season. Separate vaccines are developed for the Northern and Southern Hemispheres in preparation for their annual epidemics. In the tropics, influenza shows no clear seasonality. In the past ten years, H3N2 has tended to dominate in prevalence over H1N1, H1N2, and influenza B. Measured resistance to the standard antiviral drugs amantadine and rimantadine in H3N2 has increased from 1% in 1994 to 12% in 2003 to 91% in 2005. Seasonal H3N2 flu is a human flu from H3N2 that is slightly different from one of the previous year's flu season H3N2 variants. Seasonal influenza viruses flow out of overlapping epidemics in East Asia and Southeast Asia , then trickle around the globe before dying off. Identifying the source of the viruses allows global health officials to better predict which viruses are most likely to cause the most disease over the next year. An analysis of 13,000 samples of influenza A/H3N2 virus that were collected across six continents from 2002 to 2007 by the WHO's Global Influenza Surveillance Network showed the newly emerging strains of H3N2 appeared in East and Southeast Asian countries about six to nine months earlier than anywhere else. The strains generally reached Australia and New Zealand next, followed by North America and Europe. The new variants typically reached South America after an additional six to nine months, the group reported. A 2007 study reported: "In swine , three influenza A virus subtypes ( H1N1 , H3N2 , and H1N2 ) are circulating throughout the world. In the United States, the classic H1N1 subtype was exclusively prevalent among swine populations before 1998; however, since late August 1998, H3N2 subtypes have been isolated from pigs. Most H3N2 virus isolates are triple reassortants, containing genes from human (HA, NA, and PB1), swine (NS, NP, and M), and avian (PB2 and PA) lineages. Present vaccination strategies for swine influenza virus (SIV) control and prevention in swine farms typically include the use of one of several bivalent SIV vaccines commercially available in the United States. Of the 97 recent H3N2 isolates examined, only 41 had strong serologic cross-reactions with antiserum to three commercial SIV vaccines. Since the protective ability of influenza vaccines depends primarily on the closeness of the match between the vaccine virus and the epidemic virus, the presence of nonreactive H3N2 SIV variants suggests current commercial vaccines might not effectively protect pigs from infection with a majority of H3N2 viruses." Avian influenza virus H3N2 is endemic in pigs in China , and has been detected in pigs in Vietnam, contributing to the emergence of new variant strains. Pigs can carry human influenza viruses, which can combine (i.e. exchange homologous genome subunits by genetic reassortment ) with H5N1 , passing genes and mutating into a form which can pass easily among humans. H3N2 evolved from H2N2 by antigenic shift and caused the Hong Kong Flu pandemic of 1968 and 1969 that killed up to 750,000 humans. The dominant strain of annual flu in humans in January 2006 was H3N2. Measured resistance to the standard antiviral drugs amantadine and rimantadine in H3N2 in humans had increased to 91% by 2005. In August 2004, researchers in China found H5N1 in pigs. The Hong Kong Flu was a flu pandemic caused by a strain of H3N2 descended from H2N2 by antigenic shift , in which genes from multiple subtypes reassorted to form a new virus. This pandemic of 1968 and 1969 killed an estimated one million people worldwide. The pandemic infected an estimated 500,000 Hong Kong residents, 15% of the population, with a low death rate. In the United States, about 100,000 people died. Both the H2N2 and H3N2 pandemic flu strains contained genes from avian influenza viruses. The new subtypes arose in pigs coinfected with avian and human viruses and were soon transferred to humans. Swine were considered the original "intermediate host" for influenza, because they supported reassortment of divergent subtypes. However, other hosts appear capable of similar coinfection (e.g., many poultry species), and direct transmission of avian viruses to humans is possible. H1N1 may have been transmitted directly from birds to humans (Belshe 2005). The Hong Kong flu strain shared internal genes and the neuraminidase with the 1957 Asian flu (H2N2). Accumulated antibodies to the neuraminidase or internal proteins may have resulted in much fewer casualties than most pandemics . However, cross-immunity within and between subtypes of influenza is poorly understood. [ citation needed ] The Hong Kong flu was the first known outbreak of the H3N2 strain, though there is serologic evidence of H3N2 infections in the late 19th century. The first record of the outbreak in Hong Kong appeared on 13 July 1968 in an area with a density of about 500 people per acre in an urban setting. The outbreak reached maximum intensity in two weeks, lasting six weeks in total. The virus was isolated in Queen Mary Hospital . Flu symptoms lasted four to five days. By July 1968, extensive outbreaks were reported in Vietnam and Singapore . By September 1968, it reached India, the Philippines, northern Australia and Europe. That same month, the virus entered California from United States troops returning from the Vietnam War . It reached Japan, Africa and South America in 1969. Fujian flu refers to flu caused by either a Fujian human flu strain of the H3N2 subtype or a Fujian bird flu strain of the H5N1 subtype of the Influenza A virus. These strains are named after Fujian province in China. A/Fujian (H3N2) human flu (from A/Fujian/411/2002(H3N2)-like flu virus strains) caused an unusually severe 2003–2004 flu season. This was due to a reassortment event that caused a minor clade to provide a haemagglutinin gene that later became part of the dominant strain in the 2002–2003 flu season. A/Fujian (H3N2) was made part of the trivalent influenza vaccine for the 2004–2005 flu season . The 2004–05 trivalent influenza vaccine for the United States contained: The vaccines produced for the 2005–2006 season used: The 2006–2007 influenza vaccine composition recommended by the World Health Organization on 15 February 2006 and the US FDA's Vaccines and Related Biological Products Advisory Committee on 17 February 2006 used: an A/New Caledonia/20/99 (H1N1)-like virus an A/Wisconsin/67/2005 (H3N2)-like virus (A/Wisconsin/67/2005 and A/Hiroshima/52/2005 strains) a B/Malaysia/2506/2004-like virus from B/Malaysia/2506/2004 and B/Ohio/1/2005 strains which are of B/Victoria/2/87 lineage The composition of influenza virus vaccines for use in the 2007–2008 Northern Hemisphere influenza season recommended by the World Health Organization on 14 February 2007 was: "A/H3N2 has become the predominant flu subtype in the United States, and the record over the past 25 years shows that seasons dominated by H3N2 tend to be worse than those dominated by type A/H1N1 or type B." Many H3N2 viruses making people ill in this 2007–2008 flu season differ from the strains in the vaccine and may not be well covered by the vaccine strains. "The CDC has analyzed 250 viruses this season to determine how well they match up with the vaccine, the report says. Of 65 H3N2 isolates, 53 (81%) were characterized as A/Brisbane/10/2007-like, a variant that has evolved [notably] from the H3N2 strain in the vaccine—A/Wisconsin/67/2005." The composition of virus vaccines for use in the 2008–2009 Northern Hemisphere influenza season recommended by the World Health Organization on February 14, 2008 was: As of May 30, 2009: "CDC has antigenically characterized 1,567 seasonal human influenza viruses [947 influenza A (H1), 162 influenza A (H3) and 458 influenza B viruses] collected by U.S. laboratories since October 1, 2008, and 84 novel influenza A (H1N1) viruses. All 947 influenza seasonal A (H1) viruses are related to the influenza A (H1N1) component of the 2008–09 influenza vaccine (A/Brisbane/59/2007). All 162 influenza A (H3N2) viruses are related to the A (H3N2) vaccine component (A/Brisbane/10/2007). All 84 novel influenza A (H1N1) viruses are related to the A/California/07/2009 (H1N1) reference virus selected by WHO as a potential candidate for novel influenza A (H1N1) vaccine. Influenza B viruses currently circulating can be divided into two distinct lineages represented by the B/Yamagata/16/88 and B/Victoria/02/87 viruses. Sixty-one influenza B viruses tested belong to the B/Yamagata lineage and are related to the vaccine strain (B/Florida/04/2006). The remaining 397 viruses belong to the B/Victoria lineage and are not related to the vaccine strain." The vaccines produced for the 2009–2010 season used: an A/Brisbane/59/2007(H1N1)-like virus an A/Brisbane/10/2007 (H3N2)-like virus a B/Brisbane 60/2008-like antigens A separate vaccine was available for pandemic H1N1 influenza using the A/California/7/2009-like pandemic H1N1 strain. The vaccines produced for the 2010–2011 season used: an A/California/7/2009-like (pandemic H1N1) an A/Perth/16/2009-like (H3N2)-like virus a B/Brisbane/60/2008-like antigens The vaccines produced for the 2011–2012 season used: an A/California/07/2009 (H1N1)-like virus an A/Victoria/210/2009 (an A/Perth/16/2009-like strain) (H3N2)-like virus a B/Brisbane/60/2008-like virus The vaccines produced for the Northern Hemisphere 2012–2013 season used: In January 2013, influenza activity continued to increase in the United States and most of the country experienced high levels of influenza-like-illness (ILI), according to CDC's latest FluView report. Reports of influenza-like-illness (ILI) are nearing what have been peak levels during moderately severe seasons, and CDC continues to recommend influenza vaccination and antiviral drug treatment when appropriate at this time. On January 9, 2013, the Boston Government declared a public health emergency for H3N2 influenza. The vaccines produced for the Northern Hemisphere 2014–2015 season used: A/California/7/2009 (H1N1)pdm09-like virus A/Texas/50/2012 (H3N2)-like virus B/Massachusetts/2/2012-like virus, Quadrivalent vaccines include a B/Brisbane/60/2008-like virus. The CDC announced that drift variants of the A (H3N2) virus strain from the 2012–2013 potentially foretold a severe flu season for 2014–2015. The vaccines produced for the Northern Hemisphere 2015–2016 season used: A/California/7/2009 (H1N1)pdm09-like virus A/Switzerland/9715293/2013 (H3N2)-like virus B/Phuket/3073/2013-like virus. (This is a B/Yamagata lineage virus) The "Split Virion" vaccine distributed in 2016 contained the following strains of inactivated virus: A/California/7/2009 (H1N1)pdm09 - like strain (A/California/7/2009, NYMC X-179A) A/Hong Kong/4801/2014 (H3N2) - like strain (A/Hong Kong/4801/2014, NYMC X-263B) B/Brisbane/60/2008 - like strain (B/Brisbane/60/2008, wild type) A/California/7/2009 (H1N1)pdm09-like virus, A/Hong Kong/4801/2014 (H3N2)-like virus B/Brisbane/60/2008-like virus (B/Victoria lineage) Quadrivalent influenza vaccine adds: B/Phuket/3073/2013-like strain A/Michigan/45/2015 (H1N1)pdm09-like virus A/Hong Kong/4801/2014 (H3N2) B/Brisbane/60/2008-like virus (B/Victoria lineage) Quadrivalent influenza vaccine adds B/Phuket/3073/2013-like[B/Yamagata lineage] Quadrivalent - A/Brisbane/02/2018 (H1N1)pdm09-like virus A/SouthAustralia/34/2019 (H3N2)-like virus B/Washington/02/2019-like virus [B/Victoria lineage] B/Phuket/3073/2013-like virus [B/Yamagata lineage]The Hong Kong Flu was a flu pandemic caused by a strain of H3N2 descended from H2N2 by antigenic shift , in which genes from multiple subtypes reassorted to form a new virus. This pandemic of 1968 and 1969 killed an estimated one million people worldwide. The pandemic infected an estimated 500,000 Hong Kong residents, 15% of the population, with a low death rate. In the United States, about 100,000 people died. Both the H2N2 and H3N2 pandemic flu strains contained genes from avian influenza viruses. The new subtypes arose in pigs coinfected with avian and human viruses and were soon transferred to humans. Swine were considered the original "intermediate host" for influenza, because they supported reassortment of divergent subtypes. However, other hosts appear capable of similar coinfection (e.g., many poultry species), and direct transmission of avian viruses to humans is possible. H1N1 may have been transmitted directly from birds to humans (Belshe 2005). The Hong Kong flu strain shared internal genes and the neuraminidase with the 1957 Asian flu (H2N2). Accumulated antibodies to the neuraminidase or internal proteins may have resulted in much fewer casualties than most pandemics . However, cross-immunity within and between subtypes of influenza is poorly understood. [ citation needed ] The Hong Kong flu was the first known outbreak of the H3N2 strain, though there is serologic evidence of H3N2 infections in the late 19th century. The first record of the outbreak in Hong Kong appeared on 13 July 1968 in an area with a density of about 500 people per acre in an urban setting. The outbreak reached maximum intensity in two weeks, lasting six weeks in total. The virus was isolated in Queen Mary Hospital . Flu symptoms lasted four to five days. By July 1968, extensive outbreaks were reported in Vietnam and Singapore . By September 1968, it reached India, the Philippines, northern Australia and Europe. That same month, the virus entered California from United States troops returning from the Vietnam War . It reached Japan, Africa and South America in 1969. Fujian flu refers to flu caused by either a Fujian human flu strain of the H3N2 subtype or a Fujian bird flu strain of the H5N1 subtype of the Influenza A virus. These strains are named after Fujian province in China. A/Fujian (H3N2) human flu (from A/Fujian/411/2002(H3N2)-like flu virus strains) caused an unusually severe 2003–2004 flu season. This was due to a reassortment event that caused a minor clade to provide a haemagglutinin gene that later became part of the dominant strain in the 2002–2003 flu season. A/Fujian (H3N2) was made part of the trivalent influenza vaccine for the 2004–2005 flu season . The 2004–05 trivalent influenza vaccine for the United States contained:The vaccines produced for the 2005–2006 season used:The 2006–2007 influenza vaccine composition recommended by the World Health Organization on 15 February 2006 and the US FDA's Vaccines and Related Biological Products Advisory Committee on 17 February 2006 used: an A/New Caledonia/20/99 (H1N1)-like virus an A/Wisconsin/67/2005 (H3N2)-like virus (A/Wisconsin/67/2005 and A/Hiroshima/52/2005 strains) a B/Malaysia/2506/2004-like virus from B/Malaysia/2506/2004 and B/Ohio/1/2005 strains which are of B/Victoria/2/87 lineage The composition of influenza virus vaccines for use in the 2007–2008 Northern Hemisphere influenza season recommended by the World Health Organization on 14 February 2007 was: "A/H3N2 has become the predominant flu subtype in the United States, and the record over the past 25 years shows that seasons dominated by H3N2 tend to be worse than those dominated by type A/H1N1 or type B." Many H3N2 viruses making people ill in this 2007–2008 flu season differ from the strains in the vaccine and may not be well covered by the vaccine strains. "The CDC has analyzed 250 viruses this season to determine how well they match up with the vaccine, the report says. Of 65 H3N2 isolates, 53 (81%) were characterized as A/Brisbane/10/2007-like, a variant that has evolved [notably] from the H3N2 strain in the vaccine—A/Wisconsin/67/2005." The composition of virus vaccines for use in the 2008–2009 Northern Hemisphere influenza season recommended by the World Health Organization on February 14, 2008 was: As of May 30, 2009: "CDC has antigenically characterized 1,567 seasonal human influenza viruses [947 influenza A (H1), 162 influenza A (H3) and 458 influenza B viruses] collected by U.S. laboratories since October 1, 2008, and 84 novel influenza A (H1N1) viruses. All 947 influenza seasonal A (H1) viruses are related to the influenza A (H1N1) component of the 2008–09 influenza vaccine (A/Brisbane/59/2007). All 162 influenza A (H3N2) viruses are related to the A (H3N2) vaccine component (A/Brisbane/10/2007). All 84 novel influenza A (H1N1) viruses are related to the A/California/07/2009 (H1N1) reference virus selected by WHO as a potential candidate for novel influenza A (H1N1) vaccine. Influenza B viruses currently circulating can be divided into two distinct lineages represented by the B/Yamagata/16/88 and B/Victoria/02/87 viruses. Sixty-one influenza B viruses tested belong to the B/Yamagata lineage and are related to the vaccine strain (B/Florida/04/2006). The remaining 397 viruses belong to the B/Victoria lineage and are not related to the vaccine strain." The vaccines produced for the 2009–2010 season used: an A/Brisbane/59/2007(H1N1)-like virus an A/Brisbane/10/2007 (H3N2)-like virus a B/Brisbane 60/2008-like antigens A separate vaccine was available for pandemic H1N1 influenza using the A/California/7/2009-like pandemic H1N1 strain. The vaccines produced for the 2010–2011 season used: an A/California/7/2009-like (pandemic H1N1) an A/Perth/16/2009-like (H3N2)-like virus a B/Brisbane/60/2008-like antigens The vaccines produced for the 2011–2012 season used: an A/California/07/2009 (H1N1)-like virus an A/Victoria/210/2009 (an A/Perth/16/2009-like strain) (H3N2)-like virus a B/Brisbane/60/2008-like virus The vaccines produced for the Northern Hemisphere 2012–2013 season used: In January 2013, influenza activity continued to increase in the United States and most of the country experienced high levels of influenza-like-illness (ILI), according to CDC's latest FluView report. Reports of influenza-like-illness (ILI) are nearing what have been peak levels during moderately severe seasons, and CDC continues to recommend influenza vaccination and antiviral drug treatment when appropriate at this time. On January 9, 2013, the Boston Government declared a public health emergency for H3N2 influenza. The vaccines produced for the Northern Hemisphere 2014–2015 season used: A/California/7/2009 (H1N1)pdm09-like virus A/Texas/50/2012 (H3N2)-like virus B/Massachusetts/2/2012-like virus, Quadrivalent vaccines include a B/Brisbane/60/2008-like virus. The CDC announced that drift variants of the A (H3N2) virus strain from the 2012–2013 potentially foretold a severe flu season for 2014–2015. The vaccines produced for the Northern Hemisphere 2015–2016 season used: A/California/7/2009 (H1N1)pdm09-like virus A/Switzerland/9715293/2013 (H3N2)-like virus B/Phuket/3073/2013-like virus. (This is a B/Yamagata lineage virus) The "Split Virion" vaccine distributed in 2016 contained the following strains of inactivated virus: A/California/7/2009 (H1N1)pdm09 - like strain (A/California/7/2009, NYMC X-179A) A/Hong Kong/4801/2014 (H3N2) - like strain (A/Hong Kong/4801/2014, NYMC X-263B) B/Brisbane/60/2008 - like strain (B/Brisbane/60/2008, wild type) A/California/7/2009 (H1N1)pdm09-like virus, A/Hong Kong/4801/2014 (H3N2)-like virus B/Brisbane/60/2008-like virus (B/Victoria lineage) Quadrivalent influenza vaccine adds: B/Phuket/3073/2013-like strainA/Michigan/45/2015 (H1N1)pdm09-like virus A/Hong Kong/4801/2014 (H3N2) B/Brisbane/60/2008-like virus (B/Victoria lineage) Quadrivalent influenza vaccine adds B/Phuket/3073/2013-like[B/Yamagata lineage]Quadrivalent - A/Brisbane/02/2018 (H1N1)pdm09-like virus A/SouthAustralia/34/2019 (H3N2)-like virus B/Washington/02/2019-like virus [B/Victoria lineage] B/Phuket/3073/2013-like virus [B/Yamagata lineage]

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Avian influenza

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Orthomyxoviridae

Orthomyxoviridae (from Greek ὀρθός, orthós 'straight' + μύξα, mýxa ' mucus ') is a family of negative-sense RNA viruses . It includes seven genera : Alphainfluenzavirus , Betainfluenzavirus , Gammainfluenzavirus , Deltainfluenzavirus , Isavirus , Thogotovirus , and Quaranjavirus . The first four genera contain viruses that cause influenza in birds (see also avian influenza ) and mammals , including humans. Isaviruses infect salmon ; the thogotoviruses are arboviruses , infecting vertebrates and invertebrates (such as ticks and mosquitoes ). The Quaranjaviruses are also arboviruses , infecting vertebrates (birds) and invertebrates ( arthropods ). The four genera of Influenza virus that infect vertebrates, which are identified by antigenic differences in their nucleoprotein and matrix protein , are as follows:The influenzavirus virion is pleomorphic ; the viral envelope can occur in spherical and filamentous forms. In general, the virus's morphology is ellipsoidal with particles 100–120 nm in diameter, or filamentous with particles 80–100 nm in diameter and up to 20 µm long. There are approximately 500 distinct spike-like surface projections in the envelope each projecting 10–14 nm from the surface with varying surface densities. The major glycoprotein (HA) spike is interposed irregularly by clusters of neuraminidase (NA) spikes, with a ratio of HA to NA of about 10 to 1. The viral envelope composed of a lipid bilayer membrane in which the glycoprotein spikes are anchored encloses the nucleocapsids ; nucleoproteins of different size classes with a loop at each end; the arrangement within the virion is uncertain. The ribonuclear proteins are filamentous and fall in the range of 50–130 nm long and 9–15 nm in diameter with helical symmetry. [ citation needed ]Viruses of the family Orthomyxoviridae contain six to eight segments of linear negative-sense single stranded RNA. They have a total genome length that is 10,000–14,600 nucleotides (nt). The influenza A genome , for instance, has eight pieces of segmented negative-sense RNA (13.5 kilobases total). The best-characterised of the influenzavirus proteins are hemagglutinin and neuraminidase , two large glycoproteins found on the outside of the viral particles. Hemagglutinin is a lectin that mediates binding of the virus to target cells and entry of the viral genome into the target cell. In contrast, neuraminidase is an enzyme involved in the release of progeny virus from infected cells, by cleaving sugars that bind the mature viral particles. The hemagglutinin (H) and neuraminidase (N) proteins are key targets for antibodies and antiviral drugs, and they are used to classify the different serotypes of influenza A viruses, hence the H and N in H5N1 . The genome sequence has terminal repeated sequences; repeated at both ends. Terminal repeats at the 5′-end 12–13 nucleotides long. Nucleotide sequences of 3′-terminus identical; the same in genera of same family; most on RNA (segments), or on all RNA species. Terminal repeats at the 3′-end 9–11 nucleotides long. Encapsidated nucleic acid is solely genomic. Each virion may contain defective interfering copies. In Influenza A (H1N1) PB1-F2 is produced from an alternative reading frame in PB1. The M and NS genes produce two different genes via alternative splicing . Typically, influenza is transmitted from infected mammals through the air by coughs or sneezes, creating aerosols containing the virus, and from infected birds through their droppings . Influenza can also be transmitted by saliva , nasal secretions , feces and blood . Infections occur through contact with these bodily fluids or with contaminated surfaces. Out of a host, flu viruses can remain infectious for about one week at human body temperature, over 30 days at 0 °C (32 °F) , and indefinitely at very low temperatures (such as lakes in northeast Siberia ). They can be inactivated easily by disinfectants and detergents . The viruses bind to a cell through interactions between its hemagglutinin glycoprotein and sialic acid sugars on the surfaces of epithelial cells in the lung and throat (Stage 1 in infection figure). The cell imports the virus by endocytosis . In the acidic endosome , part of the hemagglutinin protein fuses the viral envelope with the vacuole's membrane, releasing the viral RNA (vRNA) molecules, accessory proteins and RNA-dependent RNA polymerase into the cytoplasm (Stage 2). These proteins and vRNA form a complex that is transported into the cell nucleus , where the RNA-dependent RNA polymerase begins transcribing complementary positive-sense cRNA (Steps 3a and b). The cRNA is either exported into the cytoplasm and translated (step 4), or remains in the nucleus. Newly synthesised viral proteins are either secreted through the Golgi apparatus onto the cell surface (in the case of neuraminidase and hemagglutinin, step 5b) or transported back into the nucleus to bind vRNA and form new viral genome particles (step 5a). Other viral proteins have multiple actions in the host cell, including degrading cellular mRNA and using the released nucleotides for vRNA synthesis and also inhibiting translation of host-cell mRNAs. Negative-sense vRNAs that form the genomes of future viruses, RNA-dependent RNA transcriptase, and other viral proteins are assembled into a virion. Hemagglutinin and neuraminidase molecules cluster into a bulge in the cell membrane. The vRNA and viral core proteins leave the nucleus and enter this membrane protrusion (step 6). The mature virus buds off from the cell in a sphere of host phospholipid membrane, acquiring hemagglutinin and neuraminidase with this membrane coat (step 7). As before, the viruses adhere to the cell through hemagglutinin; the mature viruses detach once their neuraminidase has cleaved sialic acid residues from the host cell. After the release of new influenza virus, the host cell dies. Orthomyxoviridae viruses are one of two RNA viruses that replicate in the nucleus (the other being retroviridae ). This is because the machinery of orthomyxo viruses cannot make their own mRNAs. They use cellular RNAs as primers for initiating the viral mRNA synthesis in a process known as cap snatching . Once in the nucleus, the RNA Polymerase Protein PB2 finds a cellular pre-mRNA and binds to its 5′ capped end. Then RNA Polymerase PA cleaves off the cellular mRNA near the 5′ end and uses this capped fragment as a primer for transcribing the rest of the viral RNA genome in viral mRNA. This is due to the need of mRNA to have a 5′ cap in order to be recognized by the cell's ribosome for translation. Since RNA proofreading enzymes are absent, the RNA-dependent RNA transcriptase makes a single nucleotide insertion error roughly every 10 thousand nucleotides, which is the approximate length of the influenza vRNA. Hence, nearly every newly manufactured influenza virus will contain a mutation in its genome. The separation of the genome into eight separate segments of vRNA allows mixing ( reassortment ) of the genes if more than one variety of influenza virus has infected the same cell ( superinfection ). The resulting alteration in the genome segments packaged into viral progeny confers new behavior, sometimes the ability to infect new host species or to overcome protective immunity of host populations to its old genome (in which case it is called an antigenic shift ). In a phylogenetic -based taxonomy , the category RNA virus includes the subcategory negative-sense ssRNA virus , which includes the order Articulavirales , and the family Orthomyxoviridae . The genera-associated species and serotypes of Orthomyxoviridae are shown in the following table.There are four genera of influenza virus, each containing only a single species, or type. Influenza A and C infect a variety of species (including humans), while influenza B almost exclusively infects humans, and influenza D infects cattle and pigs. Influenza A viruses are further classified, based on the viral surface proteins hemagglutinin (HA or H) and neuraminidase (NA or N). 18 HA subtypes (or serotypes) and 11 NA subtypes of influenza A virus have been isolated in nature. Among these, the HA subtype 1-16 and NA subtype 1-9 are found in wild waterfowl and shorebirds and the HA subtypes 17-18 and NA subtypes 10-11 have only been isolated from bats. Further variation exists; thus, specific influenza strain isolates are identified by a standard nomenclature specifying virus type, geographical location where first isolated, sequential number of isolation, year of isolation, and HA and NA subtype. Examples of the nomenclature are: A/Brisbane/59/2007 (H1N1) A/Moscow/10/99 (H3N2). The type A influenza viruses are the most virulent human pathogens among the three influenza types and cause the most severe disease. It is thought that all influenza A viruses causing outbreaks or pandemics originate from wild aquatic birds. All influenza A virus pandemics since the 1900s were caused by Avian influenza , through Reassortment with human influenza strains (seasonal flu) or through adaptation in a mixing vessel (see 2009 swine flu pandemic ). The serotypes that have been confirmed in humans , ordered by the number of confirmed human deaths, are: Influenza B virus is almost exclusively a human pathogen, and is less common than influenza A. The only other animal known to be susceptible to influenza B infection is the seal . This type of influenza mutates at a rate 2–3 times lower than type A and consequently is less genetically diverse, with only one influenza B serotype. As a result of this lack of antigenic diversity, a degree of immunity to influenza B is usually acquired at an early age. However, influenza B mutates enough that lasting immunity is not possible. This reduced rate of antigenic change, combined with its limited host range (inhibiting cross species antigenic shift ), ensures that pandemics of influenza B do not occur. The influenza C virus infects humans and pigs , and can cause severe illness and local epidemics . However, influenza C is less common than the other types and usually causes mild disease in children. This is a genus that was classified in 2016, the members of which were first isolated in 2011. This genus appears to be most closely related to Influenza C, from which it diverged several hundred years ago. There are at least two extant strains of this genus. The main hosts appear to be cattle, but the virus has been known to infect pigs as well.Influenza A viruses are further classified, based on the viral surface proteins hemagglutinin (HA or H) and neuraminidase (NA or N). 18 HA subtypes (or serotypes) and 11 NA subtypes of influenza A virus have been isolated in nature. Among these, the HA subtype 1-16 and NA subtype 1-9 are found in wild waterfowl and shorebirds and the HA subtypes 17-18 and NA subtypes 10-11 have only been isolated from bats. Further variation exists; thus, specific influenza strain isolates are identified by a standard nomenclature specifying virus type, geographical location where first isolated, sequential number of isolation, year of isolation, and HA and NA subtype. Examples of the nomenclature are: A/Brisbane/59/2007 (H1N1) A/Moscow/10/99 (H3N2). The type A influenza viruses are the most virulent human pathogens among the three influenza types and cause the most severe disease. It is thought that all influenza A viruses causing outbreaks or pandemics originate from wild aquatic birds. All influenza A virus pandemics since the 1900s were caused by Avian influenza , through Reassortment with human influenza strains (seasonal flu) or through adaptation in a mixing vessel (see 2009 swine flu pandemic ). The serotypes that have been confirmed in humans , ordered by the number of confirmed human deaths, are:Influenza B virus is almost exclusively a human pathogen, and is less common than influenza A. The only other animal known to be susceptible to influenza B infection is the seal . This type of influenza mutates at a rate 2–3 times lower than type A and consequently is less genetically diverse, with only one influenza B serotype. As a result of this lack of antigenic diversity, a degree of immunity to influenza B is usually acquired at an early age. However, influenza B mutates enough that lasting immunity is not possible. This reduced rate of antigenic change, combined with its limited host range (inhibiting cross species antigenic shift ), ensures that pandemics of influenza B do not occur. The influenza C virus infects humans and pigs , and can cause severe illness and local epidemics . However, influenza C is less common than the other types and usually causes mild disease in children. This is a genus that was classified in 2016, the members of which were first isolated in 2011. This genus appears to be most closely related to Influenza C, from which it diverged several hundred years ago. There are at least two extant strains of this genus. The main hosts appear to be cattle, but the virus has been known to infect pigs as well.Mammalian influenza viruses tend to be labile, but can survive several hours in mucus. Avian influenza virus can survive for 100 days in distilled water at room temperature, and 200 days at 17 °C (63 °F) . The avian virus is inactivated more quickly in manure, but can survive for up to two weeks in feces on cages. Avian influenza viruses can survive indefinitely when frozen. Influenza viruses are susceptible to bleach, 70% ethanol, aldehydes, oxidizing agents, and quaternary ammonium compounds. They are inactivated by heat of 133 °F (56 °C) for minimum of 60 minutes, as well as by low pH <2. Vaccines and drugs are available for the prophylaxis and treatment of influenza virus infections. Vaccines are composed of either inactivated or live attenuated virions of the H1N1 and H3N2 human influenza A viruses, as well as those of influenza B viruses. Because the antigenicities of the wild viruses evolve, vaccines are reformulated annually by updating the seed strains. [ citation needed ] When the antigenicities of the seed strains and wild viruses do not match, vaccines fail to protect the vaccinees. [ citation needed ] In addition, even when they do match, escape mutants are often generated. [ citation needed ] Drugs available for the treatment of influenza include Amantadine and Rimantadine , which inhibit the uncoating of virions by interfering with M2, and Oseltamivir (marketed under the brand name Tamiflu ), Zanamivir , and Peramivir , which inhibit the release of virions from infected cells by interfering with NA. However, escape mutants are often generated for the former drug and less frequently for the latter drug.

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Avian influenza

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Oseltamivir

ethyl (3 R ,4 R ,5 S )-5-amino-4-acetamido-3-(pentan-3-yloxy)-cyclohex-1-ene-1-carboxylate CCC(CC)OC1C=C(CC(C1NC(=O)C)N)C(=O)OCC InChI=1S/C16H28N2O4/c1-5-12(6-2)22-14-9-11(16(20)21-7-3)8-13(17)15(14)18-10(4)19/h9,12-15H,5-8,17H2,1-4H3,(H,18,19)/t13-,14+,15+/m0/s1 Y Key:VSZGPKBBMSAYNT-RRFJBIMHSA-N Y Oseltamivir , sold under the brand name Tamiflu , is an antiviral medication used to treat and prevent influenza A and influenza B , viruses that cause the flu . Many medical organizations recommend it in people who have complications or are at high risk of complications within 48 hours of first symptoms of infection. They recommend it to prevent infection in those at high risk, but not the general population. The Centers for Disease Control and Prevention (CDC) recommends that clinicians use their discretion to treat those at lower risk who present within 48 hours of first symptoms of infection. It is taken by mouth, either as a pill or liquid. Recommendations regarding oseltamivir are controversial as are criticisms of the recommendations. A 2014 Cochrane Review concluded that oseltamivir does not reduce hospitalizations, and that there is no evidence of reduction in complications of influenza. Two meta-analyses have concluded that benefits in those who are otherwise healthy do not outweigh its risks. They also found little evidence regarding whether treatment changes the risk of hospitalization or death in high risk populations. However, another meta-analysis found that oseltamivir was effective for prevention of influenza at the individual and household levels. Common side effects include vomiting , diarrhea , headache, and trouble sleeping. Other side effects may include psychiatric symptoms and seizures . In the United States it is recommended for influenza infection during pregnancy. It has been taken by a small number of pregnant women without signs of problems. Dose adjustment may be needed in those with kidney problems. Oseltamivir was approved for medical use in the US in 1999. It was the first neuraminidase inhibitor available by mouth. It is on the World Health Organization's List of Essential Medicines but was downgraded to "complementary" status in 2017. A generic version was approved in the US in 2016. In 2020, it was the 178th most commonly prescribed medication in the United States, with more than 3 million prescriptions. Oseltamivir is used for the prevention and treatment of influenza caused by influenza A and B viruses. It is on the World Health Organization's List of Essential Medicines . The WHO supports its use for severe illness due to confirmed or suspected influenza virus infection in critically ill people who have been hospitalized. Oseltamivir's risk-benefit ratio is controversial. In 2017, it was moved from the core to the complementary list based on its lower cost-effectiveness. The Expert Committee did not recommend the deletion of oseltamivir from the EML and EMLc, recognizing that it is the only medicine included on the Model Lists for critically ill patients with influenza and for influenza pandemic preparedness. However, the Committee noted that, since the inclusion of oseltamivir on the Model List in 2009, new evidence in seasonal and pandemic influenza has lowered earlier estimates of the magnitude of effect of oseltamivir on relevant clinical outcomes. The Committee recommended that the listing of oseltamivir be amended, moving the medicine from the core to the Complementary List, and that its use be restricted to severe illness due to confirmed or suspected influenza virus infection in critically ill hospitalized patients. The Expert Committee noted that WHO guidelines for pharmacological management of pandemic and seasonal influenza would be updated in 2017: unless new information is provided to support the use of oseltamivir in seasonal and pandemic outbreaks, the next Expert Committee might consider oseltamivir for deletion. The US Centers for Disease Control and Prevention (CDC), European Centre for Disease Prevention and Control (ECDC), Public Health England and the American Academy of Pediatrics (AAP) recommend the use of oseltamivir for people who have complications or are at high risk for complications. This includes those who are hospitalized, young children, those over the age of 65, people with other significant health problems, those who are pregnant, and Indigenous peoples of the Americas among others. The Infectious Disease Society of America takes the same position as the CDC. A systematic review of systematic reviews in PLoS One did not find evidence for benefits in people who are at risk, noting that "the trials were not designed or powered to give results regarding serious complications, hospitalization and mortality", as did a 2014 Cochrane Review. The Cochrane Review further recommended: "On the basis of the findings of this review, clinicians and healthcare policy-makers should urgently revise current recommendations for use of the neuraminidase inhibitors (NIs) for individuals with influenza." That is not utilizing NIs for prevention or treatment "Based on these findings there appears to be no evidence for patients, clinicians or policy-makers to use these drugs to prevent serious outcomes, both in annual influenza and pandemic influenza outbreaks." The CDC, ECDC, Public Health England, Infectious Disease Society of America, the AAP, and Roche (the originator) reject the conclusions of the Cochrane Review, arguing in part that the analysis inappropriately forms conclusions about outcomes in people who are seriously ill based on results obtained primarily in healthy populations, and that the analysis inappropriately included results from people not infected with influenza. The EMA did not change its labeling of the drug in response to the Cochrane study. A 2014 review in the New England Journal of Medicine recommended that all people admitted to intensive care units during influenza outbreaks with a diagnosis of community-acquired pneumonia receive oseltamivir until the absence of influenza infection is established by PCR testing. A 2015 systematic review and meta-analysis found oseltamivir effective at treating the symptoms of influenza, reducing the length of hospitalization, and reducing the risk of otitis media . The same review found that oseltamivir did not significantly increase the risk of adverse events. A 2016 systematic review found that oseltamivir slightly reduced the time it takes for the symptoms of influenza to be alleviated, and that it also increased the risk of "nausea, vomiting, [and] psychiatric events in adults and vomiting in children." The decrease in duration of sickness was about 18 hours. In those who are otherwise healthy the CDC states that antivirals may be considered within the first 48 hours. A German clinical practice guideline recommends against its use. Two 2013 meta-analyses have concluded that benefits in those who are otherwise healthy do not outweigh its risks. When the analysis was restricted to people with confirmed infection, the same 2014 Cochrane Review (see above) found unclear evidence of change in the risk of complications such as pneumonia , while three other reviews found a decreased risk. Together, published studies suggest that oseltamivir reduces the duration of symptoms by 0.5–1.0 day. Any benefit of treatment must be balanced against side effects, which include psychiatric symptoms and increased rates of vomiting. The 2014 Cochrane Collaboration review concluded that oseltamivir did not affect the need for hospitalizations, and that there is no proof of reduction of complications of influenza (such as pneumonia) because of a lack of diagnostic definitions, or reduction of the spread of the virus. There was also evidence that suggested that oseltamivir prevented some people from producing sufficient numbers of their own antibodies to fight infection. The authors recommended that guidance should be revised to take account of the evidence of small benefit and increased risk of harms. The US Centers for Disease Control and Prevention (CDC), the European Centre for Disease Prevention and Control (ECDC), the Public Health England (PHE), the Infectious Disease Society of America (IDSA), the American Academy of Pediatrics (AAP), and Roche (the originator) rejected the recommendations of the 2014 Cochrane Review to urgently change treatment guidelines and drug labels. As of 2017 [ update ] , the CDC does not recommend to use oseltamivir generally for prevention due to concerns that widespread use will encourage resistance development. They recommend that it be considered in those at high risk, who have been exposed to influenza within 48 hours and have not received or only recently been vaccinated. They recommended it during outbreaks in long term care facilities and in those who are significantly immunosuppressed. As of 2011 [ update ] , reviews concluded that when oseltamivir is used preventatively it decreases the risk of exposed people developing symptomatic disease. A systematic review of systematic reviews found low to moderate evidence that it decreases the risk of getting symptomatic influenza by 1 to 12% (a relative decrease of 64 to 92%). It recommended against its use in healthy, low-risk persons due to cost, the risk of resistance development, and side effects and concluded it might be useful for prevention in unvaccinated high risk persons. The US Centers for Disease Control and Prevention (CDC), European Centre for Disease Prevention and Control (ECDC), Public Health England and the American Academy of Pediatrics (AAP) recommend the use of oseltamivir for people who have complications or are at high risk for complications. This includes those who are hospitalized, young children, those over the age of 65, people with other significant health problems, those who are pregnant, and Indigenous peoples of the Americas among others. The Infectious Disease Society of America takes the same position as the CDC. A systematic review of systematic reviews in PLoS One did not find evidence for benefits in people who are at risk, noting that "the trials were not designed or powered to give results regarding serious complications, hospitalization and mortality", as did a 2014 Cochrane Review. The Cochrane Review further recommended: "On the basis of the findings of this review, clinicians and healthcare policy-makers should urgently revise current recommendations for use of the neuraminidase inhibitors (NIs) for individuals with influenza." That is not utilizing NIs for prevention or treatment "Based on these findings there appears to be no evidence for patients, clinicians or policy-makers to use these drugs to prevent serious outcomes, both in annual influenza and pandemic influenza outbreaks." The CDC, ECDC, Public Health England, Infectious Disease Society of America, the AAP, and Roche (the originator) reject the conclusions of the Cochrane Review, arguing in part that the analysis inappropriately forms conclusions about outcomes in people who are seriously ill based on results obtained primarily in healthy populations, and that the analysis inappropriately included results from people not infected with influenza. The EMA did not change its labeling of the drug in response to the Cochrane study. A 2014 review in the New England Journal of Medicine recommended that all people admitted to intensive care units during influenza outbreaks with a diagnosis of community-acquired pneumonia receive oseltamivir until the absence of influenza infection is established by PCR testing. A 2015 systematic review and meta-analysis found oseltamivir effective at treating the symptoms of influenza, reducing the length of hospitalization, and reducing the risk of otitis media . The same review found that oseltamivir did not significantly increase the risk of adverse events. A 2016 systematic review found that oseltamivir slightly reduced the time it takes for the symptoms of influenza to be alleviated, and that it also increased the risk of "nausea, vomiting, [and] psychiatric events in adults and vomiting in children." The decrease in duration of sickness was about 18 hours. In those who are otherwise healthy the CDC states that antivirals may be considered within the first 48 hours. A German clinical practice guideline recommends against its use. Two 2013 meta-analyses have concluded that benefits in those who are otherwise healthy do not outweigh its risks. When the analysis was restricted to people with confirmed infection, the same 2014 Cochrane Review (see above) found unclear evidence of change in the risk of complications such as pneumonia , while three other reviews found a decreased risk. Together, published studies suggest that oseltamivir reduces the duration of symptoms by 0.5–1.0 day. Any benefit of treatment must be balanced against side effects, which include psychiatric symptoms and increased rates of vomiting. The 2014 Cochrane Collaboration review concluded that oseltamivir did not affect the need for hospitalizations, and that there is no proof of reduction of complications of influenza (such as pneumonia) because of a lack of diagnostic definitions, or reduction of the spread of the virus. There was also evidence that suggested that oseltamivir prevented some people from producing sufficient numbers of their own antibodies to fight infection. The authors recommended that guidance should be revised to take account of the evidence of small benefit and increased risk of harms. The US Centers for Disease Control and Prevention (CDC), the European Centre for Disease Prevention and Control (ECDC), the Public Health England (PHE), the Infectious Disease Society of America (IDSA), the American Academy of Pediatrics (AAP), and Roche (the originator) rejected the recommendations of the 2014 Cochrane Review to urgently change treatment guidelines and drug labels. As of 2017 [ update ] , the CDC does not recommend to use oseltamivir generally for prevention due to concerns that widespread use will encourage resistance development. They recommend that it be considered in those at high risk, who have been exposed to influenza within 48 hours and have not received or only recently been vaccinated. They recommended it during outbreaks in long term care facilities and in those who are significantly immunosuppressed. As of 2011 [ update ] , reviews concluded that when oseltamivir is used preventatively it decreases the risk of exposed people developing symptomatic disease. A systematic review of systematic reviews found low to moderate evidence that it decreases the risk of getting symptomatic influenza by 1 to 12% (a relative decrease of 64 to 92%). It recommended against its use in healthy, low-risk persons due to cost, the risk of resistance development, and side effects and concluded it might be useful for prevention in unvaccinated high risk persons. Common adverse drug reactions (ADRs) associated with oseltamivir therapy (occurring in over 1 percent of people) include nausea and vomiting. In adults, oseltamivir increased the risk of nausea for which the number needed to harm was 28 and for vomiting was 22. So, for every 22 adult people on oseltamivir one experienced vomiting. In the treatment of children, oseltamivir also induced vomiting. The number needed to harm was 19. So, for every 19 children on oseltamivir one experienced vomiting. In prevention there were more headaches, kidney, and psychiatric events. Oseltamivir's effect on the heart is unclear: it may reduce cardiac symptoms, but may also induce serious arrhythmias. Postmarketing reports include liver inflammation and elevated liver enzymes, rash, allergic reactions including anaphylaxis , toxic epidermal necrolysis , abnormal heart rhythms , seizure, confusion, aggravation of diabetes, and haemorrhagic colitis and Stevens–Johnson syndrome . The US and EU package inserts for oseltamivir contain a warning of psychiatric effects observed in post-marketing surveillance. The frequency of these appears to be low and a causative role for oseltamivir has not been established. The 2014 Cochrane Review found a dose-response effect on psychiatric events. In trials of prevention in adults one person was harmed for every 94 treated. Neither of the two most cited published treatment trials of oseltamivir reported any drug-attributable serious adverse events. It is pregnancy category C in the United States and category B in Australia, meaning that it has been taken by a small number of women without signs of problems and in animal studies it looks safe. Dose adjustment may be needed in those with kidney problems. Oseltamivir is a neuraminidase inhibitor , a competitive inhibitor of influenza's neuraminidase enzyme. The enzyme cleaves the sialic acid which is found on glycoproteins on the surface of human cells that helps new virions to exit the cell, preventing new viral particles from being released. The vast majority of mutations conferring resistance are single amino acid residue substitutions (His274Tyr in N1) in the neuraminidase enzyme. A 2011 meta-analysis of 15 studies found a pooled incidence rate for oseltamivir resistance of 2.6%. Subgroup analyses detected higher rates among influenza A patients, especially the H1N1 subtype. It was found that a substantial number of patients might become oseltamivir-resistant as a result of oseltamivir use, and that oseltamivir resistance might be significantly associated with pneumonia. In severely immunocompromised patients there were reports of prolonged shedding of oseltamivir- (or zanamivir )-resistant virus, even after oseltamivir treatment was stopped. As of December 15, 2010 [ update ] , the World Health Organization (WHO) reported 314 samples of the prevalent 2009 pandemic H1N1 flu tested worldwide showed resistance to oseltamivir. The CDC found sporadic oseltamivir-resistant 2009 H1N1 virus infections had been identified, including with rare episodes of limited transmission, but the public health impact had been limited. Those sporadic cases of resistance were found in immunosuppressed patients during oseltamivir treatment and persons who developed illness while receiving oseltamivir chemoprophylaxis. During 2011, a new influenza A(H1N1)2009 variant with mildly reduced oseltamivir (and zanamivir) sensitivity was detected in more than 10% of community specimens in Singapore and more than 30% of samples from northern Australia. While there is concern that antiviral resistance may develop in people with haematologic malignancies due to their inability to reduce viral loads and several surveillance studies found oseltamivir-resistant pH1N1 after administration of oseltamivir in those people, as of November 2013 [ update ] , widespread transmission of oseltamivir-resistant pH1N1 has not occurred. During the 2007–08 flu season, the US CDC found 10.9% of H1N1 samples (n=1,020) to be resistant. In the 2008–09 season, the proportion of resistant H1N1 increased to 99.4%, while no other seasonal strains (H3N2, B) showed resistance. From 2009 to 2014, oseltamivir resistance was very low in seasonal flu. In the 2010–11 flu season, 99.1% of H1N1, 99.8% of H3N, and 100% of Influenza B remained oseltamivir susceptible in the US. In January 2012, the US and European CDCs reported all seasonal flu samples tested since October 2011 to be oseltamivir susceptible. In the 2013–14 season only 1% of 2009 H1N1 viruses showed oseltamivir resistance. No other influenza viruses were resistant to oseltamivir. Three studies have found resistance in 0%, 3.3%, and 18% of subjects. In the study with the 18% resistance rate, the subjects were children, many of whom had not been previously exposed to influenza virus and therefore had a weakened immune response; the results suggest that higher and earlier dosing may be necessary in such populations. In 2007, Japanese investigators detected neuraminidase-resistant influenza B virus strains in individuals not treated with these drugs. The prevalence was 1.7%. According to the CDC, As of 2019 [ update ] , transmission of oseltamivir-resistant influenza B virus strains—from persons treated with the drug—is rare. As of 2013 [ update ] , H274Y and N294S mutations that confer resistance to oseltamivir have been identified in a few H5N1 isolates from infected patients treated with oseltamivir, and have emerged spontaneously in Egypt. As of 2013 [ update ] , two of 14 adults infected with A(H7N9) and treated with oseltamivir developed oseltamivir-resistant virus with the Arg292Lys mutation. As of December 15, 2010 [ update ] , the World Health Organization (WHO) reported 314 samples of the prevalent 2009 pandemic H1N1 flu tested worldwide showed resistance to oseltamivir. The CDC found sporadic oseltamivir-resistant 2009 H1N1 virus infections had been identified, including with rare episodes of limited transmission, but the public health impact had been limited. Those sporadic cases of resistance were found in immunosuppressed patients during oseltamivir treatment and persons who developed illness while receiving oseltamivir chemoprophylaxis. During 2011, a new influenza A(H1N1)2009 variant with mildly reduced oseltamivir (and zanamivir) sensitivity was detected in more than 10% of community specimens in Singapore and more than 30% of samples from northern Australia. While there is concern that antiviral resistance may develop in people with haematologic malignancies due to their inability to reduce viral loads and several surveillance studies found oseltamivir-resistant pH1N1 after administration of oseltamivir in those people, as of November 2013 [ update ] , widespread transmission of oseltamivir-resistant pH1N1 has not occurred. During the 2007–08 flu season, the US CDC found 10.9% of H1N1 samples (n=1,020) to be resistant. In the 2008–09 season, the proportion of resistant H1N1 increased to 99.4%, while no other seasonal strains (H3N2, B) showed resistance. From 2009 to 2014, oseltamivir resistance was very low in seasonal flu. In the 2010–11 flu season, 99.1% of H1N1, 99.8% of H3N, and 100% of Influenza B remained oseltamivir susceptible in the US. In January 2012, the US and European CDCs reported all seasonal flu samples tested since October 2011 to be oseltamivir susceptible. In the 2013–14 season only 1% of 2009 H1N1 viruses showed oseltamivir resistance. No other influenza viruses were resistant to oseltamivir. Three studies have found resistance in 0%, 3.3%, and 18% of subjects. In the study with the 18% resistance rate, the subjects were children, many of whom had not been previously exposed to influenza virus and therefore had a weakened immune response; the results suggest that higher and earlier dosing may be necessary in such populations. In 2007, Japanese investigators detected neuraminidase-resistant influenza B virus strains in individuals not treated with these drugs. The prevalence was 1.7%. According to the CDC, As of 2019 [ update ] , transmission of oseltamivir-resistant influenza B virus strains—from persons treated with the drug—is rare. As of 2013 [ update ] , H274Y and N294S mutations that confer resistance to oseltamivir have been identified in a few H5N1 isolates from infected patients treated with oseltamivir, and have emerged spontaneously in Egypt. As of 2013 [ update ] , two of 14 adults infected with A(H7N9) and treated with oseltamivir developed oseltamivir-resistant virus with the Arg292Lys mutation. Its oral bioavailability is over 80% and is extensively metabolised to its active form upon first-pass through the liver. It has a volume of distribution of 23–26 litres. Its half-life is about 1–3 hours and its active carboxylate metabolite has a half-life of 6–10 hours. More than 90% of the oral dose is eliminated in the urine as the active metabolite. Oseltamivir was discovered by scientists at Gilead Sciences using shikimic acid as a starting point for synthesis ; shikimic acid was originally available only as an extract of Chinese star anise ; but by 2006, 30% of the supply was manufactured recombinantly in E. coli. Gilead exclusively licensed their relevant patents to Roche in 1996. The drug's patent has not been protected in Thailand, the Philippines, Indonesia, and several other countries. In 1999, the FDA approved oseltamivir phosphate for the treatment of influenza in adults based on two double-blind, randomized, placebo-controlled clinical trials. In June 2002, the European Medicines Agency (EMA) approved oseltamivir phosphate for prophylaxis and treatment of influenza. In 2003, a pooled analysis of ten randomised clinical trials concluded that oseltamivir reduced the risk of lower respiratory tract infections resulting in antibiotic use and hospital admissions in adults. Oseltamivir (as Tamiflu) was widely used during the H5N1 avian influenza epidemic in Southeast Asia in 2005. [ medical citation needed ] In response to the epidemic, various governments – including those of the United Kingdom, Canada, Israel, United States, and Australia – stockpiled quantities of oseltamivir in preparation for a possible pandemic and there were worldwide shortages of the drug, driven by the high demand for stockpiling. In November 2005, US President George W. Bush requested that Congress fund US$1 billion for the production and stockpile of oseltamivir, after Congress had already approved $1.8 billion for military use of the drug. Defense Secretary Donald Rumsfeld, who was a past chairman of Gilead Sciences, recused himself from all government decisions regarding the drug. In 2006, a Cochrane Review (since withdrawn) raised controversy by concluding that oseltamivir should not be used during routine seasonal influenza because of its low effectiveness. In December 2008, the Indian drug company Cipla won a case in India's court system allowing it to manufacture a cheaper generic version of Tamiflu, called Antiflu. In May 2009, Cipla won approval from the World Health Organization (WHO) certifying that its drug Antiflu was as effective as Tamiflu, and Antiflu is included in the WHO list of prequalified medicinal products. In 2009, a new A/H1N1 influenza virus was discovered to be spreading in North America. In June 2009, the WHO declared the A/H1N1 influenza a pandemic. The National Institute for Health and Care Excellence (NICE), the CDC, the WHO, and the ECDC maintained their recommendation to use oseltamivir. From 2010 to 2012, Cochrane requested Roche's full clinical study reports of their trials, which they did not provide. In 2011, a freedom of information request to the European Medicines Agency (EMA) provided Cochrane with reports from 16 Roche oseltamivir trials. In 2012, the Cochrane team published an interim review based on those reports. In 2013, Roche released 74 full clinical study reports of oseltamivir trials after GSK released the data on zanamivir studies. In 2014, Cochrane published an updated review based solely on full clinical study reports and regulatory documents. In 2016, Roche's oseltamivir patents began to expire. There have been [ when? ] reports of oseltamivir reducing disease severity and hospitalization time in canine parvovirus infection. The drug may limit the ability of the virus to invade the crypt cells of the small intestine and decrease gastrointestinal bacterial colonization and toxin production. Oseltamivir has been deemed ineffective at treating COVID-19 , consistent with the SARS-CoV-2 virus lacking influenza's neuraminidase enzyme.

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Avian influenza

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Rock dove

The rock dove , rock pigeon , or common pigeon ( / ˈ p ɪ dʒ . ə n / also / ˈ p ɪ dʒ . ɪ n / ; Columba livia ) is a member of the bird family Columbidae (doves and pigeons). : 624 In common usage, it is often simply referred to as the "pigeon", although this is the wild form of the bird; the pigeons most familiar to people are the domesticated form of the wild rock dove. The domestic pigeon ( Columba livia domestica , which includes about 1,000 different breeds ) descended from this species. Escaped domestic pigeons have increased the populations of feral pigeons around the world. Wild rock doves are pale grey with two black bars on each wing, whereas domestic and feral pigeons vary in the colour and pattern of their plumage . Few differences are seen between males and females; i.e they are not strongly sexually dimorphic . The species is generally monogamous , with two squabs (young) per brood . Both parents care for the young for a time. Habitats include various open and semi-open environments where they are able to forage on the ground. Cliffs and rock ledges are used for roosting and breeding in the wild. Originating in Southern Europe , North Africa , and Western Asia , pigeons have become established in cities around the world. The species is abundant, with an estimated population of 17 to 28 million feral and wild birds in Europe alone and up to 120 million worldwide. The official common name is rock dove , as given by the International Ornithological Congress . The rock dove was formally described in 1789 by the German naturalist Johann Friedrich Gmelin in his revised and expanded edition of Systema Naturae written by Carl Linnaeus . He placed it with all the other doves and pigeons in the genus Columba and coined the binomial name Columba livia . The genus name Columba is the Latin word meaning "pigeon, dove", whose older etymology comes from the Ancient Greek ÎºÏŒÎ»Ï Î¼Î²Î¿Ï‚ ( kolumbos ), "a diver", from ÎºÎ¿Î»Ï Î¼Î²Î¬Ï‰ (kolumbao), "dive, plunge headlong, swim". Aristophanes (Birds, 304) and others use the word ÎºÎ¿Î»Ï Î¼Î²Î¯Ï‚ ( kolumbis ), "diver", for the name of the bird, because of its swimming motion in the air. The specific epithet livia is a medieval Latin variant of livida , "livid, bluish-grey"; this was Theodorus Gaza 's translation of Greek peleia , "dove", itself thought to be derived from pellos , "dark-coloured". : 228 Its closest relative in the genus Columba is the hill pigeon , followed by the other rock pigeons: the snow , speckled , and white-collared pigeons . Pigeon chicks are called "squabs". Note that members of the lesser known pigeon genus Petrophassa and the speckled pigeon ( Columba guinea ), also have the common name " rock pigeon ". The rock dove was first described by German naturalist Johann Gmelin in 1789. The rock dove was central to Charles Darwin 's discovery of evolution , and featured in four of his works from 1859 to 1872. Darwin posited that, despite wide-ranging morphological differences, the many hundreds of breeds of domestic pigeon could all be traced back to the wild rock dove; in essence human selection of pigeon breeds was analogous to natural selection . Nine subspecies are recognised: Nine subspecies are recognised: Centuries of domestication have greatly altered the rock dove. Feral pigeons, which have escaped domestication throughout history, have significant variations in plumage. When not specified, descriptions are for assumed wild type , though the wild type may be on the verge of extinction or already extinct. The adult of the nominate subspecies of the rock dove is 29 to 37 cm (11 to 15 in) long with a 62 to 72 cm (24 to 28 in) wingspan. Weight for wild or feral rock doves ranges from 238–380 g (8.4–13.4 oz) , though overfed domestic and semidomestic individuals can exceed normal weights. It has a dark bluish-grey head, neck, and chest with glossy yellowish, greenish, and reddish-purple iridescence along its neck and wing feathers. The iris is orange, red, or golden with a paler inner ring, and the bare skin round the eye is bluish-grey. The bill is grey-black with a conspicuous off-white cere, and the feet are purplish-red. Among standard measurements, the wing chord is typically around 22.3 cm (8.8 in) , the tail is 9.5 to 11 cm (3.7 to 4.3 in) , the bill is around 1.8 cm (0.71 in) , and the tarsus is 2.6 to 3.5 cm (1.0 to 1.4 in) . The adult female is almost identical in outward appearance to the male, but the iridescence on her neck is less intense and more restricted to the rear and sides, whereas that on the breast is often very obscure. The white lower back of the pure rock dove is its best identification characteristic; the two black bars on its pale grey wings are also distinctive. The tail has a black band on the end, and the outer web of the tail feathers are margined with white. It is strong and quick on the wing, dashing out from sea caves, flying low over the water, its lighter grey rump showing well from above. [ self-published source? ] Young birds show little lustre and are duller. Eye colour of the pigeon is generally orange, but a few pigeons may have white-grey eyes. The eyelids are orange and encapsulated in a grey-white eye ring. The feet are red to pink. The subspecies gymnocycla is smaller and very much darker than the nominate subspecies . It is almost blackish on the head, rump and underparts with a white back and the iridescence of the nape extending onto the head. Subspecies targia is slightly smaller than the nominate, with similar plumage, but the back is concolorous with the mantle instead of white. Subspecies dakhlae is smaller and much paler than the nominate. Subspecies schimperi closely resembles targia , but has a distinctly paler mantle. Subspecies palaestinae is slightly larger than schimperi and has darker plumage. Subspecies gaddi is larger and paler than palaestinae, with which it intergrades in the west. Subspecies neglecta it is similar to the nominate in size but darker, with a stronger and more extensive iridescent sheen on the neck. It intergrades with gaddi in the south. Subspecies intermedia is similar to neglecta but darker, with a less contrasting back. : 176–179 There have been numerous skeletal descriptions of the rock dove and the associated muscles including those of the eye, jaw, neck, and throat. The skull is dominated by the rostrum, eye socket, and braincase. The quadrate bone is relatively small and mobile and connects the rest of the cranium to the lower jaw. The latter has an angled shape in side view because the long-axis of the front half of the lower jaw is at a 30° angle to the back half. Beneath the skull, the hyoid skeleton involves three mid-line structures and a pair of elongate structures that stem from between the junction of the back two structures. The anterior structure (the paraglossum or entoglossum) is unpaired and shaped like an arrowhead. When circling overhead, the white underwing of the bird becomes conspicuous. In its flight, behaviour, and voice, which is more of a dovecot coo than the phrase of the wood pigeon , it is a typical pigeon. Although it is a relatively strong flier, it also glides frequently, holding its wings in a very pronounced V shape as it does. As prey birds, they must keep their vigilance, and when disturbed a pigeon within a flock will take off with a noisy clapping sound that cues for other pigeons to take to flight. The noise of the take-off increases the faster a pigeon beats its wings, thus advertising the magnitude of a perceived threat to its flockmates. Feral pigeons are essentially the same size and shape as the original wild rock dove, but often display far greater variation in colour and pattern compared to their wild ancestors. The blue-barred pattern which the original wild rock dove displays is generally less common in more urban areas. Urban pigeons tend to have darker plumage than those in more rural areas. Pigeons feathers have two types of melanin (pigment) – eumelanin and pheomelanin . A study of melanin in the feathers of both wild rock and domestic pigeons, of different coloration types and known genetic background, measured the concentration, distribution and proportions of eumelanin and pheomelanin and found that gene mutations affecting the distribution, amounts and proportions of pigments accounted for the greater variation of coloration in domesticated birds than in their wild relations. Eumelanin generally causes grey or black coloration, while pheomelanin results in a reddish-brown colour. Other shades of brown may be produced through different combinations and concentrations of the two colours. As in other animals, white pigeons have little to no pigment. [ citation needed ] Darker birds may be better able to store trace metals in their feathers due to their higher concentrations of melanin, which may help mitigate the negative effects of the metals, the concentrations of which are typically higher in urban areas. Pigeons, especially homing or carrier breeds, are well known for their ability to find their way home from long distances. Despite these demonstrated abilities, wild rock doves are sedentary and rarely leave their local areas. It is hypothesized that in their natural, arid habitat, they rely on this sense to navigate back home after foraging as deserts rarely possess navigational landmarks that may be used. A rock pigeon's lifespan ranges from 3–5 years in the wild to 15 years in captivity, though longer-lived specimens have been reported. The main causes of mortality in the wild are predators and persecution by humans. [ citation needed ] Some sources state the species was first introduced to North America in 1606 at Port Royal , Nova Scotia . Although other sources cite Plymouth and Jamestown settlements in the early 17th century as the first place for species introduction in North America. The call is a soft, slightly wavering, coo. Ornithologist David Sibley describes the display call as a whoo, hoo-witoo-hoo , whereas the Cornell Lab of Ornithology describes it as a Coo, roo-c'too-coo . Variations include an alarm call, a nest call, and noises made by juveniles. Sibley describes the nest call as a repeated hu-hu-hurrr . When displaying, songs are partly sexual, partly threatening. They are accompanied by an inflated throat, tail fanning, strutting, and bowing. The alarm call, given at sight of predators, is a grunt-like oorhh . Non-vocal sounds include a loud flapping noise at take-off, feet stomping, hisses, and beak snapping. Wings may also be clapped during flights, usually during display fights or after copulation. Juveniles particularly snap their bills, usually to respond to nest invasion. The foot stomping appears deliberate, though for what purpose is unclear. Foot stomping is done with a certain foot first, showing that rock doves have "footedness", similar to human handedness . The call is a soft, slightly wavering, coo. Ornithologist David Sibley describes the display call as a whoo, hoo-witoo-hoo , whereas the Cornell Lab of Ornithology describes it as a Coo, roo-c'too-coo . Variations include an alarm call, a nest call, and noises made by juveniles. Sibley describes the nest call as a repeated hu-hu-hurrr . When displaying, songs are partly sexual, partly threatening. They are accompanied by an inflated throat, tail fanning, strutting, and bowing. The alarm call, given at sight of predators, is a grunt-like oorhh . Non-vocal sounds include a loud flapping noise at take-off, feet stomping, hisses, and beak snapping. Wings may also be clapped during flights, usually during display fights or after copulation. Juveniles particularly snap their bills, usually to respond to nest invasion. The foot stomping appears deliberate, though for what purpose is unclear. Foot stomping is done with a certain foot first, showing that rock doves have "footedness", similar to human handedness . Before the Columbian Exchange , rock doves were restricted to a natural resident range in western and southern Europe , North Africa , and extending into South Asia . They were carried into the New World aboard European ships between 1603 and 1607. The species (including ferals) has a large range, with an estimated global extent of occurrence of 10,000,000 km 2 (3,900,000 sq mi) . It has a large global population, including an estimated 17 to 28 million individuals in Europe. Fossil evidence suggests the rock dove originated in southern Asia, and skeletal remains, unearthed in Israel , confirm its existence there for at least 300,000 years. However, this species has such a long history with humans that it is impossible to identify its original range exactly. Wild pigeons reside in rock formations and cliff faces, settling in crevices to nest. They nest communally, often forming large colonies of many hundreds of individuals. Wild nesting sites include caves, canyons, and sea cliffs. They will even live in the Sahara so long as an area has rocks, water, and some plant matter. They prefer to avoid dense vegetation. Rock doves have a commensal relationship with humans, gaining both ample access to food and nesting spots in civilized areas. Human structures provide an excellent imitation of cliff structures, making rock doves very common around human habitation. Skyscrapers, highway overpasses, farm buildings, abandoned buildings, and other human structures with ample crevices are conducive to rock dove nesting. Thus the modern range of the rock dove is due in large part to humans. Agricultural settlements are favoured over forested ones. Ideal human nesting attributes combine areas with tall buildings, green spaces, ample access to human food, and schools. Conversely, suburban areas which are far from city centers and have high street density are the least conducive to pigeons. Their versatility among human structures is evidenced by a population living inside a deep well in Tunisia. Feral pigeons are usually unable to find these accommodations, so they must nest on building ledges, walls or statues. They may damage these structures via their feces; starving birds can only excrete urates, which over time corrodes masonry and metal. In contrast, a well-fed bird passes mostly solid feces, containing only small amounts of uric acid. [ citation needed ]Pigeons are often found in pairs in the breeding season, but are usually gregarious. The rock dove breeds at any time of the year, but peak times are spring and summer. Nesting sites are along coastal cliff faces, as well as the artificial cliff faces created by apartment buildings with accessible ledges or roof spaces. Pigeons can compete with native birds for nest sites. For some avian species, such as seabirds, it could be a conservation issue. Current evidence suggests that wild, domestic and feral pigeons mate for life, although their long-term bonds are not unbreakable. They are socially monogamous, but extra-pair matings do occur, often initiated by males. Due to their ability to produce crop milk , pigeons can breed at any time of year. Pigeons breed when the food supply is abundant enough to support embryonic egg development, which in cities, can be any time of the year. Laying of eggs can take place up to six times per year. [ citation needed ] Pigeons are often found in pairs during the breeding season, but usually the pigeons are gregarious , living in flocks of 50 to 500 birds (dependent on the food supply). Courtship rituals can be observed in urban parks at any time of the year. The male on the ground or rooftops puffs up the feathers on his neck to appear larger and thereby impress or attract attention. He approaches the female at a rapid walking pace while emitting repetitive quiet notes, often bowing and turning as he comes closer. At first, the female invariably walks or flies a short distance away and the male follows her until she stops. At this point, he continues the bowing motion and very often makes full- or half- pirouettes in front of the female. The male then proceeds to feed the female by regurgitating food, as they do when feeding the young. [ citation needed ] The male then mounts the female, rearing backwards to be able to join their cloacae . The mating is very brief, with the male flapping his wings to maintain balance on top of the female. The nest is a flimsy platform of straw and sticks, laid on a ledge, under cover, often on the window ledges of buildings. Two white eggs are laid; incubation, shared by both parents, lasts 17 to 19 days. The newly hatched squab (nestling) has pale yellow down and a flesh-coloured bill with a dark band. For the first few days, the baby squabs are tended and fed (through regurgitation) exclusively on " crop milk " (also called "pigeon milk" or "pigeon's milk"). The pigeon milk is produced in the crops of both parents in all species of pigeon and dove. Pigeons are altricial and their fledging period is about 30 days. Rock doves are omnivorous, but prefer plant matter: chiefly fruits and grains. Studies of pigeons in a semi-rural part of Kansas found that their diet includes the following: 92% maize , 3.2% oats , 3.7% cherry , along with small amounts of knotweed , elm , poison ivy and barley . Feral pigeons can be seen eating grass seeds and berries in parks and gardens in the spring, but plentiful sources exist throughout the year from scavenging (e.g., food remnants left inside of dropped fast food cartons, in the form of popcorn , cake , peanuts , bread and currants ) and they also eat insects and spiders . Additional food is also usually available from waste bins, tourists or residents who feed bird seed to pigeons for reasons such as empathy, fun, tradition and as a means for social interaction. Pigeons tend to congregate in large, often thick flocks when feeding on discarded food, and may be observed flying skillfully around trees, buildings, telephone poles and cables and even through moving traffic just to reach a food source. [ citation needed ] Pigeons feed on the ground in flocks or individually. Pigeons are naturally granivorous, eating seeds that fit down their gullet. They may sometimes consume small invertebrates such as worms or insect larvae as a protein supplement. As they do not possess an enlarged cecum as in European wood pigeons, they cannot digest adult plant tissue; the various seeds they eat contain the appropriate nutrients they require. While most birds take small sips and tilt their heads backwards when drinking, pigeons are able to dip their bills into the water and drink continuously, without having to tilt their heads back. In cities they typically resort to scavenging human garbage, as unprocessed grain may be impossible to find. Pigeon groups typically consist of producers, which locate and obtain food, and scroungers, which feed on food obtained by the producers. Generally, groups of pigeons contain a greater proportion of scroungers than producers. Pigeons primarily use powder down feathers for preening, which gives a soft and silky feel to their plumage. They have no preen gland or at times have very rudimentary preen glands, so oil is not used for preening. Rather, powder down feathers are spread across the body. These have a tendency to disintegrate, and the powder, akin to talcum powder, helps maintain the plumage. Some varieties of domestic pigeon have modified feathers called "fat quills". These feathers contain yellow, oil-like fat that derives from the same cells as powder down. This is used while preening and helps reduce bacterial degradation of feathers by feather bacilli. With only their flying abilities protecting them from predation, rock pigeons are a favourite almost around the world for a wide range of raptors . In fact, with feral pigeons existing in almost every city in the world, they may form the majority of prey for several raptor species that live in urban areas. Peregrine falcons and Eurasian sparrowhawks are natural predators of pigeons and quite adept at catching and feeding upon this species. Up to 80% of the diet of peregrine falcons in several cities that have breeding falcons is composed of feral pigeons. Some common predators of feral pigeons in North America are raccoons , opossums , red-tailed hawks , great horned owls , eastern screech owls , and accipiters . The birds that prey on pigeons in North America can range in size from American kestrels to golden eagles and may even include crows , gulls and ravens . [ citation needed ] On the ground the adults, their young and their eggs are at risk from feral and domestic cats . Doves and pigeons are considered to be game birds , since many species are hunted and used for food in many of the countries in which they are native. The body feathers have dense, fluffy bases and are loosely attached to the skin, hence they drop out easily. When a predator catches a pigeon large numbers of feathers come out in the attacker's mouth and the pigeon may use this temporary distraction to make an escape. It also tends to drop the tail feathers when preyed upon or under traumatic conditions, probably as a distraction mechanism. Pigeons may harbour a diverse parasite fauna. They often host the intestinal helminths Capillaria columbae and Ascaridia columbae . Their ectoparasites include the ischnoceran lice Columbicola columbae , Campanulotes bidentatus compar , the amblyceran lice Bonomiella columbae , Hohorstiella lata , Colpocephalum turbinatum , the mites Tinaminyssus melloi , Dermanyssus gallinae , Dermoglyphus columbae , Falculifer rostratus and Diplaegidia columbae . The hippoboscid fly Pseudolynchia canariensis is a typical blood-sucking ectoparasite of pigeons in tropical and subtropical regions.The rock dove breeds at any time of the year, but peak times are spring and summer. Nesting sites are along coastal cliff faces, as well as the artificial cliff faces created by apartment buildings with accessible ledges or roof spaces. Pigeons can compete with native birds for nest sites. For some avian species, such as seabirds, it could be a conservation issue. Current evidence suggests that wild, domestic and feral pigeons mate for life, although their long-term bonds are not unbreakable. They are socially monogamous, but extra-pair matings do occur, often initiated by males. Due to their ability to produce crop milk , pigeons can breed at any time of year. Pigeons breed when the food supply is abundant enough to support embryonic egg development, which in cities, can be any time of the year. Laying of eggs can take place up to six times per year. [ citation needed ] Pigeons are often found in pairs during the breeding season, but usually the pigeons are gregarious , living in flocks of 50 to 500 birds (dependent on the food supply). Courtship rituals can be observed in urban parks at any time of the year. The male on the ground or rooftops puffs up the feathers on his neck to appear larger and thereby impress or attract attention. He approaches the female at a rapid walking pace while emitting repetitive quiet notes, often bowing and turning as he comes closer. At first, the female invariably walks or flies a short distance away and the male follows her until she stops. At this point, he continues the bowing motion and very often makes full- or half- pirouettes in front of the female. The male then proceeds to feed the female by regurgitating food, as they do when feeding the young. [ citation needed ] The male then mounts the female, rearing backwards to be able to join their cloacae . The mating is very brief, with the male flapping his wings to maintain balance on top of the female. The nest is a flimsy platform of straw and sticks, laid on a ledge, under cover, often on the window ledges of buildings. Two white eggs are laid; incubation, shared by both parents, lasts 17 to 19 days. The newly hatched squab (nestling) has pale yellow down and a flesh-coloured bill with a dark band. For the first few days, the baby squabs are tended and fed (through regurgitation) exclusively on " crop milk " (also called "pigeon milk" or "pigeon's milk"). The pigeon milk is produced in the crops of both parents in all species of pigeon and dove. Pigeons are altricial and their fledging period is about 30 days. Rock doves are omnivorous, but prefer plant matter: chiefly fruits and grains. Studies of pigeons in a semi-rural part of Kansas found that their diet includes the following: 92% maize , 3.2% oats , 3.7% cherry , along with small amounts of knotweed , elm , poison ivy and barley . Feral pigeons can be seen eating grass seeds and berries in parks and gardens in the spring, but plentiful sources exist throughout the year from scavenging (e.g., food remnants left inside of dropped fast food cartons, in the form of popcorn , cake , peanuts , bread and currants ) and they also eat insects and spiders . Additional food is also usually available from waste bins, tourists or residents who feed bird seed to pigeons for reasons such as empathy, fun, tradition and as a means for social interaction. Pigeons tend to congregate in large, often thick flocks when feeding on discarded food, and may be observed flying skillfully around trees, buildings, telephone poles and cables and even through moving traffic just to reach a food source. [ citation needed ] Pigeons feed on the ground in flocks or individually. Pigeons are naturally granivorous, eating seeds that fit down their gullet. They may sometimes consume small invertebrates such as worms or insect larvae as a protein supplement. As they do not possess an enlarged cecum as in European wood pigeons, they cannot digest adult plant tissue; the various seeds they eat contain the appropriate nutrients they require. While most birds take small sips and tilt their heads backwards when drinking, pigeons are able to dip their bills into the water and drink continuously, without having to tilt their heads back. In cities they typically resort to scavenging human garbage, as unprocessed grain may be impossible to find. Pigeon groups typically consist of producers, which locate and obtain food, and scroungers, which feed on food obtained by the producers. Generally, groups of pigeons contain a greater proportion of scroungers than producers. Pigeons primarily use powder down feathers for preening, which gives a soft and silky feel to their plumage. They have no preen gland or at times have very rudimentary preen glands, so oil is not used for preening. Rather, powder down feathers are spread across the body. These have a tendency to disintegrate, and the powder, akin to talcum powder, helps maintain the plumage. Some varieties of domestic pigeon have modified feathers called "fat quills". These feathers contain yellow, oil-like fat that derives from the same cells as powder down. This is used while preening and helps reduce bacterial degradation of feathers by feather bacilli. With only their flying abilities protecting them from predation, rock pigeons are a favourite almost around the world for a wide range of raptors . In fact, with feral pigeons existing in almost every city in the world, they may form the majority of prey for several raptor species that live in urban areas. Peregrine falcons and Eurasian sparrowhawks are natural predators of pigeons and quite adept at catching and feeding upon this species. Up to 80% of the diet of peregrine falcons in several cities that have breeding falcons is composed of feral pigeons. Some common predators of feral pigeons in North America are raccoons , opossums , red-tailed hawks , great horned owls , eastern screech owls , and accipiters . The birds that prey on pigeons in North America can range in size from American kestrels to golden eagles and may even include crows , gulls and ravens . [ citation needed ] On the ground the adults, their young and their eggs are at risk from feral and domestic cats . Doves and pigeons are considered to be game birds , since many species are hunted and used for food in many of the countries in which they are native. The body feathers have dense, fluffy bases and are loosely attached to the skin, hence they drop out easily. When a predator catches a pigeon large numbers of feathers come out in the attacker's mouth and the pigeon may use this temporary distraction to make an escape. It also tends to drop the tail feathers when preyed upon or under traumatic conditions, probably as a distraction mechanism. Pigeons may harbour a diverse parasite fauna. They often host the intestinal helminths Capillaria columbae and Ascaridia columbae . Their ectoparasites include the ischnoceran lice Columbicola columbae , Campanulotes bidentatus compar , the amblyceran lice Bonomiella columbae , Hohorstiella lata , Colpocephalum turbinatum , the mites Tinaminyssus melloi , Dermanyssus gallinae , Dermoglyphus columbae , Falculifer rostratus and Diplaegidia columbae . The hippoboscid fly Pseudolynchia canariensis is a typical blood-sucking ectoparasite of pigeons in tropical and subtropical regions.With only their flying abilities protecting them from predation, rock pigeons are a favourite almost around the world for a wide range of raptors . In fact, with feral pigeons existing in almost every city in the world, they may form the majority of prey for several raptor species that live in urban areas. Peregrine falcons and Eurasian sparrowhawks are natural predators of pigeons and quite adept at catching and feeding upon this species. Up to 80% of the diet of peregrine falcons in several cities that have breeding falcons is composed of feral pigeons. Some common predators of feral pigeons in North America are raccoons , opossums , red-tailed hawks , great horned owls , eastern screech owls , and accipiters . The birds that prey on pigeons in North America can range in size from American kestrels to golden eagles and may even include crows , gulls and ravens . [ citation needed ] On the ground the adults, their young and their eggs are at risk from feral and domestic cats . Doves and pigeons are considered to be game birds , since many species are hunted and used for food in many of the countries in which they are native. The body feathers have dense, fluffy bases and are loosely attached to the skin, hence they drop out easily. When a predator catches a pigeon large numbers of feathers come out in the attacker's mouth and the pigeon may use this temporary distraction to make an escape. It also tends to drop the tail feathers when preyed upon or under traumatic conditions, probably as a distraction mechanism. Pigeons may harbour a diverse parasite fauna. They often host the intestinal helminths Capillaria columbae and Ascaridia columbae . Their ectoparasites include the ischnoceran lice Columbicola columbae , Campanulotes bidentatus compar , the amblyceran lice Bonomiella columbae , Hohorstiella lata , Colpocephalum turbinatum , the mites Tinaminyssus melloi , Dermanyssus gallinae , Dermoglyphus columbae , Falculifer rostratus and Diplaegidia columbae . The hippoboscid fly Pseudolynchia canariensis is a typical blood-sucking ectoparasite of pigeons in tropical and subtropical regions.Rock doves have been domesticated for several thousand years, giving rise to the domestic pigeon ( Columba livia domestica ). They may have been domesticated as long as 5,000 years ago. Numerous breeds of fancy pigeons of all sizes, colours, and types have been bred. Domesticated pigeons are used as homing pigeons as well as food and pets. They were in the past also used as carrier pigeons . So-called war pigeons have played significant roles during wartime, and many pigeons have received awards and medals for their services in saving hundreds of human lives. Pigeons have notably been "employed" as medical imaging data sorters. They have been successfully trained under research conditions to examine data on a screen for the purposes of detecting breast cancer. They appear to use their innate visual navigation skills to do so. Many domestic birds have got lost, escaped or been released over the years and have given rise to feral pigeons. These show a variety of plumages, although many have the blue-barred pattern as does the pure rock dove. Feral pigeons are found in cities and towns all over the world. The scarcity of the pure wild species is partly due to interbreeding with feral birds. Contact with pigeon droppings poses a minor risk of contracting histoplasmosis , cryptococcosis and psittacosis , and long-term exposure to both droppings and feathers can induce an allergy known as bird fancier's lung . Pigeons are not a major concern in the spread of West Nile virus : though they can contract it, they apparently do not transmit it. Some contagions are transmitted by pigeons; for example, the bacteria Chlamydophila psittaci is endemic among pigeons and causes psittacosis in humans. It is generally transmitted from handling pigeons or their droppings (more commonly the latter). Psittacosis is a serious disease but rarely fatal (less than 1%). Pigeons are also important vectors for various species of the bacteria Salmonella , which causes diseases such as salmonellosis and paratyphoid fever. Pigeons are also known to host avian mites, which can infest human habitation and bite humans, a condition known as gamasoidosis . However, infesting mammals is relatively rare. Pigeons may, however, carry and spread avian influenza . One study has shown that adult pigeons are not clinically susceptible to the most dangerous strain of avian influenza, H5N1 , and that they do not transmit the virus to poultry. Other studies have presented evidence of clinical signs and neurological lesions resulting from infection but found that the pigeons did not transmit the disease to poultry reared in direct contact with them. Pigeons were found to be "resistant or minimally susceptible" to other strains of avian influenza, such as the H7N7 . Research into whether pigeons play a part in spreading bird flu have shown pigeons do not carry the deadly H5N1 strain. Three studies have been done since the late 1990s by the US Agriculture Department's Southeast Poultry Research Laboratory in Athens, Georgia, according to the center's director, David Swayne. The lab has been working on bird flu since the 1970s. In one experiment, researchers squirted into pigeons' mouths liquid drops that contained the highly pathogenic H5N1 virus from a Hong Kong sample. The birds received 100 to 1,000 times the concentration that wild birds would encounter in nature. "We couldn't infect the pigeons", Swayne said. "So that's good news." Rock doves have been domesticated for several thousand years, giving rise to the domestic pigeon ( Columba livia domestica ). They may have been domesticated as long as 5,000 years ago. Numerous breeds of fancy pigeons of all sizes, colours, and types have been bred. Domesticated pigeons are used as homing pigeons as well as food and pets. They were in the past also used as carrier pigeons . So-called war pigeons have played significant roles during wartime, and many pigeons have received awards and medals for their services in saving hundreds of human lives. Pigeons have notably been "employed" as medical imaging data sorters. They have been successfully trained under research conditions to examine data on a screen for the purposes of detecting breast cancer. They appear to use their innate visual navigation skills to do so. Many domestic birds have got lost, escaped or been released over the years and have given rise to feral pigeons. These show a variety of plumages, although many have the blue-barred pattern as does the pure rock dove. Feral pigeons are found in cities and towns all over the world. The scarcity of the pure wild species is partly due to interbreeding with feral birds. So-called war pigeons have played significant roles during wartime, and many pigeons have received awards and medals for their services in saving hundreds of human lives.Pigeons have notably been "employed" as medical imaging data sorters. They have been successfully trained under research conditions to examine data on a screen for the purposes of detecting breast cancer. They appear to use their innate visual navigation skills to do so. Many domestic birds have got lost, escaped or been released over the years and have given rise to feral pigeons. These show a variety of plumages, although many have the blue-barred pattern as does the pure rock dove. Feral pigeons are found in cities and towns all over the world. The scarcity of the pure wild species is partly due to interbreeding with feral birds. Contact with pigeon droppings poses a minor risk of contracting histoplasmosis , cryptococcosis and psittacosis , and long-term exposure to both droppings and feathers can induce an allergy known as bird fancier's lung . Pigeons are not a major concern in the spread of West Nile virus : though they can contract it, they apparently do not transmit it. Some contagions are transmitted by pigeons; for example, the bacteria Chlamydophila psittaci is endemic among pigeons and causes psittacosis in humans. It is generally transmitted from handling pigeons or their droppings (more commonly the latter). Psittacosis is a serious disease but rarely fatal (less than 1%). Pigeons are also important vectors for various species of the bacteria Salmonella , which causes diseases such as salmonellosis and paratyphoid fever. Pigeons are also known to host avian mites, which can infest human habitation and bite humans, a condition known as gamasoidosis . However, infesting mammals is relatively rare. Pigeons may, however, carry and spread avian influenza . One study has shown that adult pigeons are not clinically susceptible to the most dangerous strain of avian influenza, H5N1 , and that they do not transmit the virus to poultry. Other studies have presented evidence of clinical signs and neurological lesions resulting from infection but found that the pigeons did not transmit the disease to poultry reared in direct contact with them. Pigeons were found to be "resistant or minimally susceptible" to other strains of avian influenza, such as the H7N7 . Research into whether pigeons play a part in spreading bird flu have shown pigeons do not carry the deadly H5N1 strain. Three studies have been done since the late 1990s by the US Agriculture Department's Southeast Poultry Research Laboratory in Athens, Georgia, according to the center's director, David Swayne. The lab has been working on bird flu since the 1970s. In one experiment, researchers squirted into pigeons' mouths liquid drops that contained the highly pathogenic H5N1 virus from a Hong Kong sample. The birds received 100 to 1,000 times the concentration that wild birds would encounter in nature. "We couldn't infect the pigeons", Swayne said. "So that's good news."

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Avian influenza

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Influenza A virus subtype H2N2

Influenza A virus subtype H2N2 ( A/H2N2 ) is a subtype of Influenza A virus . H2N2 has mutated into various strains including the " Asian flu " strain (now extinct in the wild), H3N2 , and various strains found in birds . It is also suspected of causing a human pandemic in 1889. The geographic spreading of the 1889 Russian flu has been studied and published. Some believe that the 1889–1890 Russian flu was caused by the influenzavirus A virus subtype H2N2, but the evidence is not conclusive. It is the earliest flu pandemic for which detailed records are available. More recently, there are speculations that it might have been caused by one of the coronaviruses first discovered in the 1960s. The "Asian Flu" was a category 2 flu pandemic outbreak of influenzavirus A that first appeared in Guizhou , China in early 1957 and lasted until 1958. The first cases were reported in Singapore in February 1957. In February 1957, a new influenza A (H2N2) virus emerged in East Asia, triggering a pandemic ("Asian Flu"). This H2N2 virus was composed of three different genes from an H2N2 virus that originated from an avian influenza A virus, including the H2 hemagglutinin and the N2 neuraminidase genes. It was first reported in Singapore in February 1957, Hong Kong in April 1957, and in coastal cities in the United States in summer 1957. Some authors believe it originated from mutation in wild ducks combining with a pre-existing human strain. Other authors are less certain. It reached Hong Kong by April, and US by June. Estimates of US and worldwide deaths caused by this pandemic varies widely depending on source; ranging from approximately 69,800 to 116,000 in the United States, and worldwide from 1 million to 4 million, with the World Health Organization (WHO) settling on "about 2 million," with an overall mortality rate of 0.6%. Asian Flu was of the H2N2 subtype (a notation that refers to the configuration of the hemagglutinin and neuraminidase proteins in the virus) of type A influenza, and an influenza vaccine was developed in 1957 to contain its outbreak. [ citation needed ] The Asian Flu strain later evolved via antigenic shift into H3N2 which caused a milder pandemic from 1968 to 1969. Both the H2N2 and H3N2 pandemic strains contained avian influenza virus RNA segments. From October 2004 to February 2005, approximately 3,700 test kits of the 1957 H2N2 virus were accidentally spread around the world from the College of American Pathologists (CAP). CAP assists laboratories in accuracy by providing unidentified samples of viruses ; private contractor Meridian Bioscience in Cincinnati , U.S. , chose the 1957 strain instead of one of the less deadly avian influenza virus subtypes. The 1957 H2N2 virus is considered deadly and the U.S. government called for the vials containing the strain to be destroyed. [ citation needed ]

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Avian influenza

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Influenza A virus subtype H10N8

The influenza A virus subtype H10N8 is an avian influenza virus. It is one of three H10 subtype avian influenza viruses isolated from domestic ducks in China, designated as SH602/H10N8, FJ1761/H10N3 and SX3180/H10N7. The first A/H10N8 virus was isolated from a duck in Guangdong province , China, in 2012. The virus shows high pathogenicity in mice. It was also found in waterfowls , feral dogs , and live poultry markets. While multiple H10 genotype viruses (e.g. H10N8, H10N3, and H10N7) are circulating in live poultry markets in China, their potential to infect mammals remains largely unknown. Genome sequencing and virus characterization suggest that the virus strains that infected humans originated from poultry markets. H10N8, as well as H10N7, and H6N8, have been detected in people to a lesser extent than other strains.

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Avian influenza

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Influenza A virus subtype H5N6

H5N6 is a subtype of the species Influenza A virus (sometimes called bird flu virus). Infected birds shed the virus in their saliva, mucous, and feces. The virus was first detected in poultry in 2013, since then spreading among wild bird populations and poultry around the world. Humans can be infected through unprotected contact with infected birds or contaminated surfaces. The virus transmits by getting into a person's eyes, nose, mouth, and through inhalation. Human infections are rare. Since 2014, at least 87 cases have occurred in humans. 29 people have died. A spike in human cases was reported in 2021. There have been no confirmed cases of human-to-human transmission . Some infections have been identified where no direct contact with infected birds or contaminated surfaces has been known to had occurred. Only one infected woman has said that she never came into any contact with poultry. In November and December human cases of H5N6 were reported in China. From October to December, four outbreaks were also reported in China, resulting in the culling of over 170,000 birds. In December, H5N6 avian influenza was reported in bird droppings in Hong Kong. In December, South Korea raised its bird flu alert to highest level for the first time. An Australian test confirmed that the August 2017 bird flu outbreak in Pampanga was of the subtype H5N6. Coinciding with the COVID-19 pandemic , H5N6 caused the deaths of 1,840 of 2,497 birds at a poultry farm in China's Sichuan province . 25,000 birds were culled in total in a Philippines poultry outbreak. A 7-mile zone constricting poultry movement was also established. The first reported human case outside of China was detected in Laos . A five-year-old boy from Luang Prabang Province tested positive after being exposed to poultry . At least 16 isolated cases were reported in China between July and September 2021, including a case in a 26-year-old woman from Guilin who died. A 61-year-old woman who was infected in July has denied ever coming into contact with poultry. On 3 October, the World Health Organization said wider surveillance was urgently required to better understand the risk and the recent increase of spill over to humans . On October 26, 2021, Thijs Kuiken, a professor of comparative pathology at Erasmus University Medical Centre in Rotterdam, said the rise in human cases could be explained by a new variant which is "a little more infectious" to people. On January 7, 2022, a 43-year-old woman in the Guangdong province of China was hospitalised. On January 13, 2022, five more people in the Guangxi autonomous region , the Sichuan province, and the Zhejiang province of China were reported to be infected, two of whom have died. On March 18, 2022, a 28-year-old man from Puyang in Henan Province, was hospitalized. On March 24, 2022, a 53-year-old woman from Zhenjiang City in Jiangsu Province, was hospitalized. A 56-year-old male living in Deyang City (Sichuan Province) became the 13th case of 2022 when on March 31, 2022, he developed symptoms. He was hospitalized on April 4. On August 23 a 27-year-old woman from Sichuan province was reported. On September 27, 2023, a fatal case in a 68-year-old man from Chongqing was reported. This was 6th case of H5N6 in 2023 within China.

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Avian influenza

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2020–2024 H5N1 outbreak

Since 2020, global cases of avian influenza subtype H5N1 have been rising, with cases reported from every continent as of February 2023 except for Australia and Antarctica . In late 2023, H5N1 was discovered in the Antarctic for the first time, raising fears of imminent spread throughout the region, potentially leading to a "catastrophic breeding failure" among animals that had not previously been exposed to avian influenza viruses. The virus involved in the outbreak is classified in H5 clade 2.3.4.4b. H5N6 and H5N8 viruses with the H5-2.3.4.4b hemagglutinin (HA) gene became prominent globally among poultry in 2018 – 2020. In 2020, reassortment (genetic "swapping") between these H5-2.3.4.4b poultry viruses and N1 wild bird viruses led to the emergence of a H5N1 with a H5-2.3.4.4b gene. The virus then spread across Europe, detected there in autumn , before spreading to Africa and Asia . It continues to swap genes with local flu viruses as it travels the globe. : (fig.1) In May 2021, H5N1 was detected in wild red foxes in the Netherlands . It was later detected in December in Estonia in wild foxes. In January 2022, an infection in an eighty-year-old man was reported, who raised ducks in England . Also in January, infections were reported from the United States in wild birds. In February, infections were reported from commercial poultry centres in the U.S., and Peru reported infections in sea lions . The virus continued to spread further, infecting additional species of mammals. In October, a mink farm in northwest Spain was affected. A human case of H5N1 was reported in the U.S. in April, "though this detection may have been the result of contamination of the nasal passages with the virus rather than actual infection." In September, Spain reported a human case; this was followed by a second case in November, in a person who worked at the same poultry farm as the first. Both were asymptomatic. In November, China reported a human case, infected due to contact with poultry. The case died from their infection. H5N1 was first detected in the islands of the Antarctic region in October 2023, via a brown skua on Bird Island, near South Georgia . Within several months, hundreds of elephant seals were found dead, as well as fur seals, kelp gulls and further brown skua. In December 2023, conservation officials confirmed that a polar bear had died of H5N1 near Alaska's northernmost city, Utqiagvik . In February 2023, Cambodia reported the death of a girl due to H5N1 infection after developing symptoms on 16 February. The girl's father also tested positive for the virus. The World Health Organization (WHO) described the situation as "worrying" and urged "heightened vigilance". Further sequencing determined that at least one of the two cases was from an older H5N1 clade, 2.3.2.1c, which had circulated as a common H5N1 strain in Cambodia for many years, rather than the more recent clade 2.3.4.4b, which had caused mass poultry deaths since 2020. This older clade had jumped to humans in the past yet hadn't previously resulted in any known human-to-human transmission. On March 1, 2023, as Taiwan raised its travel alert for Cambodia, the WHO and the U.S. Center for Disease and Control and Prevention (CDC) , in concert with Cambodian authorities, determined that both of the individuals had been infected through direct contact with poultry. In late February 2023, Argentina confirmed a case of H5N1 in industrial poultry, in the Rio Negro province. Avian product exports were suspended as a result. In March 2023, H5N1 was detected in black-necked swan populations in Carlos Anwandter Nature Sanctuary , Chile and Uruguay . In Uruguay the death of ten swans found in the locality of Estación Tapia was attributed to flu. Previously in Uruguay ten hens had died because of the flu in El Monarca, Montevideo . In late March 2023, Chile detected H5N1 in a 53 year-old man who had severe symptoms. The patient survived but had to stay on a ventilator. The virus was determined to be in the 2.3.4.4b lineage. In September 2023, Uruguay reported upwards of 400 seals and sea lions found dead of H5N1 on the nation's Atlantic coastline and along the River Plate . According to a 2024 paper, a large outbreak of H5N1 killed 70% of elephant seal pups born in the 2023 breeding season. In surveyed areas of Península Valdés , Argentina, seal mortality rates exceed 96%. A February 2024 article reports that the outbreak in South America has, since 2022, killed at least 600,000 wild birds and 50,000 mammals. On April 1 a domestic dog in Ottawa , Canada was tested positive for H5N1. On May 22, Brazil declared an 180-day "animal health emergency" in response to eight cases of H5N1 found in wild birds. Although Brazil's major poultry-producing regions are in the country's south and the infections were found in Espirito Santo state and Rio de Janeiro state, Brazil, as the world's largest exporter of chicken meat, created an emergency operations center to plan for and mitigate potential further spread of H5N1. A cluster of five human infections of H5N1 occurred in Cambodia in late January and early February. All patients had recent contact with sick poultry. One patient died. Sequencing of two of the patients indicate that they were infected by clade 2.3.2.1c, which is not the same same as the 2.3.4.4b clade virus that is causing global outbreaks in the US and beyond. A person in Vietnam died of H5N1 infection around the same time. It remains unreported which clade of H5 virus the patient in Vietnam was infected by. However, an April 2024 statement from the FAO reports that recent (~2023) reassortment in the Greater Mekong Subregion has produced viruses that carry internal genes from the new 2.3.4.4b virus but the H5 gene from the old 2.3.2.1c lineage. The FAO also states that the new type of virus is implicate in human cases, but it does not specify which. On April 5, the Philippines reported a H5N1 outbreak on a poultry farm in Leyte , which killed 4,475 birds. Earlier in the year, the Philippines Department of Agriculture temporarily banned poultry exports from several countries including Japan, Belgium, and France. On April 18, a H5N1 outbreak was detected in ducks in two parts in Alappuzha district , Kerala . The disease was confirmed in a lab for ducks reared in the area. The District Collector has decided to initiate the process of culling domestic birds within a 1 kilometre radius from the epicentre of the outbreak. The US CDC continues to report "widespread" occurrence in wild birds, "sporadic outbreaks" in poultry flocks, and "sporadic infections" as of March 2024. As of March 8, 2024, the United States Department of Agriculture's (USDA) Animal and Plant Health Inspection Service (APHIS) had recorded around 20 mammal species confirmed as being able to be infected by H5N1. Also in March 2024, H5N1 was confirmed to have infected farmed goats and cows in the USA. On April 2, a dairy worker in Texas became infected and strong indications of cow-to-cow spread were evident as cow herds in five different states became ill. A few days later on April 4, H5N1 was confirmed to have spread to several additional dairy herds in six US states including Texas, along with Idaho, Kansas, New Mexico, Ohio and Michigan. Scientists have deemed these to be either cow-to-cow transmission or spillover from wild birds . On April 11, H5N1 was found in dairy cattle herds in North Carolina and South Dakota. On April 10, researchers found several cases of HPAI H5N1 in animals in New York City, including three Canada geese, a red-tailed hawk, a peregrine falcon, and a chicken. H5N1 was detected in dead birds on the Antarctic mainland for the first time in February 2024. In February, scientists found H5N1 in 12 Antarctic skua seabirds carcasses on Beak Island . Additional cases have also been found at Hope Bay and on the Devil and Paulet islands . In March, scientists detected the virus in the nine Adélie penguins and one Antarctic cormorant . H5N6 and H5N8 viruses with the H5-2.3.4.4b hemagglutinin (HA) gene became prominent globally among poultry in 2018 – 2020. In 2020, reassortment (genetic "swapping") between these H5-2.3.4.4b poultry viruses and N1 wild bird viruses led to the emergence of a H5N1 with a H5-2.3.4.4b gene. The virus then spread across Europe, detected there in autumn , before spreading to Africa and Asia . It continues to swap genes with local flu viruses as it travels the globe. : (fig.1)In May 2021, H5N1 was detected in wild red foxes in the Netherlands . It was later detected in December in Estonia in wild foxes. In January 2022, an infection in an eighty-year-old man was reported, who raised ducks in England . Also in January, infections were reported from the United States in wild birds. In February, infections were reported from commercial poultry centres in the U.S., and Peru reported infections in sea lions . The virus continued to spread further, infecting additional species of mammals. In October, a mink farm in northwest Spain was affected. A human case of H5N1 was reported in the U.S. in April, "though this detection may have been the result of contamination of the nasal passages with the virus rather than actual infection." In September, Spain reported a human case; this was followed by a second case in November, in a person who worked at the same poultry farm as the first. Both were asymptomatic. In November, China reported a human case, infected due to contact with poultry. The case died from their infection. H5N1 was first detected in the islands of the Antarctic region in October 2023, via a brown skua on Bird Island, near South Georgia . Within several months, hundreds of elephant seals were found dead, as well as fur seals, kelp gulls and further brown skua. In December 2023, conservation officials confirmed that a polar bear had died of H5N1 near Alaska's northernmost city, Utqiagvik . In February 2023, Cambodia reported the death of a girl due to H5N1 infection after developing symptoms on 16 February. The girl's father also tested positive for the virus. The World Health Organization (WHO) described the situation as "worrying" and urged "heightened vigilance". Further sequencing determined that at least one of the two cases was from an older H5N1 clade, 2.3.2.1c, which had circulated as a common H5N1 strain in Cambodia for many years, rather than the more recent clade 2.3.4.4b, which had caused mass poultry deaths since 2020. This older clade had jumped to humans in the past yet hadn't previously resulted in any known human-to-human transmission. On March 1, 2023, as Taiwan raised its travel alert for Cambodia, the WHO and the U.S. Center for Disease and Control and Prevention (CDC) , in concert with Cambodian authorities, determined that both of the individuals had been infected through direct contact with poultry. In late February 2023, Argentina confirmed a case of H5N1 in industrial poultry, in the Rio Negro province. Avian product exports were suspended as a result. In March 2023, H5N1 was detected in black-necked swan populations in Carlos Anwandter Nature Sanctuary , Chile and Uruguay . In Uruguay the death of ten swans found in the locality of Estación Tapia was attributed to flu. Previously in Uruguay ten hens had died because of the flu in El Monarca, Montevideo . In late March 2023, Chile detected H5N1 in a 53 year-old man who had severe symptoms. The patient survived but had to stay on a ventilator. The virus was determined to be in the 2.3.4.4b lineage. In September 2023, Uruguay reported upwards of 400 seals and sea lions found dead of H5N1 on the nation's Atlantic coastline and along the River Plate . According to a 2024 paper, a large outbreak of H5N1 killed 70% of elephant seal pups born in the 2023 breeding season. In surveyed areas of Península Valdés , Argentina, seal mortality rates exceed 96%. A February 2024 article reports that the outbreak in South America has, since 2022, killed at least 600,000 wild birds and 50,000 mammals. On April 1 a domestic dog in Ottawa , Canada was tested positive for H5N1. On May 22, Brazil declared an 180-day "animal health emergency" in response to eight cases of H5N1 found in wild birds. Although Brazil's major poultry-producing regions are in the country's south and the infections were found in Espirito Santo state and Rio de Janeiro state, Brazil, as the world's largest exporter of chicken meat, created an emergency operations center to plan for and mitigate potential further spread of H5N1. H5N1 was first detected in the islands of the Antarctic region in October 2023, via a brown skua on Bird Island, near South Georgia . Within several months, hundreds of elephant seals were found dead, as well as fur seals, kelp gulls and further brown skua. In December 2023, conservation officials confirmed that a polar bear had died of H5N1 near Alaska's northernmost city, Utqiagvik . In February 2023, Cambodia reported the death of a girl due to H5N1 infection after developing symptoms on 16 February. The girl's father also tested positive for the virus. The World Health Organization (WHO) described the situation as "worrying" and urged "heightened vigilance". Further sequencing determined that at least one of the two cases was from an older H5N1 clade, 2.3.2.1c, which had circulated as a common H5N1 strain in Cambodia for many years, rather than the more recent clade 2.3.4.4b, which had caused mass poultry deaths since 2020. This older clade had jumped to humans in the past yet hadn't previously resulted in any known human-to-human transmission. On March 1, 2023, as Taiwan raised its travel alert for Cambodia, the WHO and the U.S. Center for Disease and Control and Prevention (CDC) , in concert with Cambodian authorities, determined that both of the individuals had been infected through direct contact with poultry. In late February 2023, Argentina confirmed a case of H5N1 in industrial poultry, in the Rio Negro province. Avian product exports were suspended as a result. In March 2023, H5N1 was detected in black-necked swan populations in Carlos Anwandter Nature Sanctuary , Chile and Uruguay . In Uruguay the death of ten swans found in the locality of Estación Tapia was attributed to flu. Previously in Uruguay ten hens had died because of the flu in El Monarca, Montevideo . In late March 2023, Chile detected H5N1 in a 53 year-old man who had severe symptoms. The patient survived but had to stay on a ventilator. The virus was determined to be in the 2.3.4.4b lineage. In September 2023, Uruguay reported upwards of 400 seals and sea lions found dead of H5N1 on the nation's Atlantic coastline and along the River Plate . According to a 2024 paper, a large outbreak of H5N1 killed 70% of elephant seal pups born in the 2023 breeding season. In surveyed areas of Península Valdés , Argentina, seal mortality rates exceed 96%. A February 2024 article reports that the outbreak in South America has, since 2022, killed at least 600,000 wild birds and 50,000 mammals. On April 1 a domestic dog in Ottawa , Canada was tested positive for H5N1. On May 22, Brazil declared an 180-day "animal health emergency" in response to eight cases of H5N1 found in wild birds. Although Brazil's major poultry-producing regions are in the country's south and the infections were found in Espirito Santo state and Rio de Janeiro state, Brazil, as the world's largest exporter of chicken meat, created an emergency operations center to plan for and mitigate potential further spread of H5N1. A cluster of five human infections of H5N1 occurred in Cambodia in late January and early February. All patients had recent contact with sick poultry. One patient died. Sequencing of two of the patients indicate that they were infected by clade 2.3.2.1c, which is not the same same as the 2.3.4.4b clade virus that is causing global outbreaks in the US and beyond. A person in Vietnam died of H5N1 infection around the same time. It remains unreported which clade of H5 virus the patient in Vietnam was infected by. However, an April 2024 statement from the FAO reports that recent (~2023) reassortment in the Greater Mekong Subregion has produced viruses that carry internal genes from the new 2.3.4.4b virus but the H5 gene from the old 2.3.2.1c lineage. The FAO also states that the new type of virus is implicate in human cases, but it does not specify which. On April 5, the Philippines reported a H5N1 outbreak on a poultry farm in Leyte , which killed 4,475 birds. Earlier in the year, the Philippines Department of Agriculture temporarily banned poultry exports from several countries including Japan, Belgium, and France. On April 18, a H5N1 outbreak was detected in ducks in two parts in Alappuzha district , Kerala . The disease was confirmed in a lab for ducks reared in the area. The District Collector has decided to initiate the process of culling domestic birds within a 1 kilometre radius from the epicentre of the outbreak. The US CDC continues to report "widespread" occurrence in wild birds, "sporadic outbreaks" in poultry flocks, and "sporadic infections" as of March 2024. As of March 8, 2024, the United States Department of Agriculture's (USDA) Animal and Plant Health Inspection Service (APHIS) had recorded around 20 mammal species confirmed as being able to be infected by H5N1. Also in March 2024, H5N1 was confirmed to have infected farmed goats and cows in the USA. On April 2, a dairy worker in Texas became infected and strong indications of cow-to-cow spread were evident as cow herds in five different states became ill. A few days later on April 4, H5N1 was confirmed to have spread to several additional dairy herds in six US states including Texas, along with Idaho, Kansas, New Mexico, Ohio and Michigan. Scientists have deemed these to be either cow-to-cow transmission or spillover from wild birds . On April 11, H5N1 was found in dairy cattle herds in North Carolina and South Dakota. On April 10, researchers found several cases of HPAI H5N1 in animals in New York City, including three Canada geese, a red-tailed hawk, a peregrine falcon, and a chicken. H5N1 was detected in dead birds on the Antarctic mainland for the first time in February 2024. In February, scientists found H5N1 in 12 Antarctic skua seabirds carcasses on Beak Island . Additional cases have also been found at Hope Bay and on the Devil and Paulet islands . In March, scientists detected the virus in the nine Adélie penguins and one Antarctic cormorant . A cluster of five human infections of H5N1 occurred in Cambodia in late January and early February. All patients had recent contact with sick poultry. One patient died. Sequencing of two of the patients indicate that they were infected by clade 2.3.2.1c, which is not the same same as the 2.3.4.4b clade virus that is causing global outbreaks in the US and beyond. A person in Vietnam died of H5N1 infection around the same time. It remains unreported which clade of H5 virus the patient in Vietnam was infected by. However, an April 2024 statement from the FAO reports that recent (~2023) reassortment in the Greater Mekong Subregion has produced viruses that carry internal genes from the new 2.3.4.4b virus but the H5 gene from the old 2.3.2.1c lineage. The FAO also states that the new type of virus is implicate in human cases, but it does not specify which. On April 5, the Philippines reported a H5N1 outbreak on a poultry farm in Leyte , which killed 4,475 birds. Earlier in the year, the Philippines Department of Agriculture temporarily banned poultry exports from several countries including Japan, Belgium, and France. On April 18, a H5N1 outbreak was detected in ducks in two parts in Alappuzha district , Kerala . The disease was confirmed in a lab for ducks reared in the area. The District Collector has decided to initiate the process of culling domestic birds within a 1 kilometre radius from the epicentre of the outbreak. The US CDC continues to report "widespread" occurrence in wild birds, "sporadic outbreaks" in poultry flocks, and "sporadic infections" as of March 2024. As of March 8, 2024, the United States Department of Agriculture's (USDA) Animal and Plant Health Inspection Service (APHIS) had recorded around 20 mammal species confirmed as being able to be infected by H5N1. Also in March 2024, H5N1 was confirmed to have infected farmed goats and cows in the USA. On April 2, a dairy worker in Texas became infected and strong indications of cow-to-cow spread were evident as cow herds in five different states became ill. A few days later on April 4, H5N1 was confirmed to have spread to several additional dairy herds in six US states including Texas, along with Idaho, Kansas, New Mexico, Ohio and Michigan. Scientists have deemed these to be either cow-to-cow transmission or spillover from wild birds . On April 11, H5N1 was found in dairy cattle herds in North Carolina and South Dakota. On April 10, researchers found several cases of HPAI H5N1 in animals in New York City, including three Canada geese, a red-tailed hawk, a peregrine falcon, and a chicken. H5N1 was detected in dead birds on the Antarctic mainland for the first time in February 2024. In February, scientists found H5N1 in 12 Antarctic skua seabirds carcasses on Beak Island . Additional cases have also been found at Hope Bay and on the Devil and Paulet islands . In March, scientists detected the virus in the nine Adélie penguins and one Antarctic cormorant . H5-2.3.4.4b can be prevented by vaccination in chickens. The H5-Re14 (2.3.4.4b) strain used in updated vaccines since 2022 is a reasonably good match for the new virus.

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Avian influenza

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Spanish flu

The 1918–1920 flu pandemic , also known as the Great Influenza epidemic or by the common misnomer Spanish flu , was an exceptionally deadly global influenza pandemic caused by the H1N1 influenza A virus . The earliest documented case was March 1918 in the state of Kansas in the United States, with further cases recorded in France, Germany and the United Kingdom in April. Two years later, nearly a third of the global population, or an estimated 500 million people, had been infected in four successive waves. Estimates of deaths range from 17 million to 50 million, and possibly as high as 100 million, making it one of the deadliest pandemics in history . The pandemic broke out near the end of World War I , when wartime censors in the belligerent countries suppressed bad news to maintain morale , but newspapers freely reported the outbreak in neutral Spain , creating a false impression of Spain as the epicenter and leading to the "Spanish flu" misnomer. Limited historical epidemiological data make the pandemic's geographic origin indeterminate, with competing hypotheses on the initial spread. Most influenza outbreaks disproportionately kill the young and old, with a higher survival rate in-between, but this pandemic had unusually high mortality for young adults. Scientists offer several explanations for the high mortality, including a six-year climate anomaly affecting migration of disease vectors with increased likelihood of spread through bodies of water. The virus was particularly deadly because it triggered a cytokine storm , ravaging the stronger immune system of young adults, although the viral infection was apparently no more aggressive than previous influenza strains. However, the claim that young adults had a high mortality during the pandemic has been contested. Malnourishment, overcrowded medical camps and hospitals, and poor hygiene , exacerbated by the war, promoted bacterial superinfection , killing most of the victims after a typically prolonged death bed. The 1918 Spanish flu was the first of three flu pandemics caused by H1N1 influenza A virus ; the most recent one was the 2009 swine flu pandemic . The 1977 Russian flu was also caused by H1N1 virus. This pandemic was known by many different names—some old, some new—depending on place, time, and context. The etymology of alternative names historicises the scourge and its effects on people who would only learn years later that invisible viruses caused influenza . The lack of scientific answers led the Sierra Leone Weekly News ( Freetown ) to suggest a biblical framing in July 1918, using an interrogative from Exodus 16 in ancient Hebrew : [lower-alpha 1] "One thing is for certain—the doctors are at present flabbergasted; and we suggest that rather than calling the disease influenza they should for the present until they have it in hand, say Man hu —'What is it?'" Outbreaks of influenza-like illness were documented in 1916–17 at British military hospitals in Étaples , France , and just across the English Channel at Aldershot , England . Clinical indications in common with the 1918 pandemic included rapid symptom progression to a "dusky" heliotrope cyanosis of the face. This characteristic blue-violet cyanosis in expiring patients led to the name 'purple death'. The Aldershot physicians later wrote in The Lancet , "the influenza pneumococcal purulent bronchitis we and others described in 1916 and 1917 is fundamentally the same condition as the influenza of this present pandemic." This " purulent bronchitis " is not yet linked to the same A/H1N1 virus, but it may be a precursor. In 1918, ' epidemic influenza ' ( Italian : influenza , influence ), also known at the time as 'the grip' ( French : la grippe , grasp), appeared in Kansas in the U.S. during late spring, and early reports from Spain began appearing on 21 May. Reports from both places called it 'three-day fever' ( fiebre de los tres días ). Many alternative names are exonyms in the practice of making new infectious diseases seem foreign. This pattern was observed even before the 1889–1890 pandemic , also known as the 'Russian flu', when the Russians already called epidemic influenza the 'Chinese catarrh', the Germans called it the 'Russian pest', while the Italians in turn called it the 'German disease'. These epithets were re-used in the 1918 pandemic, along with new ones. Outside Spain, the disease was soon misnamed 'Spanish influenza'. In a 2 June 1918 The Times of London dispatch titled, "The Spanish Epidemic," a correspondent in Madrid reported over 100,000 victims of, "The unknown disease…clearly of a gripal character," without referring to "Spanish influenza" directly. Three weeks later The Times reported that, "Everybody thinks of it as the 'Spanish' influenza to-day." Three days after that an advertisement appeared in The Times for Formamint tablets to prevent "Spanish influenza". When it reached Moscow, Pravda announced, " Ispánka (the Spanish lady) is in town," making 'the Spanish lady' another common name. The outbreak did not originate in Spain (see below ), but reporting did, due to wartime censorship in belligerent nations. Spain was a neutral country unconcerned with appearances of combat readiness , and without a wartime propaganda machine to prop up morale ; so its newspapers freely reported epidemic effects, including King Alfonso XIII 's illness, making Spain the apparent locus of the epidemic. The censorship was so effective that Spain's health officials were unaware its neighboring countries were similarly affected. In an October 1918 "Madrid Letter" to the Journal of the American Medical Association , a Spanish official protested, "we were surprised to learn that the disease was making ravages in other countries, and that people there were calling it the 'Spanish grip'. And wherefore Spanish? …this epidemic was not born in Spain, and this should be recorded as a historic vindication." But before this letter could be published, The Serbian Newspaper ( Corfu ) said, "Various countries have been assigning the origin of this imposing guest to each other for quite some time, and at one point in time they agreed to assign its origin to the kind and neutral Spain…" French press initially used 'American flu', but adopted 'Spanish flu' in lieu of antagonizing an ally. In the spring of 1918, British soldiers called it 'Flanders flu', while German soldiers used ' Flandern-Fieber ' (Flemish fever), both after a famous battlefield in Belgium where many soldiers on both sides fell ill. In Senegal it was named 'Brazilian flu', and in Brazil , 'German flu'. In Spain it was also known as the 'French flu' ( gripe francesa ), or the 'Naples Soldier' ( Soldado de Nápoles ), after a popular song from a zarzuela . [lower-alpha 2] Spanish flu ( gripe española ) is now a common name in Spain, but remains controversial there. Other names derived from geopolitical borders and social boundaries. In Poland it was the ' Bolshevik disease', while the Bolsheviks referred to it as the ' Kirghiz disease'. Some Africans called it a 'white man's sickness', but in South Africa , white men also used the ethnophaulism 'kaffersiekte' (lit. negro disease). Japan blamed sumo wrestlers for bringing the disease home from a match in Taiwan by calling it 'sumo flu' ( Sumo Kaze ), even though three top wrestlers died there. World Health Organization 'best practices' first published in 2015 now aim to prevent social stigma by no longer associating culturally significant names with new diseases, listing "Spanish flu" under "examples to be avoided". Many authors now eschew calling this the Spanish flu, instead using variations of '1918–19/20 flu/influenza pandemic'. Some language endonyms did not name specific regions or groups of people. Examples specific to this pandemic include: Northern Ndebele : 'Malibuzwe' (let enquiries be made concerning it), Swahili : 'Ugonjo huo kichwa na kukohoa na kiuno' (the disease of head and coughing and spine), Yao : 'chipindupindu' (disease from seeking to make a profit in wartime), Otjiherero : 'kaapitohanga' (disease which passes through like a bullet), and Persian : 'nakhushi-yi bad' (disease of the wind). This outbreak was also commonly known as the 'great influenza epidemic', after the 'great war', a common name for World War I before World War II . French military doctors originally called it 'disease 11' ( maladie onze ). German doctors downplayed the severity by calling it 'pseudo influenza' ( Latin: pseudo , false), while in Africa, doctors tried to get patients to take it more seriously by calling it 'influenza vera' ( Latin: vera , true). A children's song from the 1889–90 flu pandemic was shortened and adapted into a skipping-rope rhyme popular in 1918. It is a metaphor for the transmissibility of 'Influenza', where that name was clipped to the apheresis 'Enza': I had a little bird, its name was Enza. I opened the window, and in-flu-enza.Outbreaks of influenza-like illness were documented in 1916–17 at British military hospitals in Étaples , France , and just across the English Channel at Aldershot , England . Clinical indications in common with the 1918 pandemic included rapid symptom progression to a "dusky" heliotrope cyanosis of the face. This characteristic blue-violet cyanosis in expiring patients led to the name 'purple death'. The Aldershot physicians later wrote in The Lancet , "the influenza pneumococcal purulent bronchitis we and others described in 1916 and 1917 is fundamentally the same condition as the influenza of this present pandemic." This " purulent bronchitis " is not yet linked to the same A/H1N1 virus, but it may be a precursor. In 1918, ' epidemic influenza ' ( Italian : influenza , influence ), also known at the time as 'the grip' ( French : la grippe , grasp), appeared in Kansas in the U.S. during late spring, and early reports from Spain began appearing on 21 May. Reports from both places called it 'three-day fever' ( fiebre de los tres días ). Many alternative names are exonyms in the practice of making new infectious diseases seem foreign. This pattern was observed even before the 1889–1890 pandemic , also known as the 'Russian flu', when the Russians already called epidemic influenza the 'Chinese catarrh', the Germans called it the 'Russian pest', while the Italians in turn called it the 'German disease'. These epithets were re-used in the 1918 pandemic, along with new ones. Outside Spain, the disease was soon misnamed 'Spanish influenza'. In a 2 June 1918 The Times of London dispatch titled, "The Spanish Epidemic," a correspondent in Madrid reported over 100,000 victims of, "The unknown disease…clearly of a gripal character," without referring to "Spanish influenza" directly. Three weeks later The Times reported that, "Everybody thinks of it as the 'Spanish' influenza to-day." Three days after that an advertisement appeared in The Times for Formamint tablets to prevent "Spanish influenza". When it reached Moscow, Pravda announced, " Ispánka (the Spanish lady) is in town," making 'the Spanish lady' another common name. The outbreak did not originate in Spain (see below ), but reporting did, due to wartime censorship in belligerent nations. Spain was a neutral country unconcerned with appearances of combat readiness , and without a wartime propaganda machine to prop up morale ; so its newspapers freely reported epidemic effects, including King Alfonso XIII 's illness, making Spain the apparent locus of the epidemic. The censorship was so effective that Spain's health officials were unaware its neighboring countries were similarly affected. In an October 1918 "Madrid Letter" to the Journal of the American Medical Association , a Spanish official protested, "we were surprised to learn that the disease was making ravages in other countries, and that people there were calling it the 'Spanish grip'. And wherefore Spanish? …this epidemic was not born in Spain, and this should be recorded as a historic vindication." But before this letter could be published, The Serbian Newspaper ( Corfu ) said, "Various countries have been assigning the origin of this imposing guest to each other for quite some time, and at one point in time they agreed to assign its origin to the kind and neutral Spain…" French press initially used 'American flu', but adopted 'Spanish flu' in lieu of antagonizing an ally. In the spring of 1918, British soldiers called it 'Flanders flu', while German soldiers used ' Flandern-Fieber ' (Flemish fever), both after a famous battlefield in Belgium where many soldiers on both sides fell ill. In Senegal it was named 'Brazilian flu', and in Brazil , 'German flu'. In Spain it was also known as the 'French flu' ( gripe francesa ), or the 'Naples Soldier' ( Soldado de Nápoles ), after a popular song from a zarzuela . [lower-alpha 2] Spanish flu ( gripe española ) is now a common name in Spain, but remains controversial there. Other names derived from geopolitical borders and social boundaries. In Poland it was the ' Bolshevik disease', while the Bolsheviks referred to it as the ' Kirghiz disease'. Some Africans called it a 'white man's sickness', but in South Africa , white men also used the ethnophaulism 'kaffersiekte' (lit. negro disease). Japan blamed sumo wrestlers for bringing the disease home from a match in Taiwan by calling it 'sumo flu' ( Sumo Kaze ), even though three top wrestlers died there. World Health Organization 'best practices' first published in 2015 now aim to prevent social stigma by no longer associating culturally significant names with new diseases, listing "Spanish flu" under "examples to be avoided". Many authors now eschew calling this the Spanish flu, instead using variations of '1918–19/20 flu/influenza pandemic'. Outside Spain, the disease was soon misnamed 'Spanish influenza'. In a 2 June 1918 The Times of London dispatch titled, "The Spanish Epidemic," a correspondent in Madrid reported over 100,000 victims of, "The unknown disease…clearly of a gripal character," without referring to "Spanish influenza" directly. Three weeks later The Times reported that, "Everybody thinks of it as the 'Spanish' influenza to-day." Three days after that an advertisement appeared in The Times for Formamint tablets to prevent "Spanish influenza". When it reached Moscow, Pravda announced, " Ispánka (the Spanish lady) is in town," making 'the Spanish lady' another common name. The outbreak did not originate in Spain (see below ), but reporting did, due to wartime censorship in belligerent nations. Spain was a neutral country unconcerned with appearances of combat readiness , and without a wartime propaganda machine to prop up morale ; so its newspapers freely reported epidemic effects, including King Alfonso XIII 's illness, making Spain the apparent locus of the epidemic. The censorship was so effective that Spain's health officials were unaware its neighboring countries were similarly affected. In an October 1918 "Madrid Letter" to the Journal of the American Medical Association , a Spanish official protested, "we were surprised to learn that the disease was making ravages in other countries, and that people there were calling it the 'Spanish grip'. And wherefore Spanish? …this epidemic was not born in Spain, and this should be recorded as a historic vindication." But before this letter could be published, The Serbian Newspaper ( Corfu ) said, "Various countries have been assigning the origin of this imposing guest to each other for quite some time, and at one point in time they agreed to assign its origin to the kind and neutral Spain…" French press initially used 'American flu', but adopted 'Spanish flu' in lieu of antagonizing an ally. In the spring of 1918, British soldiers called it 'Flanders flu', while German soldiers used ' Flandern-Fieber ' (Flemish fever), both after a famous battlefield in Belgium where many soldiers on both sides fell ill. In Senegal it was named 'Brazilian flu', and in Brazil , 'German flu'. In Spain it was also known as the 'French flu' ( gripe francesa ), or the 'Naples Soldier' ( Soldado de Nápoles ), after a popular song from a zarzuela . [lower-alpha 2] Spanish flu ( gripe española ) is now a common name in Spain, but remains controversial there. Other names derived from geopolitical borders and social boundaries. In Poland it was the ' Bolshevik disease', while the Bolsheviks referred to it as the ' Kirghiz disease'. Some Africans called it a 'white man's sickness', but in South Africa , white men also used the ethnophaulism 'kaffersiekte' (lit. negro disease). Japan blamed sumo wrestlers for bringing the disease home from a match in Taiwan by calling it 'sumo flu' ( Sumo Kaze ), even though three top wrestlers died there. World Health Organization 'best practices' first published in 2015 now aim to prevent social stigma by no longer associating culturally significant names with new diseases, listing "Spanish flu" under "examples to be avoided". Many authors now eschew calling this the Spanish flu, instead using variations of '1918–19/20 flu/influenza pandemic'. Some language endonyms did not name specific regions or groups of people. Examples specific to this pandemic include: Northern Ndebele : 'Malibuzwe' (let enquiries be made concerning it), Swahili : 'Ugonjo huo kichwa na kukohoa na kiuno' (the disease of head and coughing and spine), Yao : 'chipindupindu' (disease from seeking to make a profit in wartime), Otjiherero : 'kaapitohanga' (disease which passes through like a bullet), and Persian : 'nakhushi-yi bad' (disease of the wind). This outbreak was also commonly known as the 'great influenza epidemic', after the 'great war', a common name for World War I before World War II . French military doctors originally called it 'disease 11' ( maladie onze ). German doctors downplayed the severity by calling it 'pseudo influenza' ( Latin: pseudo , false), while in Africa, doctors tried to get patients to take it more seriously by calling it 'influenza vera' ( Latin: vera , true). A children's song from the 1889–90 flu pandemic was shortened and adapted into a skipping-rope rhyme popular in 1918. It is a metaphor for the transmissibility of 'Influenza', where that name was clipped to the apheresis 'Enza': I had a little bird, its name was Enza. I opened the window, and in-flu-enza.The pandemic is conventionally marked as having begun on 4 March 1918 with the recording of the case of Albert Gitchell, an army cook at Camp Funston in Kansas , United States, despite there having been cases before him. The disease had already been observed 200 miles (320 km) away in Haskell County as early as January 1918, prompting local doctor Loring Miner to warn the editors of the U.S. Public Health Service 's academic journal Public Health Reports . Within days of the 4 March first case at Camp Funston, 522 men at the camp had reported sick. By 11 March 1918, the virus had reached Queens , New York. Failure to take preventive measures in March/April was later criticized. As the U.S. had entered World War I, the disease quickly spread from Camp Funston, a major training ground for troops of the American Expeditionary Forces , to other U.S. Army camps and Europe, becoming an epidemic in the Midwest , East Coast , and French ports by April 1918, and reaching the Western Front by the middle of the month. It then quickly spread to the rest of France, Great Britain, Italy, and Spain and in May reached Wrocław and Odessa . After the signing of the Treaty of Brest-Litovsk (March 1918), Germany started releasing Russian prisoners of war, who then brought the disease to their country. It reached North Africa, India, and Japan in May, and soon after had likely gone around the world as there had been recorded cases in Southeast Asia in April. In June an outbreak was reported in China . After reaching Australia in July, the wave started to recede. The first wave of the flu lasted from the first quarter of 1918 and was relatively mild. Mortality rates were not appreciably above normal; in the United States ~75,000 flu-related deaths were reported in the first six months of 1918, compared to ~63,000 deaths during the same time period in 1915. In Madrid, Spain, fewer than 1,000 people died from influenza between May and June 1918. There were no reported quarantines during the first quarter of 1918. However, the first wave caused a significant disruption in the military operations of World War I , with three-quarters of French troops, half the British forces, and over 900,000 German soldiers sick. The second wave began in the second half of August 1918, probably spreading to Boston , Massachusetts and Freetown , Sierra Leone , by ships from Brest , where it had likely arrived with American troops or French recruits for naval training. From the Boston Navy Yard and Camp Devens (later renamed Fort Devens ), about 30 miles west of Boston, other U.S. military sites were soon afflicted, as were troops being transported to Europe. Helped by troop movements, it spread over the next two months to all of North America, and then to Central and South America , also reaching Brazil and the Caribbean on ships. In July 1918, the Ottoman Empire saw its first cases in some soldiers. From Freetown, the pandemic continued to spread through West Africa along the coast, rivers, and the colonial railways, and from railheads to more remote communities, while South Africa received it in September on ships bringing back members of the South African Native Labour Corps returning from France. From there it spread around southern Africa and beyond the Zambezi , reaching Ethiopia in November. On 15 September, New York City saw its first fatality from influenza. The Philadelphia Liberty Loans Parade , held in Philadelphia , Pennsylvania , on 28 September 1918 to promote government bonds for World War I, resulted in 12,000 deaths after a major outbreak of the illness spread among people who had attended the parade. From Europe, the second wave swept through Russia in a southwest–northeast diagonal front, as well as being brought to Arkhangelsk by the North Russia intervention , and then spread throughout Asia following the Russian Civil War and the Trans-Siberian railway , reaching Iran (where it spread through the holy city of Mashhad ), and then later India in September, as well as China and Japan in October. The celebrations of the Armistice of 11 November 1918 also caused outbreaks in Lima and Nairobi , but by December the wave was mostly over. The second wave of the 1918 pandemic was much more deadly than the first. The first wave had resembled typical flu epidemics; those most at risk were the sick and elderly, while younger, healthier people recovered easily. October 1918 was the month with the highest fatality rate of the whole pandemic. In the United States, ~292,000 deaths were reported between September–December 1918, compared to ~26,000 during the same time period in 1915. The Netherlands reported over 40,000 deaths from influenza and acute respiratory disease. Bombay reported ~15,000 deaths in a population of 1.1 million. The 1918 flu pandemic in India was especially deadly, with an estimated 12.5–20 million deaths in the last quarter of 1918 alone. [ page needed ] Pandemic activity persisted, in general, into 1919 in many places. This persistence in activity is possibly attributable to climate, specifically in the Northern Hemisphere , where it was winter and thus the usual time for influenza activity. The pandemic nonetheless continued into 1919 largely independent of region and climate. Cases began to rise again in some parts of the United States as early as late November 1918, with the Public Health Service issuing its first report of a "recrudescence of the disease" being felt in "widely scattered localities" in early December. This resurgent activity varied across the country, however, possibly on account of differing restrictions. Michigan , for example, experienced a swift resurgence of influenza that reached its peak in December, possibly as a result of the lifting of the ban on public gatherings. Pandemic interventions, such as bans on public gatherings and the closing of schools, were reimposed in many places in an attempt to suppress the spread. There was "a very sudden and very marked rise in general death rate" in most cities in January 1919; nearly all experienced "some degree of recrudescence" of the flu in January and February. : 153–154 Significant outbreaks occurred in cities including Los Angeles , New York City, Memphis , Nashville , San Francisco , and St. Louis . By 21 February, with some local variation, influenza activity was reported to have been declining since mid-January in all parts of the country. Following this "first great epidemic period" that had commenced in October 1918, deaths from pneumonia and influenza were "somewhat below average" in the large cities of the United States between May 1919 and January 1920. : 158 Nonetheless, nearly 160,000 deaths were attributed to these causes in the first six months of 1919. It was not until later in the winter and into the spring that a clearer resurgence appeared in Europe. A significant third wave had developed in England and Wales by mid-February, peaking in early March, though it did not fully subside until May. France also experienced a significant wave that peaked in February, alongside the Netherlands. Norway , Finland , and Switzerland saw recrudescences of pandemic activity in March, and Sweden in April. Much of Spain was affected by "a substantial recrudescent wave" of influenza between January and April 1919. Portugal experienced a resurgence in pandemic activity that lasted from March to September 1919, with the greatest impact being felt on the west coast and in the north of the country; all districts were affected between April and May specifically. Influenza entered Australia for the first time in January 1919 after a strict maritime quarantine had shielded the country through the latter part of 1918. It assumed epidemic proportions first in Melbourne , peaking in mid-February. The flu soon appeared in neighboring New South Wales and South Australia and then spread across the country throughout the year. New South Wales experienced its first wave of infection between mid-March and late May, while a second, more severe wave occurred in Victoria between April and June. Land quarantine measures hindered the spread of the disease, resulting in varied experiences of exposures and outbreaks among the various states. Queensland was not infected until late April; Western Australia avoided the disease until early June, and Tasmania remained free from it until mid-August. Out of the six states, Victoria and New South Wales experienced generally more extensive epidemics. Each experienced another significant wave of illness over the winter. The second epidemic in New South Wales was more severe than the first, while Victoria saw a third wave that was somewhat less extensive than its second, more akin to its first. The disease also reached other parts of the world for the first time in 1919, such as Madagascar , which saw its first cases in April; the outbreak had spread to practically all sections of the island by June. In other parts, influenza recurred in the form of a true "third wave". Hong Kong experienced another outbreak in June, as did South Africa during its fall and winter months in the Southern Hemisphere . New Zealand also experienced some cases in May. Parts of South America experienced a resurgence of pandemic activity throughout 1919. A third wave hit Brazil between January and June. Between July 1919 and February 1920, Chile , which had been affected for the first time just in October 1918, experienced a severe second wave, with mortality peaking in August 1919. Montevideo similarly experienced a second outbreak between July and September. The third wave particularly affected Spain, Serbia , Mexico and Great Britain, resulting in hundreds of thousands of deaths. It was in general less severe than the second wave but still much more deadly than the initial first wave. In the Northern Hemisphere, fears of a "recurrence" of the flu grew as fall approached. Experts cited the history of past flu epidemics, such as that of 1889–1890, to predict that such a recurrence a year later was not unlikely, though not all agreed. In September 1919, U.S. Surgeon General Rupert Blue said a return of the flu later in the year would "probably, but by no means certainly," occur. France had readied a public information campaign before the end of the summer, and Britain began preparations in the fall with the manufacture of vaccine. In Japan, the flu broke out again in December and spread rapidly throughout the country, a fact attributed at the time to the coming of cold weather. Pandemic-related measures were renewed to check the spread of the outbreak, and health authorities recommended the use of masks. The epidemic intensified in the latter part of December before swiftly peaking in January. Between October 1919 and 23 January 1920, 780,000 cases were reported across the country, with at least 20,000 deaths recorded by that date. This apparently reflected "a condition of severity three times greater than for the corresponding period of" 1918–1919, during Japan's first epidemic. Nonetheless, the disease was regarded as being milder than it had been the year before, albeit more infectious. Despite its rapid peak at the beginning of the year, the outbreak persisted throughout the winter, before subsiding in the spring. In the United States, there were "almost continuously isolated or solitary cases" of flu throughout the spring and summer months of 1919. An increase in scattered cases became apparent as early as September, but Chicago experienced one of the first major outbreaks of the flu beginning in the middle of January. The Public Health Service announced it would take steps to "localize the epidemic", but the disease was already causing a simultaneous outbreak in Kansas City and quickly spread outward from the center of the country in no clear direction. A few days after its first announcement, PHS issued another assuring that the disease was under the control of state health authorities and that an outbreak of epidemic proportions was not expected. It became apparent within days of the start of Chicago's explosive growth in cases that the flu was spreading in the city at an even faster rate than in winter 1919, though fewer were dying. Within a week, new cases in the city had surpassed its peak during the 1919 wave. Around the same time, New York City began to see its own sudden increase in cases, and other cities around the country were soon to follow. Certain pandemic restrictions, such as the closing of schools and theaters and the staggering of business hours to avoid congestion, were reimposed in cities like Chicago, Memphis, and New York City. As they had during the epidemic in fall 1918, schools in New York City remained open, while those in Memphis were shuttered as part of more general restrictions on public gatherings. The fourth wave in the United States subsided as swiftly as it had appeared, reaching a peak in early February. "An epidemic of considerable proportions marked the early months of 1920", the U.S. Mortality Statistics would later note; according to data at this time, the epidemic resulted in one third as many deaths as the 1918–1919 experience. New York City alone reported 6,374 deaths between December 1919 and April 1920, almost twice the number of the first wave in spring 1918. Other U.S. cities including Detroit, Milwaukee, Kansas City, Minneapolis, and St. Louis were hit particularly hard, with death rates higher than all of 1918. The Territory of Hawaii experienced its peak of the pandemic in early 1920, recording 1,489 deaths from flu-related causes, compared with 615 in 1918 and 796 in 1919. Poland experienced a devastating outbreak during the winter months, with its capital Warsaw reaching a peak of 158 deaths in a single week, compared to the peak of 92 reached in December 1918; however, the 1920 epidemic passed in a matter of weeks, while the 1918–1919 wave had developed over the entire second half of 1918. By contrast, the outbreak in western Europe was considered "benign", with the age distribution of deaths beginning to take on that of seasonal flu . Five countries in Europe (Spain, Denmark, Finland, Germany and Switzerland) recorded a late peak between January–April 1920. Mexico experienced a fourth wave between February and March. In South America, Peru experienced "asynchronous recrudescent waves" throughout the year. A severe third wave hit Lima , the capital city, between January and March, resulting in an all-cause excess mortality rate approximately four times greater than that of the 1918–1919 wave. Ica similarly experienced another severe pandemic wave in 1920, between July and October. A fourth wave also occurred in Brazil, in February. Korea and Taiwan , both colonies of Japan at this time, also experienced pronounced outbreaks in late 1919 and early 1920. By mid-1920, the pandemic was largely considered to be "over" by the public as well as governments. Though parts of Chile experienced a third, milder wave between November 1920 and March 1921, the flu seemed to be mostly absent through the winter of 1920–1921. : 167 In the United States, for example, deaths from pneumonia and influenza were "very much lower than for many years". : 167 Influenza began to be reported again from many places in 1921. : 168 The pandemic continued to be felt in Chile, where a fourth wave affected seven of its 24 provinces between June and December 1921. The winter of 1921–1922 was the first major reappearance of influenza in the Northern Hemisphere, in many parts its most significant occurrence since the main pandemic in late 1918. Northwestern Europe was particularly affected. All-cause mortality in the Netherlands approximately doubled in January 1922 alone. : 168 In Helsinki , a major epidemic (the fifth since 1918) prevailed between November and December 1921. The flu was also widespread in the United States, its prevalence in California reportedly greater in early March 1922 than at any point since 1920. : 172 In the years after 1920, the disease, a novel one in 1918, assumed a more familiar nature, coming to represent at least one form of the "seasonal flu". The virus, H1N1, remained endemic, occasionally causing more severe or otherwise notable outbreaks as it gradually evolved over the years. The period since its initial appearance in 1918 has been termed a "pandemic era", in which all flu pandemics since its emergence have been caused by its own descendants. Following the first of these post-1918 pandemics , in 1957, the virus was totally displaced by the novel H2N2 , the reassortant product of the human H1N1 and an avian influenza virus, which thereafter became the active influenza A virus in humans. In 1977, an influenza virus bearing a very close resemblance to the seasonal H1N1, which had not been seen since the 1950s, appeared in Russia and subsequently initiated a "technical" pandemic that principally affected those 26 years of age and younger. While some natural explanations, such as the virus remaining in some frozen state for 20 years, have been proposed to explain this unprecedented phenomenon, the nature of influenza itself has been cited in favor of human involvement of some kind, such as an accidental leak from a lab where the old virus had been preserved for research purposes. Following this miniature pandemic, the reemerged H1N1 became endemic once again but did not displace the other active influenza A virus, H3N2 (which itself had displaced H2N2 through a pandemic in 1968 ). For the first time, two influenza A viruses were observed in cocirculation. This state of affairs has persisted even after 2009, when a novel H1N1 virus emerged, sparked a pandemic , and thereafter took the place of the seasonal H1N1 to circulate alongside H3N2. Despite its name, historical and epidemiological data cannot identify the geographic origin of the Spanish flu. However, several theories have been proposed. The first confirmed cases originated in the United States. Historian Alfred W. Crosby stated in 2003 that the flu originated in Kansas , and author John M. Barry described a January 1918 outbreak in Haskell County, Kansas , as the point of origin in his 2004 article. A 2018 study of tissue slides and medical reports led by evolutionary biology professor Michael Worobey found evidence against the disease originating from Kansas, as those cases were milder and had fewer deaths compared to the infections in New York City in the same period. The study did find evidence through phylogenetic analyses that the virus likely had a North American origin, though it was not conclusive. In addition, the haemagglutinin glycoproteins of the virus suggest that it originated long before 1918, and other studies suggest that the reassortment of the H1N1 virus likely occurred in or around 1915. The major U.K. troop staging and hospital camp in Étaples in France has been theorized by virologist John Oxford as being at the center of the Spanish flu. His study found that in late 1916 the Étaples camp was hit by the onset of a new disease with high mortality that caused symptoms similar to the flu. According to Oxford, a similar outbreak occurred in March 1917 at army barracks in Aldershot , and military pathologists later recognized these early outbreaks as the same disease as the Spanish flu. The overcrowded camp and hospital at Étaples was an ideal environment for the spread of a respiratory virus. The hospital treated thousands of victims of poison gas attacks, and other casualties of war, and 100,000 soldiers passed through the camp every day. It also was home to a piggery and poultry was regularly brought in from surrounding villages to feed the camp. Oxford and his team postulated that a precursor virus, harbored in birds, mutated and then migrated to pigs kept near the front. A report published in 2016 in the Journal of the Chinese Medical Association found evidence that the 1918 virus had been circulating in the European armies for months and possibly years before the 1918 pandemic. Political scientist Andrew Price-Smith published data from the Austrian archives suggesting the influenza began in Austria in early 1917. A 2009 study in Influenza and Other Respiratory Viruses found that Spanish flu mortality simultaneously peaked within the two-month period of October and November 1918 in all fourteen European countries analyzed, which is inconsistent with the pattern that researchers would expect if the virus had originated somewhere in Europe and then spread outwards. In 1993, Claude Hannoun, the leading expert on the Spanish flu at the Pasteur Institute , asserted the precursor virus was likely to have come from China and then mutated in the United States near Boston and from there spread to Brest , France, Europe's battlefields, the rest of Europe, and the rest of the world, with Allied soldiers and sailors as the main disseminators. Hannoun considered several alternative hypotheses of origin, such as Spain, Kansas, and Brest, as being possible, but not likely. In 2014, historian Mark Humphries argued that the mobilization of 96,000 Chinese laborers to work behind the British and French lines might have been the source of the pandemic. Humphries, of the Memorial University of Newfoundland in St. John's , based his conclusions on newly unearthed records. He found archival evidence that a respiratory illness that struck northern China (where the laborers came from) in November 1917 was identified a year later by Chinese health officials as identical to the Spanish flu. Unfortunately, no tissue samples have survived for modern comparison. Nevertheless, there were some reports of respiratory illness on parts of the path the laborers took to get to Europe, which also passed through North America. China was one of the few regions of the world seemingly less affected by the Spanish flu pandemic, where several studies have documented a comparatively mild flu season in 1918. (Although this is disputed due to lack of data during the Warlord Period , see Around the globe .) This has led to speculation that the Spanish flu pandemic originated in China, as the lower rates of flu mortality may be explained by the Chinese population's previously acquired immunity to the flu virus. In the Guangdong Province it was reported that early outbreaks of influenza in 1918 disproportionately impacted young men. The June outbreak infected children and adolescents between 11 and 20 years of age, while the October outbreak was most common in those aged 11 to 15. A report published in 2016 in the Journal of the Chinese Medical Association found no evidence that the 1918 virus was imported to Europe via Chinese and Southeast Asian soldiers and workers and instead found evidence of its circulation in Europe before the pandemic. The 2016 study found that the low flu mortality rate (an estimated one in a thousand) recorded among the Chinese and Southeast Asian workers in Europe suggests that the Asian units were not different from other Allied military units in France at the end of 1918 and, thus, were not a likely source of a new lethal virus. Further evidence against the disease being spread by Chinese workers was that workers entered Europe through other routes that did not result in a detectable spread, making them unlikely to have been the original hosts. The pandemic is conventionally marked as having begun on 4 March 1918 with the recording of the case of Albert Gitchell, an army cook at Camp Funston in Kansas , United States, despite there having been cases before him. The disease had already been observed 200 miles (320 km) away in Haskell County as early as January 1918, prompting local doctor Loring Miner to warn the editors of the U.S. Public Health Service 's academic journal Public Health Reports . Within days of the 4 March first case at Camp Funston, 522 men at the camp had reported sick. By 11 March 1918, the virus had reached Queens , New York. Failure to take preventive measures in March/April was later criticized. As the U.S. had entered World War I, the disease quickly spread from Camp Funston, a major training ground for troops of the American Expeditionary Forces , to other U.S. Army camps and Europe, becoming an epidemic in the Midwest , East Coast , and French ports by April 1918, and reaching the Western Front by the middle of the month. It then quickly spread to the rest of France, Great Britain, Italy, and Spain and in May reached Wrocław and Odessa . After the signing of the Treaty of Brest-Litovsk (March 1918), Germany started releasing Russian prisoners of war, who then brought the disease to their country. It reached North Africa, India, and Japan in May, and soon after had likely gone around the world as there had been recorded cases in Southeast Asia in April. In June an outbreak was reported in China . After reaching Australia in July, the wave started to recede. The first wave of the flu lasted from the first quarter of 1918 and was relatively mild. Mortality rates were not appreciably above normal; in the United States ~75,000 flu-related deaths were reported in the first six months of 1918, compared to ~63,000 deaths during the same time period in 1915. In Madrid, Spain, fewer than 1,000 people died from influenza between May and June 1918. There were no reported quarantines during the first quarter of 1918. However, the first wave caused a significant disruption in the military operations of World War I , with three-quarters of French troops, half the British forces, and over 900,000 German soldiers sick. The second wave began in the second half of August 1918, probably spreading to Boston , Massachusetts and Freetown , Sierra Leone , by ships from Brest , where it had likely arrived with American troops or French recruits for naval training. From the Boston Navy Yard and Camp Devens (later renamed Fort Devens ), about 30 miles west of Boston, other U.S. military sites were soon afflicted, as were troops being transported to Europe. Helped by troop movements, it spread over the next two months to all of North America, and then to Central and South America , also reaching Brazil and the Caribbean on ships. In July 1918, the Ottoman Empire saw its first cases in some soldiers. From Freetown, the pandemic continued to spread through West Africa along the coast, rivers, and the colonial railways, and from railheads to more remote communities, while South Africa received it in September on ships bringing back members of the South African Native Labour Corps returning from France. From there it spread around southern Africa and beyond the Zambezi , reaching Ethiopia in November. On 15 September, New York City saw its first fatality from influenza. The Philadelphia Liberty Loans Parade , held in Philadelphia , Pennsylvania , on 28 September 1918 to promote government bonds for World War I, resulted in 12,000 deaths after a major outbreak of the illness spread among people who had attended the parade. From Europe, the second wave swept through Russia in a southwest–northeast diagonal front, as well as being brought to Arkhangelsk by the North Russia intervention , and then spread throughout Asia following the Russian Civil War and the Trans-Siberian railway , reaching Iran (where it spread through the holy city of Mashhad ), and then later India in September, as well as China and Japan in October. The celebrations of the Armistice of 11 November 1918 also caused outbreaks in Lima and Nairobi , but by December the wave was mostly over. The second wave of the 1918 pandemic was much more deadly than the first. The first wave had resembled typical flu epidemics; those most at risk were the sick and elderly, while younger, healthier people recovered easily. October 1918 was the month with the highest fatality rate of the whole pandemic. In the United States, ~292,000 deaths were reported between September–December 1918, compared to ~26,000 during the same time period in 1915. The Netherlands reported over 40,000 deaths from influenza and acute respiratory disease. Bombay reported ~15,000 deaths in a population of 1.1 million. The 1918 flu pandemic in India was especially deadly, with an estimated 12.5–20 million deaths in the last quarter of 1918 alone. [ page needed ] Pandemic activity persisted, in general, into 1919 in many places. This persistence in activity is possibly attributable to climate, specifically in the Northern Hemisphere , where it was winter and thus the usual time for influenza activity. The pandemic nonetheless continued into 1919 largely independent of region and climate. Cases began to rise again in some parts of the United States as early as late November 1918, with the Public Health Service issuing its first report of a "recrudescence of the disease" being felt in "widely scattered localities" in early December. This resurgent activity varied across the country, however, possibly on account of differing restrictions. Michigan , for example, experienced a swift resurgence of influenza that reached its peak in December, possibly as a result of the lifting of the ban on public gatherings. Pandemic interventions, such as bans on public gatherings and the closing of schools, were reimposed in many places in an attempt to suppress the spread. There was "a very sudden and very marked rise in general death rate" in most cities in January 1919; nearly all experienced "some degree of recrudescence" of the flu in January and February. : 153–154 Significant outbreaks occurred in cities including Los Angeles , New York City, Memphis , Nashville , San Francisco , and St. Louis . By 21 February, with some local variation, influenza activity was reported to have been declining since mid-January in all parts of the country. Following this "first great epidemic period" that had commenced in October 1918, deaths from pneumonia and influenza were "somewhat below average" in the large cities of the United States between May 1919 and January 1920. : 158 Nonetheless, nearly 160,000 deaths were attributed to these causes in the first six months of 1919. It was not until later in the winter and into the spring that a clearer resurgence appeared in Europe. A significant third wave had developed in England and Wales by mid-February, peaking in early March, though it did not fully subside until May. France also experienced a significant wave that peaked in February, alongside the Netherlands. Norway , Finland , and Switzerland saw recrudescences of pandemic activity in March, and Sweden in April. Much of Spain was affected by "a substantial recrudescent wave" of influenza between January and April 1919. Portugal experienced a resurgence in pandemic activity that lasted from March to September 1919, with the greatest impact being felt on the west coast and in the north of the country; all districts were affected between April and May specifically. Influenza entered Australia for the first time in January 1919 after a strict maritime quarantine had shielded the country through the latter part of 1918. It assumed epidemic proportions first in Melbourne , peaking in mid-February. The flu soon appeared in neighboring New South Wales and South Australia and then spread across the country throughout the year. New South Wales experienced its first wave of infection between mid-March and late May, while a second, more severe wave occurred in Victoria between April and June. Land quarantine measures hindered the spread of the disease, resulting in varied experiences of exposures and outbreaks among the various states. Queensland was not infected until late April; Western Australia avoided the disease until early June, and Tasmania remained free from it until mid-August. Out of the six states, Victoria and New South Wales experienced generally more extensive epidemics. Each experienced another significant wave of illness over the winter. The second epidemic in New South Wales was more severe than the first, while Victoria saw a third wave that was somewhat less extensive than its second, more akin to its first. The disease also reached other parts of the world for the first time in 1919, such as Madagascar , which saw its first cases in April; the outbreak had spread to practically all sections of the island by June. In other parts, influenza recurred in the form of a true "third wave". Hong Kong experienced another outbreak in June, as did South Africa during its fall and winter months in the Southern Hemisphere . New Zealand also experienced some cases in May. Parts of South America experienced a resurgence of pandemic activity throughout 1919. A third wave hit Brazil between January and June. Between July 1919 and February 1920, Chile , which had been affected for the first time just in October 1918, experienced a severe second wave, with mortality peaking in August 1919. Montevideo similarly experienced a second outbreak between July and September. The third wave particularly affected Spain, Serbia , Mexico and Great Britain, resulting in hundreds of thousands of deaths. It was in general less severe than the second wave but still much more deadly than the initial first wave. In the Northern Hemisphere, fears of a "recurrence" of the flu grew as fall approached. Experts cited the history of past flu epidemics, such as that of 1889–1890, to predict that such a recurrence a year later was not unlikely, though not all agreed. In September 1919, U.S. Surgeon General Rupert Blue said a return of the flu later in the year would "probably, but by no means certainly," occur. France had readied a public information campaign before the end of the summer, and Britain began preparations in the fall with the manufacture of vaccine. In Japan, the flu broke out again in December and spread rapidly throughout the country, a fact attributed at the time to the coming of cold weather. Pandemic-related measures were renewed to check the spread of the outbreak, and health authorities recommended the use of masks. The epidemic intensified in the latter part of December before swiftly peaking in January. Between October 1919 and 23 January 1920, 780,000 cases were reported across the country, with at least 20,000 deaths recorded by that date. This apparently reflected "a condition of severity three times greater than for the corresponding period of" 1918–1919, during Japan's first epidemic. Nonetheless, the disease was regarded as being milder than it had been the year before, albeit more infectious. Despite its rapid peak at the beginning of the year, the outbreak persisted throughout the winter, before subsiding in the spring. In the United States, there were "almost continuously isolated or solitary cases" of flu throughout the spring and summer months of 1919. An increase in scattered cases became apparent as early as September, but Chicago experienced one of the first major outbreaks of the flu beginning in the middle of January. The Public Health Service announced it would take steps to "localize the epidemic", but the disease was already causing a simultaneous outbreak in Kansas City and quickly spread outward from the center of the country in no clear direction. A few days after its first announcement, PHS issued another assuring that the disease was under the control of state health authorities and that an outbreak of epidemic proportions was not expected. It became apparent within days of the start of Chicago's explosive growth in cases that the flu was spreading in the city at an even faster rate than in winter 1919, though fewer were dying. Within a week, new cases in the city had surpassed its peak during the 1919 wave. Around the same time, New York City began to see its own sudden increase in cases, and other cities around the country were soon to follow. Certain pandemic restrictions, such as the closing of schools and theaters and the staggering of business hours to avoid congestion, were reimposed in cities like Chicago, Memphis, and New York City. As they had during the epidemic in fall 1918, schools in New York City remained open, while those in Memphis were shuttered as part of more general restrictions on public gatherings. The fourth wave in the United States subsided as swiftly as it had appeared, reaching a peak in early February. "An epidemic of considerable proportions marked the early months of 1920", the U.S. Mortality Statistics would later note; according to data at this time, the epidemic resulted in one third as many deaths as the 1918–1919 experience. New York City alone reported 6,374 deaths between December 1919 and April 1920, almost twice the number of the first wave in spring 1918. Other U.S. cities including Detroit, Milwaukee, Kansas City, Minneapolis, and St. Louis were hit particularly hard, with death rates higher than all of 1918. The Territory of Hawaii experienced its peak of the pandemic in early 1920, recording 1,489 deaths from flu-related causes, compared with 615 in 1918 and 796 in 1919. Poland experienced a devastating outbreak during the winter months, with its capital Warsaw reaching a peak of 158 deaths in a single week, compared to the peak of 92 reached in December 1918; however, the 1920 epidemic passed in a matter of weeks, while the 1918–1919 wave had developed over the entire second half of 1918. By contrast, the outbreak in western Europe was considered "benign", with the age distribution of deaths beginning to take on that of seasonal flu . Five countries in Europe (Spain, Denmark, Finland, Germany and Switzerland) recorded a late peak between January–April 1920. Mexico experienced a fourth wave between February and March. In South America, Peru experienced "asynchronous recrudescent waves" throughout the year. A severe third wave hit Lima , the capital city, between January and March, resulting in an all-cause excess mortality rate approximately four times greater than that of the 1918–1919 wave. Ica similarly experienced another severe pandemic wave in 1920, between July and October. A fourth wave also occurred in Brazil, in February. Korea and Taiwan , both colonies of Japan at this time, also experienced pronounced outbreaks in late 1919 and early 1920. By mid-1920, the pandemic was largely considered to be "over" by the public as well as governments. Though parts of Chile experienced a third, milder wave between November 1920 and March 1921, the flu seemed to be mostly absent through the winter of 1920–1921. : 167 In the United States, for example, deaths from pneumonia and influenza were "very much lower than for many years". : 167 Influenza began to be reported again from many places in 1921. : 168 The pandemic continued to be felt in Chile, where a fourth wave affected seven of its 24 provinces between June and December 1921. The winter of 1921–1922 was the first major reappearance of influenza in the Northern Hemisphere, in many parts its most significant occurrence since the main pandemic in late 1918. Northwestern Europe was particularly affected. All-cause mortality in the Netherlands approximately doubled in January 1922 alone. : 168 In Helsinki , a major epidemic (the fifth since 1918) prevailed between November and December 1921. The flu was also widespread in the United States, its prevalence in California reportedly greater in early March 1922 than at any point since 1920. : 172 In the years after 1920, the disease, a novel one in 1918, assumed a more familiar nature, coming to represent at least one form of the "seasonal flu". The virus, H1N1, remained endemic, occasionally causing more severe or otherwise notable outbreaks as it gradually evolved over the years. The period since its initial appearance in 1918 has been termed a "pandemic era", in which all flu pandemics since its emergence have been caused by its own descendants. Following the first of these post-1918 pandemics , in 1957, the virus was totally displaced by the novel H2N2 , the reassortant product of the human H1N1 and an avian influenza virus, which thereafter became the active influenza A virus in humans. In 1977, an influenza virus bearing a very close resemblance to the seasonal H1N1, which had not been seen since the 1950s, appeared in Russia and subsequently initiated a "technical" pandemic that principally affected those 26 years of age and younger. While some natural explanations, such as the virus remaining in some frozen state for 20 years, have been proposed to explain this unprecedented phenomenon, the nature of influenza itself has been cited in favor of human involvement of some kind, such as an accidental leak from a lab where the old virus had been preserved for research purposes. Following this miniature pandemic, the reemerged H1N1 became endemic once again but did not displace the other active influenza A virus, H3N2 (which itself had displaced H2N2 through a pandemic in 1968 ). For the first time, two influenza A viruses were observed in cocirculation. This state of affairs has persisted even after 2009, when a novel H1N1 virus emerged, sparked a pandemic , and thereafter took the place of the seasonal H1N1 to circulate alongside H3N2. The pandemic is conventionally marked as having begun on 4 March 1918 with the recording of the case of Albert Gitchell, an army cook at Camp Funston in Kansas , United States, despite there having been cases before him. The disease had already been observed 200 miles (320 km) away in Haskell County as early as January 1918, prompting local doctor Loring Miner to warn the editors of the U.S. Public Health Service 's academic journal Public Health Reports . Within days of the 4 March first case at Camp Funston, 522 men at the camp had reported sick. By 11 March 1918, the virus had reached Queens , New York. Failure to take preventive measures in March/April was later criticized. As the U.S. had entered World War I, the disease quickly spread from Camp Funston, a major training ground for troops of the American Expeditionary Forces , to other U.S. Army camps and Europe, becoming an epidemic in the Midwest , East Coast , and French ports by April 1918, and reaching the Western Front by the middle of the month. It then quickly spread to the rest of France, Great Britain, Italy, and Spain and in May reached Wrocław and Odessa . After the signing of the Treaty of Brest-Litovsk (March 1918), Germany started releasing Russian prisoners of war, who then brought the disease to their country. It reached North Africa, India, and Japan in May, and soon after had likely gone around the world as there had been recorded cases in Southeast Asia in April. In June an outbreak was reported in China . After reaching Australia in July, the wave started to recede. The first wave of the flu lasted from the first quarter of 1918 and was relatively mild. Mortality rates were not appreciably above normal; in the United States ~75,000 flu-related deaths were reported in the first six months of 1918, compared to ~63,000 deaths during the same time period in 1915. In Madrid, Spain, fewer than 1,000 people died from influenza between May and June 1918. There were no reported quarantines during the first quarter of 1918. However, the first wave caused a significant disruption in the military operations of World War I , with three-quarters of French troops, half the British forces, and over 900,000 German soldiers sick. The second wave began in the second half of August 1918, probably spreading to Boston , Massachusetts and Freetown , Sierra Leone , by ships from Brest , where it had likely arrived with American troops or French recruits for naval training. From the Boston Navy Yard and Camp Devens (later renamed Fort Devens ), about 30 miles west of Boston, other U.S. military sites were soon afflicted, as were troops being transported to Europe. Helped by troop movements, it spread over the next two months to all of North America, and then to Central and South America , also reaching Brazil and the Caribbean on ships. In July 1918, the Ottoman Empire saw its first cases in some soldiers. From Freetown, the pandemic continued to spread through West Africa along the coast, rivers, and the colonial railways, and from railheads to more remote communities, while South Africa received it in September on ships bringing back members of the South African Native Labour Corps returning from France. From there it spread around southern Africa and beyond the Zambezi , reaching Ethiopia in November. On 15 September, New York City saw its first fatality from influenza. The Philadelphia Liberty Loans Parade , held in Philadelphia , Pennsylvania , on 28 September 1918 to promote government bonds for World War I, resulted in 12,000 deaths after a major outbreak of the illness spread among people who had attended the parade. From Europe, the second wave swept through Russia in a southwest–northeast diagonal front, as well as being brought to Arkhangelsk by the North Russia intervention , and then spread throughout Asia following the Russian Civil War and the Trans-Siberian railway , reaching Iran (where it spread through the holy city of Mashhad ), and then later India in September, as well as China and Japan in October. The celebrations of the Armistice of 11 November 1918 also caused outbreaks in Lima and Nairobi , but by December the wave was mostly over. The second wave of the 1918 pandemic was much more deadly than the first. The first wave had resembled typical flu epidemics; those most at risk were the sick and elderly, while younger, healthier people recovered easily. October 1918 was the month with the highest fatality rate of the whole pandemic. In the United States, ~292,000 deaths were reported between September–December 1918, compared to ~26,000 during the same time period in 1915. The Netherlands reported over 40,000 deaths from influenza and acute respiratory disease. Bombay reported ~15,000 deaths in a population of 1.1 million. The 1918 flu pandemic in India was especially deadly, with an estimated 12.5–20 million deaths in the last quarter of 1918 alone. [ page needed ]Pandemic activity persisted, in general, into 1919 in many places. This persistence in activity is possibly attributable to climate, specifically in the Northern Hemisphere , where it was winter and thus the usual time for influenza activity. The pandemic nonetheless continued into 1919 largely independent of region and climate. Cases began to rise again in some parts of the United States as early as late November 1918, with the Public Health Service issuing its first report of a "recrudescence of the disease" being felt in "widely scattered localities" in early December. This resurgent activity varied across the country, however, possibly on account of differing restrictions. Michigan , for example, experienced a swift resurgence of influenza that reached its peak in December, possibly as a result of the lifting of the ban on public gatherings. Pandemic interventions, such as bans on public gatherings and the closing of schools, were reimposed in many places in an attempt to suppress the spread. There was "a very sudden and very marked rise in general death rate" in most cities in January 1919; nearly all experienced "some degree of recrudescence" of the flu in January and February. : 153–154 Significant outbreaks occurred in cities including Los Angeles , New York City, Memphis , Nashville , San Francisco , and St. Louis . By 21 February, with some local variation, influenza activity was reported to have been declining since mid-January in all parts of the country. Following this "first great epidemic period" that had commenced in October 1918, deaths from pneumonia and influenza were "somewhat below average" in the large cities of the United States between May 1919 and January 1920. : 158 Nonetheless, nearly 160,000 deaths were attributed to these causes in the first six months of 1919. It was not until later in the winter and into the spring that a clearer resurgence appeared in Europe. A significant third wave had developed in England and Wales by mid-February, peaking in early March, though it did not fully subside until May. France also experienced a significant wave that peaked in February, alongside the Netherlands. Norway , Finland , and Switzerland saw recrudescences of pandemic activity in March, and Sweden in April. Much of Spain was affected by "a substantial recrudescent wave" of influenza between January and April 1919. Portugal experienced a resurgence in pandemic activity that lasted from March to September 1919, with the greatest impact being felt on the west coast and in the north of the country; all districts were affected between April and May specifically. Influenza entered Australia for the first time in January 1919 after a strict maritime quarantine had shielded the country through the latter part of 1918. It assumed epidemic proportions first in Melbourne , peaking in mid-February. The flu soon appeared in neighboring New South Wales and South Australia and then spread across the country throughout the year. New South Wales experienced its first wave of infection between mid-March and late May, while a second, more severe wave occurred in Victoria between April and June. Land quarantine measures hindered the spread of the disease, resulting in varied experiences of exposures and outbreaks among the various states. Queensland was not infected until late April; Western Australia avoided the disease until early June, and Tasmania remained free from it until mid-August. Out of the six states, Victoria and New South Wales experienced generally more extensive epidemics. Each experienced another significant wave of illness over the winter. The second epidemic in New South Wales was more severe than the first, while Victoria saw a third wave that was somewhat less extensive than its second, more akin to its first. The disease also reached other parts of the world for the first time in 1919, such as Madagascar , which saw its first cases in April; the outbreak had spread to practically all sections of the island by June. In other parts, influenza recurred in the form of a true "third wave". Hong Kong experienced another outbreak in June, as did South Africa during its fall and winter months in the Southern Hemisphere . New Zealand also experienced some cases in May. Parts of South America experienced a resurgence of pandemic activity throughout 1919. A third wave hit Brazil between January and June. Between July 1919 and February 1920, Chile , which had been affected for the first time just in October 1918, experienced a severe second wave, with mortality peaking in August 1919. Montevideo similarly experienced a second outbreak between July and September. The third wave particularly affected Spain, Serbia , Mexico and Great Britain, resulting in hundreds of thousands of deaths. It was in general less severe than the second wave but still much more deadly than the initial first wave.In the Northern Hemisphere, fears of a "recurrence" of the flu grew as fall approached. Experts cited the history of past flu epidemics, such as that of 1889–1890, to predict that such a recurrence a year later was not unlikely, though not all agreed. In September 1919, U.S. Surgeon General Rupert Blue said a return of the flu later in the year would "probably, but by no means certainly," occur. France had readied a public information campaign before the end of the summer, and Britain began preparations in the fall with the manufacture of vaccine. In Japan, the flu broke out again in December and spread rapidly throughout the country, a fact attributed at the time to the coming of cold weather. Pandemic-related measures were renewed to check the spread of the outbreak, and health authorities recommended the use of masks. The epidemic intensified in the latter part of December before swiftly peaking in January. Between October 1919 and 23 January 1920, 780,000 cases were reported across the country, with at least 20,000 deaths recorded by that date. This apparently reflected "a condition of severity three times greater than for the corresponding period of" 1918–1919, during Japan's first epidemic. Nonetheless, the disease was regarded as being milder than it had been the year before, albeit more infectious. Despite its rapid peak at the beginning of the year, the outbreak persisted throughout the winter, before subsiding in the spring. In the United States, there were "almost continuously isolated or solitary cases" of flu throughout the spring and summer months of 1919. An increase in scattered cases became apparent as early as September, but Chicago experienced one of the first major outbreaks of the flu beginning in the middle of January. The Public Health Service announced it would take steps to "localize the epidemic", but the disease was already causing a simultaneous outbreak in Kansas City and quickly spread outward from the center of the country in no clear direction. A few days after its first announcement, PHS issued another assuring that the disease was under the control of state health authorities and that an outbreak of epidemic proportions was not expected. It became apparent within days of the start of Chicago's explosive growth in cases that the flu was spreading in the city at an even faster rate than in winter 1919, though fewer were dying. Within a week, new cases in the city had surpassed its peak during the 1919 wave. Around the same time, New York City began to see its own sudden increase in cases, and other cities around the country were soon to follow. Certain pandemic restrictions, such as the closing of schools and theaters and the staggering of business hours to avoid congestion, were reimposed in cities like Chicago, Memphis, and New York City. As they had during the epidemic in fall 1918, schools in New York City remained open, while those in Memphis were shuttered as part of more general restrictions on public gatherings. The fourth wave in the United States subsided as swiftly as it had appeared, reaching a peak in early February. "An epidemic of considerable proportions marked the early months of 1920", the U.S. Mortality Statistics would later note; according to data at this time, the epidemic resulted in one third as many deaths as the 1918–1919 experience. New York City alone reported 6,374 deaths between December 1919 and April 1920, almost twice the number of the first wave in spring 1918. Other U.S. cities including Detroit, Milwaukee, Kansas City, Minneapolis, and St. Louis were hit particularly hard, with death rates higher than all of 1918. The Territory of Hawaii experienced its peak of the pandemic in early 1920, recording 1,489 deaths from flu-related causes, compared with 615 in 1918 and 796 in 1919. Poland experienced a devastating outbreak during the winter months, with its capital Warsaw reaching a peak of 158 deaths in a single week, compared to the peak of 92 reached in December 1918; however, the 1920 epidemic passed in a matter of weeks, while the 1918–1919 wave had developed over the entire second half of 1918. By contrast, the outbreak in western Europe was considered "benign", with the age distribution of deaths beginning to take on that of seasonal flu . Five countries in Europe (Spain, Denmark, Finland, Germany and Switzerland) recorded a late peak between January–April 1920. Mexico experienced a fourth wave between February and March. In South America, Peru experienced "asynchronous recrudescent waves" throughout the year. A severe third wave hit Lima , the capital city, between January and March, resulting in an all-cause excess mortality rate approximately four times greater than that of the 1918–1919 wave. Ica similarly experienced another severe pandemic wave in 1920, between July and October. A fourth wave also occurred in Brazil, in February. Korea and Taiwan , both colonies of Japan at this time, also experienced pronounced outbreaks in late 1919 and early 1920. By mid-1920, the pandemic was largely considered to be "over" by the public as well as governments. Though parts of Chile experienced a third, milder wave between November 1920 and March 1921, the flu seemed to be mostly absent through the winter of 1920–1921. : 167 In the United States, for example, deaths from pneumonia and influenza were "very much lower than for many years". : 167 Influenza began to be reported again from many places in 1921. : 168 The pandemic continued to be felt in Chile, where a fourth wave affected seven of its 24 provinces between June and December 1921. The winter of 1921–1922 was the first major reappearance of influenza in the Northern Hemisphere, in many parts its most significant occurrence since the main pandemic in late 1918. Northwestern Europe was particularly affected. All-cause mortality in the Netherlands approximately doubled in January 1922 alone. : 168 In Helsinki , a major epidemic (the fifth since 1918) prevailed between November and December 1921. The flu was also widespread in the United States, its prevalence in California reportedly greater in early March 1922 than at any point since 1920. : 172 In the years after 1920, the disease, a novel one in 1918, assumed a more familiar nature, coming to represent at least one form of the "seasonal flu". The virus, H1N1, remained endemic, occasionally causing more severe or otherwise notable outbreaks as it gradually evolved over the years. The period since its initial appearance in 1918 has been termed a "pandemic era", in which all flu pandemics since its emergence have been caused by its own descendants. Following the first of these post-1918 pandemics , in 1957, the virus was totally displaced by the novel H2N2 , the reassortant product of the human H1N1 and an avian influenza virus, which thereafter became the active influenza A virus in humans. In 1977, an influenza virus bearing a very close resemblance to the seasonal H1N1, which had not been seen since the 1950s, appeared in Russia and subsequently initiated a "technical" pandemic that principally affected those 26 years of age and younger. While some natural explanations, such as the virus remaining in some frozen state for 20 years, have been proposed to explain this unprecedented phenomenon, the nature of influenza itself has been cited in favor of human involvement of some kind, such as an accidental leak from a lab where the old virus had been preserved for research purposes. Following this miniature pandemic, the reemerged H1N1 became endemic once again but did not displace the other active influenza A virus, H3N2 (which itself had displaced H2N2 through a pandemic in 1968 ). For the first time, two influenza A viruses were observed in cocirculation. This state of affairs has persisted even after 2009, when a novel H1N1 virus emerged, sparked a pandemic , and thereafter took the place of the seasonal H1N1 to circulate alongside H3N2. Despite its name, historical and epidemiological data cannot identify the geographic origin of the Spanish flu. However, several theories have been proposed. The first confirmed cases originated in the United States. Historian Alfred W. Crosby stated in 2003 that the flu originated in Kansas , and author John M. Barry described a January 1918 outbreak in Haskell County, Kansas , as the point of origin in his 2004 article. A 2018 study of tissue slides and medical reports led by evolutionary biology professor Michael Worobey found evidence against the disease originating from Kansas, as those cases were milder and had fewer deaths compared to the infections in New York City in the same period. The study did find evidence through phylogenetic analyses that the virus likely had a North American origin, though it was not conclusive. In addition, the haemagglutinin glycoproteins of the virus suggest that it originated long before 1918, and other studies suggest that the reassortment of the H1N1 virus likely occurred in or around 1915. The major U.K. troop staging and hospital camp in Étaples in France has been theorized by virologist John Oxford as being at the center of the Spanish flu. His study found that in late 1916 the Étaples camp was hit by the onset of a new disease with high mortality that caused symptoms similar to the flu. According to Oxford, a similar outbreak occurred in March 1917 at army barracks in Aldershot , and military pathologists later recognized these early outbreaks as the same disease as the Spanish flu. The overcrowded camp and hospital at Étaples was an ideal environment for the spread of a respiratory virus. The hospital treated thousands of victims of poison gas attacks, and other casualties of war, and 100,000 soldiers passed through the camp every day. It also was home to a piggery and poultry was regularly brought in from surrounding villages to feed the camp. Oxford and his team postulated that a precursor virus, harbored in birds, mutated and then migrated to pigs kept near the front. A report published in 2016 in the Journal of the Chinese Medical Association found evidence that the 1918 virus had been circulating in the European armies for months and possibly years before the 1918 pandemic. Political scientist Andrew Price-Smith published data from the Austrian archives suggesting the influenza began in Austria in early 1917. A 2009 study in Influenza and Other Respiratory Viruses found that Spanish flu mortality simultaneously peaked within the two-month period of October and November 1918 in all fourteen European countries analyzed, which is inconsistent with the pattern that researchers would expect if the virus had originated somewhere in Europe and then spread outwards. In 1993, Claude Hannoun, the leading expert on the Spanish flu at the Pasteur Institute , asserted the precursor virus was likely to have come from China and then mutated in the United States near Boston and from there spread to Brest , France, Europe's battlefields, the rest of Europe, and the rest of the world, with Allied soldiers and sailors as the main disseminators. Hannoun considered several alternative hypotheses of origin, such as Spain, Kansas, and Brest, as being possible, but not likely. In 2014, historian Mark Humphries argued that the mobilization of 96,000 Chinese laborers to work behind the British and French lines might have been the source of the pandemic. Humphries, of the Memorial University of Newfoundland in St. John's , based his conclusions on newly unearthed records. He found archival evidence that a respiratory illness that struck northern China (where the laborers came from) in November 1917 was identified a year later by Chinese health officials as identical to the Spanish flu. Unfortunately, no tissue samples have survived for modern comparison. Nevertheless, there were some reports of respiratory illness on parts of the path the laborers took to get to Europe, which also passed through North America. China was one of the few regions of the world seemingly less affected by the Spanish flu pandemic, where several studies have documented a comparatively mild flu season in 1918. (Although this is disputed due to lack of data during the Warlord Period , see Around the globe .) This has led to speculation that the Spanish flu pandemic originated in China, as the lower rates of flu mortality may be explained by the Chinese population's previously acquired immunity to the flu virus. In the Guangdong Province it was reported that early outbreaks of influenza in 1918 disproportionately impacted young men. The June outbreak infected children and adolescents between 11 and 20 years of age, while the October outbreak was most common in those aged 11 to 15. A report published in 2016 in the Journal of the Chinese Medical Association found no evidence that the 1918 virus was imported to Europe via Chinese and Southeast Asian soldiers and workers and instead found evidence of its circulation in Europe before the pandemic. The 2016 study found that the low flu mortality rate (an estimated one in a thousand) recorded among the Chinese and Southeast Asian workers in Europe suggests that the Asian units were not different from other Allied military units in France at the end of 1918 and, thus, were not a likely source of a new lethal virus. Further evidence against the disease being spread by Chinese workers was that workers entered Europe through other routes that did not result in a detectable spread, making them unlikely to have been the original hosts. The first confirmed cases originated in the United States. Historian Alfred W. Crosby stated in 2003 that the flu originated in Kansas , and author John M. Barry described a January 1918 outbreak in Haskell County, Kansas , as the point of origin in his 2004 article. A 2018 study of tissue slides and medical reports led by evolutionary biology professor Michael Worobey found evidence against the disease originating from Kansas, as those cases were milder and had fewer deaths compared to the infections in New York City in the same period. The study did find evidence through phylogenetic analyses that the virus likely had a North American origin, though it was not conclusive. In addition, the haemagglutinin glycoproteins of the virus suggest that it originated long before 1918, and other studies suggest that the reassortment of the H1N1 virus likely occurred in or around 1915. The major U.K. troop staging and hospital camp in Étaples in France has been theorized by virologist John Oxford as being at the center of the Spanish flu. His study found that in late 1916 the Étaples camp was hit by the onset of a new disease with high mortality that caused symptoms similar to the flu. According to Oxford, a similar outbreak occurred in March 1917 at army barracks in Aldershot , and military pathologists later recognized these early outbreaks as the same disease as the Spanish flu. The overcrowded camp and hospital at Étaples was an ideal environment for the spread of a respiratory virus. The hospital treated thousands of victims of poison gas attacks, and other casualties of war, and 100,000 soldiers passed through the camp every day. It also was home to a piggery and poultry was regularly brought in from surrounding villages to feed the camp. Oxford and his team postulated that a precursor virus, harbored in birds, mutated and then migrated to pigs kept near the front. A report published in 2016 in the Journal of the Chinese Medical Association found evidence that the 1918 virus had been circulating in the European armies for months and possibly years before the 1918 pandemic. Political scientist Andrew Price-Smith published data from the Austrian archives suggesting the influenza began in Austria in early 1917. A 2009 study in Influenza and Other Respiratory Viruses found that Spanish flu mortality simultaneously peaked within the two-month period of October and November 1918 in all fourteen European countries analyzed, which is inconsistent with the pattern that researchers would expect if the virus had originated somewhere in Europe and then spread outwards. In 1993, Claude Hannoun, the leading expert on the Spanish flu at the Pasteur Institute , asserted the precursor virus was likely to have come from China and then mutated in the United States near Boston and from there spread to Brest , France, Europe's battlefields, the rest of Europe, and the rest of the world, with Allied soldiers and sailors as the main disseminators. Hannoun considered several alternative hypotheses of origin, such as Spain, Kansas, and Brest, as being possible, but not likely. In 2014, historian Mark Humphries argued that the mobilization of 96,000 Chinese laborers to work behind the British and French lines might have been the source of the pandemic. Humphries, of the Memorial University of Newfoundland in St. John's , based his conclusions on newly unearthed records. He found archival evidence that a respiratory illness that struck northern China (where the laborers came from) in November 1917 was identified a year later by Chinese health officials as identical to the Spanish flu. Unfortunately, no tissue samples have survived for modern comparison. Nevertheless, there were some reports of respiratory illness on parts of the path the laborers took to get to Europe, which also passed through North America. China was one of the few regions of the world seemingly less affected by the Spanish flu pandemic, where several studies have documented a comparatively mild flu season in 1918. (Although this is disputed due to lack of data during the Warlord Period , see Around the globe .) This has led to speculation that the Spanish flu pandemic originated in China, as the lower rates of flu mortality may be explained by the Chinese population's previously acquired immunity to the flu virus. In the Guangdong Province it was reported that early outbreaks of influenza in 1918 disproportionately impacted young men. The June outbreak infected children and adolescents between 11 and 20 years of age, while the October outbreak was most common in those aged 11 to 15. A report published in 2016 in the Journal of the Chinese Medical Association found no evidence that the 1918 virus was imported to Europe via Chinese and Southeast Asian soldiers and workers and instead found evidence of its circulation in Europe before the pandemic. The 2016 study found that the low flu mortality rate (an estimated one in a thousand) recorded among the Chinese and Southeast Asian workers in Europe suggests that the Asian units were not different from other Allied military units in France at the end of 1918 and, thus, were not a likely source of a new lethal virus. Further evidence against the disease being spread by Chinese workers was that workers entered Europe through other routes that did not result in a detectable spread, making them unlikely to have been the original hosts. The basic reproduction number of the virus was between 2 and 3. The close quarters and massive troop movements of World War I hastened the pandemic, and probably both increased transmission and augmented mutation. The war may also have reduced people's resistance to the virus. Some speculate the soldiers' immune systems were weakened by malnourishment, as well as the stresses of combat and chemical attacks, increasing their susceptibility. A large factor in the worldwide occurrence of the flu was increased travel. Modern transportation systems made it easier for soldiers, sailors, and civilian travelers to spread the disease. Another was lies and denial by governments, leaving the population ill-prepared to handle the outbreaks. The severity of the second wave has been attributed to the circumstances of the First World War. In civilian life, natural selection favors a mild strain. Those who get very ill stay home, and those mildly ill continue with their lives, preferentially spreading the mild strain. In the trenches, natural selection was reversed. Soldiers with a mild strain stayed where they were, while the severely ill were sent on crowded trains to crowded field hospitals, spreading the deadlier virus. The second wave began, and the flu quickly spread around the world again. Consequently, during modern pandemics, health officials look for deadlier strains of a virus when it reaches places with social upheaval. The fact that most of those who recovered from first-wave infections had become immune showed that it must have been the same strain of flu. This was most dramatically illustrated in Copenhagen , which escaped with a combined mortality rate of just 0.29% (0.02% in the first wave and 0.27% in the second wave) because of exposure to the less-lethal first wave. For the rest of the population, the second wave was far more deadly; the most vulnerable people were those like the soldiers in the trenches – adults who were young and fit. After the lethal second wave struck in late 1918, new cases dropped abruptly. In Philadelphia, for example, 4,597 people died in the week ending 16 October, but by 11 November, influenza had almost disappeared from the city. One explanation for the rapid decline in the lethality of the disease is that doctors became more effective in the prevention and treatment of pneumonia that developed after the victims had contracted the virus. However, John Barry stated in his 2004 book The Great Influenza: The Epic Story of the Deadliest Plague In History that researchers have found no evidence to support this position. Another theory holds that the 1918 virus mutated extremely rapidly to a less lethal strain. Such evolution of influenza is a common occurrence: there is a tendency for pathogenic viruses to become less lethal with time, as the hosts of more dangerous strains tend to die out. Fatal cases did continue into 1919, however. One notable example was that of ice hockey player Joe Hall , who, while playing for the Montreal Canadiens , fell victim to the flu in April after an outbreak that resulted in the cancellation of the 1919 Stanley Cup Finals . The majority of the infected experienced only the typical flu symptoms of sore throat, headache, and fever, especially during the first wave. However, during the second wave, the disease was much more serious, often complicated by bacterial pneumonia , which was often the cause of death. This more serious type would cause heliotrope cyanosis to develop, whereby the skin would first develop two mahogany spots over the cheekbones which would then over a few hours spread to color the entire face blue, followed by black coloration first in the extremities and then further spreading to the limbs and the torso. After this, death would follow within hours or days due to the lungs being filled with fluids. Other signs and symptoms reported included spontaneous mouth and nosebleeds, miscarriages for pregnant women, a peculiar smell, teeth and hair falling out, delirium , dizziness, insomnia, loss of hearing or smell, and impaired vision. One observer wrote, "One of the most striking of the complications was hemorrhage from mucous membranes , especially from the nose, stomach, and intestine. Bleeding from the ears and petechial hemorrhages in the skin also occurred". The severity of the symptoms was believed to be caused by cytokine storms . The majority of deaths were from bacterial pneumonia , a common secondary infection associated with influenza. This pneumonia was itself caused by common upper respiratory-tract bacteria, which were able to get into the lungs via the damaged bronchial tubes of the victims. The virus also killed people directly by causing massive hemorrhages and edema in the lungs. Modern analysis has shown the virus to be particularly deadly because it triggers a cytokine storm (overreaction of the body's immune system). One group of researchers recovered the virus from the bodies of frozen victims and transfected animals with it. The animals suffered rapidly progressive respiratory failure and death through a cytokine storm. The strong immune reactions of young adults were postulated to have ravaged the body, whereas the weaker immune reactions of children and middle-aged adults resulted in fewer deaths among those groups. Because the virus that caused the disease was too small to be seen under a microscope at the time, there were problems with correctly diagnosing it. The bacterium Haemophilus influenzae was instead mistakenly thought to be the cause, as it was big enough to be seen and was present in many, though not all, patients. For this reason, a vaccine that was used against that bacillus did not make an infection rarer but did decrease the death rate. During the deadly second wave there were also fears that it was in fact plague , dengue fever , or cholera . Another common misdiagnosis was typhus , which was common in circumstances of social upheaval, and was therefore also affecting Russia in the aftermath of the October Revolution . In Chile , the view of the country's elite was that the nation was in severe decline, and therefore doctors assumed that the disease was typhus caused by poor hygiene, and not an infectious one, causing a mismanaged response which did not ban mass gatherings. Studies have shown that the immune system of Spanish flu victims was weakened by adverse climate conditions which were particularly unseasonably cold and wet for extended periods of time during the duration of the pandemic. This affected especially WWI troops exposed to incessant rains and lower-than-average temperatures for the duration of the conflict, and especially during the second wave of the pandemic. Ultra-high-resolution climate data combined with highly detailed mortality records analyzed at Harvard University and the Climate Change Institute at the University of Maine identified a severe climate anomaly that impacted Europe from 1914 to 1919, with several environmental indicators directly influencing the severity and spread of the Spanish flu pandemic. Specifically, a significant increase in precipitation affected all of Europe during the second wave of the pandemic, from September to December 1918. Mortality figures follow closely the concurrent increase in precipitation and decrease in temperatures. Several explanations have been proposed for this, including the fact that lower temperatures and increased precipitation provided ideal conditions for virus replication and transmission, while also negatively affecting the immune systems of soldiers and other people exposed to the inclement weather, a factor proven to increase likelihood of infection by both viruses and pneumococcal co-morbid infections documented to have affected a large percentage of pandemic victims (one fifth of them, with a 36% mortality rate). A six-year climate anomaly (1914–1919) brought cold, marine air to Europe, drastically changing its weather, as documented by eyewitness accounts and instrumental records, reaching as far as the Gallipoli campaign , in Turkey, where ANZAC troops suffered extremely cold temperatures despite the normally Mediterranean climate of the region. The climate anomaly likely influenced the migration of H1N1 avian vectors which contaminate bodies of water with their droppings, reaching 60% infection rates in autumn. The climate anomaly has been associated with an anthropogenic increase in atmospheric dust, due to the incessant bombardment; increased nucleation due to dust particles ( cloud condensation nuclei ) contributed to increased precipitation. The basic reproduction number of the virus was between 2 and 3. The close quarters and massive troop movements of World War I hastened the pandemic, and probably both increased transmission and augmented mutation. The war may also have reduced people's resistance to the virus. Some speculate the soldiers' immune systems were weakened by malnourishment, as well as the stresses of combat and chemical attacks, increasing their susceptibility. A large factor in the worldwide occurrence of the flu was increased travel. Modern transportation systems made it easier for soldiers, sailors, and civilian travelers to spread the disease. Another was lies and denial by governments, leaving the population ill-prepared to handle the outbreaks. The severity of the second wave has been attributed to the circumstances of the First World War. In civilian life, natural selection favors a mild strain. Those who get very ill stay home, and those mildly ill continue with their lives, preferentially spreading the mild strain. In the trenches, natural selection was reversed. Soldiers with a mild strain stayed where they were, while the severely ill were sent on crowded trains to crowded field hospitals, spreading the deadlier virus. The second wave began, and the flu quickly spread around the world again. Consequently, during modern pandemics, health officials look for deadlier strains of a virus when it reaches places with social upheaval. The fact that most of those who recovered from first-wave infections had become immune showed that it must have been the same strain of flu. This was most dramatically illustrated in Copenhagen , which escaped with a combined mortality rate of just 0.29% (0.02% in the first wave and 0.27% in the second wave) because of exposure to the less-lethal first wave. For the rest of the population, the second wave was far more deadly; the most vulnerable people were those like the soldiers in the trenches – adults who were young and fit. After the lethal second wave struck in late 1918, new cases dropped abruptly. In Philadelphia, for example, 4,597 people died in the week ending 16 October, but by 11 November, influenza had almost disappeared from the city. One explanation for the rapid decline in the lethality of the disease is that doctors became more effective in the prevention and treatment of pneumonia that developed after the victims had contracted the virus. However, John Barry stated in his 2004 book The Great Influenza: The Epic Story of the Deadliest Plague In History that researchers have found no evidence to support this position. Another theory holds that the 1918 virus mutated extremely rapidly to a less lethal strain. Such evolution of influenza is a common occurrence: there is a tendency for pathogenic viruses to become less lethal with time, as the hosts of more dangerous strains tend to die out. Fatal cases did continue into 1919, however. One notable example was that of ice hockey player Joe Hall , who, while playing for the Montreal Canadiens , fell victim to the flu in April after an outbreak that resulted in the cancellation of the 1919 Stanley Cup Finals . The majority of the infected experienced only the typical flu symptoms of sore throat, headache, and fever, especially during the first wave. However, during the second wave, the disease was much more serious, often complicated by bacterial pneumonia , which was often the cause of death. This more serious type would cause heliotrope cyanosis to develop, whereby the skin would first develop two mahogany spots over the cheekbones which would then over a few hours spread to color the entire face blue, followed by black coloration first in the extremities and then further spreading to the limbs and the torso. After this, death would follow within hours or days due to the lungs being filled with fluids. Other signs and symptoms reported included spontaneous mouth and nosebleeds, miscarriages for pregnant women, a peculiar smell, teeth and hair falling out, delirium , dizziness, insomnia, loss of hearing or smell, and impaired vision. One observer wrote, "One of the most striking of the complications was hemorrhage from mucous membranes , especially from the nose, stomach, and intestine. Bleeding from the ears and petechial hemorrhages in the skin also occurred". The severity of the symptoms was believed to be caused by cytokine storms . The majority of deaths were from bacterial pneumonia , a common secondary infection associated with influenza. This pneumonia was itself caused by common upper respiratory-tract bacteria, which were able to get into the lungs via the damaged bronchial tubes of the victims. The virus also killed people directly by causing massive hemorrhages and edema in the lungs. Modern analysis has shown the virus to be particularly deadly because it triggers a cytokine storm (overreaction of the body's immune system). One group of researchers recovered the virus from the bodies of frozen victims and transfected animals with it. The animals suffered rapidly progressive respiratory failure and death through a cytokine storm. The strong immune reactions of young adults were postulated to have ravaged the body, whereas the weaker immune reactions of children and middle-aged adults resulted in fewer deaths among those groups. Because the virus that caused the disease was too small to be seen under a microscope at the time, there were problems with correctly diagnosing it. The bacterium Haemophilus influenzae was instead mistakenly thought to be the cause, as it was big enough to be seen and was present in many, though not all, patients. For this reason, a vaccine that was used against that bacillus did not make an infection rarer but did decrease the death rate. During the deadly second wave there were also fears that it was in fact plague , dengue fever , or cholera . Another common misdiagnosis was typhus , which was common in circumstances of social upheaval, and was therefore also affecting Russia in the aftermath of the October Revolution . In Chile , the view of the country's elite was that the nation was in severe decline, and therefore doctors assumed that the disease was typhus caused by poor hygiene, and not an infectious one, causing a mismanaged response which did not ban mass gatherings. Studies have shown that the immune system of Spanish flu victims was weakened by adverse climate conditions which were particularly unseasonably cold and wet for extended periods of time during the duration of the pandemic. This affected especially WWI troops exposed to incessant rains and lower-than-average temperatures for the duration of the conflict, and especially during the second wave of the pandemic. Ultra-high-resolution climate data combined with highly detailed mortality records analyzed at Harvard University and the Climate Change Institute at the University of Maine identified a severe climate anomaly that impacted Europe from 1914 to 1919, with several environmental indicators directly influencing the severity and spread of the Spanish flu pandemic. Specifically, a significant increase in precipitation affected all of Europe during the second wave of the pandemic, from September to December 1918. Mortality figures follow closely the concurrent increase in precipitation and decrease in temperatures. Several explanations have been proposed for this, including the fact that lower temperatures and increased precipitation provided ideal conditions for virus replication and transmission, while also negatively affecting the immune systems of soldiers and other people exposed to the inclement weather, a factor proven to increase likelihood of infection by both viruses and pneumococcal co-morbid infections documented to have affected a large percentage of pandemic victims (one fifth of them, with a 36% mortality rate). A six-year climate anomaly (1914–1919) brought cold, marine air to Europe, drastically changing its weather, as documented by eyewitness accounts and instrumental records, reaching as far as the Gallipoli campaign , in Turkey, where ANZAC troops suffered extremely cold temperatures despite the normally Mediterranean climate of the region. The climate anomaly likely influenced the migration of H1N1 avian vectors which contaminate bodies of water with their droppings, reaching 60% infection rates in autumn. The climate anomaly has been associated with an anthropogenic increase in atmospheric dust, due to the incessant bombardment; increased nucleation due to dust particles ( cloud condensation nuclei ) contributed to increased precipitation. While systems for alerting public health authorities of infectious spread did exist in 1918, they did not generally include influenza, leading to a delayed response. Nevertheless, actions were taken. Maritime quarantines were declared on islands such as Iceland, Australia, and American Samoa, saving many lives. Social distancing measures were introduced, for example closing schools, theatres, and places of worship, limiting public transportation, and banning mass gatherings. Wearing face masks became common in some places, such as Japan, though there were debates over their efficacy. There was also some resistance to their use, as exemplified by the Anti-Mask League of San Francisco . Vaccines were also developed, but as these were based on bacteria and not the actual virus, they could only help with secondary infections. The actual enforcement of various restrictions varied. To a large extent, the New York City health commissioner ordered businesses to open and close on staggered shifts to avoid overcrowding on the subways. A later study found that measures such as banning mass gatherings and requiring the wearing of face masks could cut the death rate up to 50 percent, but this was dependent on their being imposed early in the outbreak and not being lifted prematurely. As there were no antiviral drugs to treat the virus, and no antibiotics to treat the secondary bacterial infections, doctors would rely on a random assortment of medicines with varying degrees of effectiveness, such as aspirin , quinine , arsenics , digitalis , strychnine , epsom salts , castor oil , and iodine . Treatments of traditional medicine , such as bloodletting , ayurveda , and kampo were also applied. Due to World War I , many countries engaged in wartime censorship, and suppressed reporting of the pandemic. For example, the Italian newspaper Corriere della Sera was prohibited from reporting daily death tolls. The newspapers of the time were also generally paternalistic and worried about mass panic. Misinformation also spread along with the disease. In Ireland there was a belief that noxious gases were rising from the mass graves of Flanders Fields and being "blown all over the world by winds". There were also rumors that the Germans were behind it, for example by poisoning the aspirin manufactured by Bayer , or by releasing poison gas from U-boats . While systems for alerting public health authorities of infectious spread did exist in 1918, they did not generally include influenza, leading to a delayed response. Nevertheless, actions were taken. Maritime quarantines were declared on islands such as Iceland, Australia, and American Samoa, saving many lives. Social distancing measures were introduced, for example closing schools, theatres, and places of worship, limiting public transportation, and banning mass gatherings. Wearing face masks became common in some places, such as Japan, though there were debates over their efficacy. There was also some resistance to their use, as exemplified by the Anti-Mask League of San Francisco . Vaccines were also developed, but as these were based on bacteria and not the actual virus, they could only help with secondary infections. The actual enforcement of various restrictions varied. To a large extent, the New York City health commissioner ordered businesses to open and close on staggered shifts to avoid overcrowding on the subways. A later study found that measures such as banning mass gatherings and requiring the wearing of face masks could cut the death rate up to 50 percent, but this was dependent on their being imposed early in the outbreak and not being lifted prematurely. As there were no antiviral drugs to treat the virus, and no antibiotics to treat the secondary bacterial infections, doctors would rely on a random assortment of medicines with varying degrees of effectiveness, such as aspirin , quinine , arsenics , digitalis , strychnine , epsom salts , castor oil , and iodine . Treatments of traditional medicine , such as bloodletting , ayurveda , and kampo were also applied. Due to World War I , many countries engaged in wartime censorship, and suppressed reporting of the pandemic. For example, the Italian newspaper Corriere della Sera was prohibited from reporting daily death tolls. The newspapers of the time were also generally paternalistic and worried about mass panic. Misinformation also spread along with the disease. In Ireland there was a belief that noxious gases were rising from the mass graves of Flanders Fields and being "blown all over the world by winds". There were also rumors that the Germans were behind it, for example by poisoning the aspirin manufactured by Bayer , or by releasing poison gas from U-boats . The Spanish flu infected around 500 million people, about one-third of the world's population. Estimates as to how many infected people died vary greatly, but the flu is regardless considered to be one of the deadliest pandemics in history. An early estimate from 1927 put global mortality at 21.6 million. An estimate from 1991 states that the virus killed between 25 and 39 million people. A 2005 estimate put the death toll at 50 million (about 3% of the global population), and possibly as high as 100 million (more than 5%). However, a 2018 reassessment in the American Journal of Epidemiology estimated the total to be about 17 million, though this has been contested. With a world population of 1.8 to 1.9 billion, these estimates correspond to between 1 and 6 percent of the population. A 2009 study in Influenza and Other Respiratory Viruses based on data from fourteen European countries estimated a total of 2.64 million excess deaths in Europe attributable to the Spanish flu during the major 1918–1919 phase of the pandemic, in line with the three prior studies from 1991, 2002, and 2006 that calculated a European death toll of between 2 million and 2.3 million. This represents a mortality rate of about 1.1% of the European population ( c. 250 million in 1918), considerably higher than the mortality rate in the U.S., which the authors hypothesize is likely due to the severe effects of the war in Europe. The excess mortality rate in the U.K. has been estimated at 0.28%–0.4%, far below this European average. Some 12–17 million people died in India , about 5% of the population. The death toll in India's British-ruled districts was 13.88 million. Another estimate gives at least 12 million dead. The decade between 1911 and 1921 was the only census period in which India's population fell, mostly due to devastation of the Spanish flu pandemic. While India is generally described as the country most severely affected by the Spanish flu, at least one study argues that other factors may partially account for the very high excess mortality rates observed in 1918, citing unusually high 1917 mortality and wide regional variation (ranging from 0.47% to 6.66%). A 2006 study in The Lancet also noted that Indian provinces had excess mortality rates ranging from 2.1% to 7.8%, stating: "Commentators at the time attributed this huge variation to differences in nutritional status and diurnal fluctuations in temperature." In Finland, 20,000 died out of 210,000 infected. In Sweden, 34,000 died. In Japan, the flu killed nearly 500,000 people over two waves between 1918 and 1920, with nearly 300,000 excess deaths between October 1918 and May 1919 and 182,000 between December 1919 and May 1920. In the Dutch East Indies (now Indonesia ), 1.5 million were assumed to have died among 30 million inhabitants. In Tahiti , 13% of the population died during one month. Similarly, in Western Samoa 22% of the population of 38,000 died within two months. In Istanbul , capital of the Ottoman Empire, 6,403 to 10,000 died, giving the city a mortality rate of at least 0.56%. In New Zealand, the flu killed an estimated 6,400 Pākehā (or "New Zealanders primarily of European descent") and 2,500 indigenous Māori in six weeks, with Māori dying at eight times the rate of Pākehā. In Australia, the flu killed around 12,000 to 20,000 people. The country's death rate, 2.7 per 1,000 people, was one of the lowest recorded compared with other countries at the time; however, as much as 40 percent of the population were infected, and a mortality rate of 50 percent was recorded by some Aboriginal communities. New South Wales and Victoria saw the greatest relative mortality, with 3.19 and 2.40 deaths per 1,000 people respectively, while Western Australia, Queensland, Southern Australia, and Tasmania experienced rates of 1.70, 1.14, 1.13, and 1.09 per 1,000 respectively. In Queensland, at least one-third of deaths recorded were in the Aboriginal population. In the U.S., about 28% of the population of 105 million became infected, and 500,000 to 850,000 died (0.48 to 0.81 percent of the population). Native American tribes were particularly hard hit. In the Four Corners area, there were 3,293 registered deaths among Native Americans . Entire Inuit and Alaskan Native village communities died in Alaska . In Canada, 50,000 died. In Brazil, 300,000 died, including president Rodrigues Alves . In the UK, as many as 250,000 died; in France, more than 400,000. In Ghana , the influenza epidemic killed at least 100,000 people. Tafari Makonnen (the future Haile Selassie , Emperor of Ethiopia ) was one of the first Ethiopians who contracted influenza but survived. Many of his subjects did not; estimates for fatalities in the capital city, Addis Ababa , range from 5,000 to 10,000, or higher. The death toll in Russia has been estimated at 450,000, though the epidemiologists who suggested this number called it a "shot in the dark". If it is correct, Russia lost roughly 0.4% of its population, meaning it suffered the lowest influenza-related mortality in Europe. Another study considers this number unlikely, given that the country was in the grip of a civil war , and the infrastructure of daily life had broken down; the study suggests that Russia's death toll was closer to 2%, or 2.7 million people. Even in areas where mortality was low, so many adults were incapacitated that much of everyday life was hampered. Some communities closed all stores or required customers to leave orders outside. There were reports that healthcare workers could not tend the sick nor the gravediggers bury the dead because they too were ill. Mass graves were dug by steam shovel and bodies buried without coffins in many places. Bristol Bay , a region of Alaska populated by indigenous people , suffered a death rate of 40 percent of the total population, with some villages entirely disappearing. Nenana, Alaska , managed to avoid the extent of the pandemic between 1918 and 1919, but the flu at last reached the town in spring 1920. Reports suggested that during the first two weeks of May, the majority of the town's population became infected; 10% of the population were estimated to have died, most of whom were Alaska Natives. Several Pacific island territories were hit particularly hard. The pandemic reached them from New Zealand, which was too slow to implement measures to prevent ships, such as Talune , carrying the flu from leaving its ports. From New Zealand, the flu reached Tonga (killing 8% of the population), Nauru (16%), and Fiji (5%, 9,000 people). Worst affected was Western Samoa, formerly German Samoa , which had been occupied by New Zealand in 1914. 90% of the population was infected; 30% of adult men, 22% of adult women, and 10% of children died. By contrast, Governor John Martin Poyer prevented the flu from reaching neighboring American Samoa by imposing a blockade. The disease spread fastest through the higher social classes among the indigenous peoples, because of the custom of gathering oral tradition from chiefs on their deathbeds; many community elders were infected through this process. In Iran , the mortality was very high: according to an estimate, between 902,400 and 2,431,000, or 8% to 22% of the total population died. The country was going through the Persian famine of 1917–1919 concurrently. In Ireland , during the worst 12 months, the Spanish flu accounted for one-third of all deaths. In South Africa it is estimated that about 300,000 people amounting to 6% of the population died within six weeks. Government actions in the early stages of the virus' arrival in the country in September 1918 are believed to have unintentionally accelerated its spread throughout the country. Almost a quarter of the working population of Kimberley , consisting of workers in the diamond mines, died. In British Somaliland , one official estimated that 7% of the native population died. This huge death toll resulted from an extremely high infection rate of up to 50% and the extreme severity of the symptoms, suspected to be caused by cytokine storms . In the Pacific, American Samoa and the French colony of New Caledonia succeeded in preventing even a single death from influenza through effective quarantines . However, the outbreak was delayed into 1926 for American Samoa and 1921 for New Caledonia as the quarantine period ended. On American Samoa, at least 25% of the island residents were clinically attacked and 0.1% died, and on New Caledonia, there was widespread illness and 0.1% population died. Australia also managed to avoid the first two waves with a quarantine. Iceland protected a third of its population from exposure by blocking the main road of the island. By the end of the pandemic, the isolated island of Marajó , in Brazil's Amazon River Delta had not reported an outbreak. Saint Helena also reported no deaths. Estimates for the death toll in China have varied widely, a range which reflects the lack of centralized collection of health data at the time due to the Warlord period . China may have experienced a relatively mild flu season in 1918 compared to other areas of the world. However, some reports from its interior suggest that mortality rates from influenza were perhaps higher in at least a few locations in China in 1918. At the very least, there is little evidence that China as a whole was seriously affected by the flu compared to other countries in the world. The first estimate of the Chinese death toll was made in 1991 by Patterson and Pyle, which estimated a toll of between 5 and 9 million. However, this 1991 study was criticized by later studies due to flawed methodology, and newer studies have published estimates of a far lower mortality rate in China. For instance, Iijima in 1998 estimates the death toll in China to be between 1 and 1.28 million based on data available from Chinese port cities. The lower estimates of the Chinese death toll are based on the low mortality rates that were found in Chinese port cities (for example, Hong Kong) and on the assumption that poor communications prevented the flu from penetrating the interior of China. However, some contemporary newspaper and post office reports, as well as reports from missionary doctors, suggest that the flu did penetrate the Chinese interior and that influenza was severe in at least some locations in the countryside of China. Although medical records from China's interior are lacking, extensive medical data were recorded in Chinese port cities, such as then British -controlled Hong Kong, Canton , Peking , Harbin and Shanghai . These data were collected by the Chinese Maritime Customs Service , which was largely staffed by non-Chinese foreigners, such as the British, French, and other European colonial officials in China. As a whole, data from China's port cities show low mortality rates compared to other cities in Asia. For example, the British authorities at Hong Kong and Canton reported a mortality rate from influenza at a rate of 0.25% and 0.32%, much lower than the reported mortality rate of other cities in Asia, such as Calcutta or Bombay, where influenza was much more devastating. Similarly, in the city of Shanghai – which had a population of over 2 million in 1918 – there were only 266 recorded deaths from influenza among the Chinese population in 1918. If extrapolated from the extensive data recorded from Chinese cities, the suggested mortality rate from influenza in China as a whole in 1918 was likely lower than 1% – much lower than the world average (which was around 3–5%). In contrast, Japan and Taiwan had reported a mortality rate from influenza around 0.45% and 0.69% respectively, higher than the mortality rate collected from data in Chinese port cities, such as Hong Kong (0.25%), Canton (0.32%), and Shanghai. However, it is noted that the influenza mortality rate in Hong Kong and Canton are under-recorded, because only the deaths that occurred in colony hospitals were counted. Similarly, in Shanghai, these statistics are limited to that area of the city under the control of the health section of the Shanghai International Settlement, and the actual death toll in Shanghai was much higher. The medical records from China's interior indicate that, compared to cities, rural communities have substantially higher mortality rate. A published influenza survey in Houlu County, Hebei Province, found that the case fatality rate was 9.77% and 0.79% of county population died from influenza in October and November 1918. The pandemic mostly killed young adults. In 1918–1919, 99% of pandemic influenza deaths in the U.S. occurred in people under 65, and nearly half of deaths were in young adults 20 to 40 years old. In 1920, the mortality rate among people under 65 had decreased sixfold to half the mortality rate of people over 65, but 92% of deaths still occurred in people under 65. This is unusual since influenza is typically most deadly to weak individuals, such as infants under age two, adults over age 70, and the immunocompromised . In 1918, older adults may have had partial protection caused by exposure to the 1889–1890 flu pandemic, known as the "Russian flu". According to historian John M. Barry, the most vulnerable of all – "those most likely, of the most likely", to die – were pregnant women. He reported that in thirteen studies of hospitalized women in the pandemic, the death rate ranged from 23% to 71%. Of the pregnant women who survived childbirth, over one-quarter (26%) lost the child. Another oddity was that the outbreak was widespread in the summer and autumn (in the Northern Hemisphere); influenza is usually worse in winter. There were also geographic patterns to the disease's fatality. Some parts of Asia had 30 times higher death rates than some parts of Europe, and generally, Africa and Asia had higher rates, while Europe and North America had lower ones. There was also great variation within continents, with three times higher mortality in Hungary and Spain compared to Denmark, two to three times higher chance of death in Sub-Saharan Africa compared to North Africa, and possibly up to ten times higher rates between the extremes of Asia. Cities were affected worse than rural areas. There were also differences between cities, which might have reflected exposure to the milder first wave giving immunity, as well as the introduction of social distancing measures. Another major pattern was the differences between social classes. In Oslo , death rates were inversely correlated with apartment size, as the poorer people living in smaller apartments died at a higher rate. Social status was also reflected in the higher mortality among immigrant communities, with Italian Americans , a recently arrived group at the time, were nearly twice as likely to die compared to the average Americans. These disparities reflected worse diets, crowded living conditions, and problems accessing healthcare. Paradoxically, however, African Americans were relatively spared by the pandemic. More men than women were killed by the flu, as they were more likely to go out and be exposed, while women would tend to stay at home . For the same reason men also were more likely to have pre-existing tuberculosis , which severely worsened the chances of recovery. However, in India the opposite was true, potentially because Indian women were neglected with poorer nutrition, and were expected to care for the sick. A study conducted by He et al . (2011) used a mechanistic modeling approach to study the three waves of the 1918 influenza pandemic. They examined the factors that underlie variability in temporal patterns and their correlation to patterns of mortality and morbidity. Their analysis suggests that temporal variations in transmission rate provide the best explanation, and the variation in transmission required to generate these three waves is within biologically plausible values. Another study by He et al . (2013) used a simple epidemic model incorporating three factors to infer the cause of the three waves of the 1918 influenza pandemic. These factors were school opening and closing, temperature changes throughout the outbreak, and human behavioral changes in response to the outbreak. Their modeling results showed that all three factors are important, but human behavioral responses showed the most significant effects. The Spanish flu infected around 500 million people, about one-third of the world's population. Estimates as to how many infected people died vary greatly, but the flu is regardless considered to be one of the deadliest pandemics in history. An early estimate from 1927 put global mortality at 21.6 million. An estimate from 1991 states that the virus killed between 25 and 39 million people. A 2005 estimate put the death toll at 50 million (about 3% of the global population), and possibly as high as 100 million (more than 5%). However, a 2018 reassessment in the American Journal of Epidemiology estimated the total to be about 17 million, though this has been contested. With a world population of 1.8 to 1.9 billion, these estimates correspond to between 1 and 6 percent of the population. A 2009 study in Influenza and Other Respiratory Viruses based on data from fourteen European countries estimated a total of 2.64 million excess deaths in Europe attributable to the Spanish flu during the major 1918–1919 phase of the pandemic, in line with the three prior studies from 1991, 2002, and 2006 that calculated a European death toll of between 2 million and 2.3 million. This represents a mortality rate of about 1.1% of the European population ( c. 250 million in 1918), considerably higher than the mortality rate in the U.S., which the authors hypothesize is likely due to the severe effects of the war in Europe. The excess mortality rate in the U.K. has been estimated at 0.28%–0.4%, far below this European average. Some 12–17 million people died in India , about 5% of the population. The death toll in India's British-ruled districts was 13.88 million. Another estimate gives at least 12 million dead. The decade between 1911 and 1921 was the only census period in which India's population fell, mostly due to devastation of the Spanish flu pandemic. While India is generally described as the country most severely affected by the Spanish flu, at least one study argues that other factors may partially account for the very high excess mortality rates observed in 1918, citing unusually high 1917 mortality and wide regional variation (ranging from 0.47% to 6.66%). A 2006 study in The Lancet also noted that Indian provinces had excess mortality rates ranging from 2.1% to 7.8%, stating: "Commentators at the time attributed this huge variation to differences in nutritional status and diurnal fluctuations in temperature." In Finland, 20,000 died out of 210,000 infected. In Sweden, 34,000 died. In Japan, the flu killed nearly 500,000 people over two waves between 1918 and 1920, with nearly 300,000 excess deaths between October 1918 and May 1919 and 182,000 between December 1919 and May 1920. In the Dutch East Indies (now Indonesia ), 1.5 million were assumed to have died among 30 million inhabitants. In Tahiti , 13% of the population died during one month. Similarly, in Western Samoa 22% of the population of 38,000 died within two months. In Istanbul , capital of the Ottoman Empire, 6,403 to 10,000 died, giving the city a mortality rate of at least 0.56%. In New Zealand, the flu killed an estimated 6,400 Pākehā (or "New Zealanders primarily of European descent") and 2,500 indigenous Māori in six weeks, with Māori dying at eight times the rate of Pākehā. In Australia, the flu killed around 12,000 to 20,000 people. The country's death rate, 2.7 per 1,000 people, was one of the lowest recorded compared with other countries at the time; however, as much as 40 percent of the population were infected, and a mortality rate of 50 percent was recorded by some Aboriginal communities. New South Wales and Victoria saw the greatest relative mortality, with 3.19 and 2.40 deaths per 1,000 people respectively, while Western Australia, Queensland, Southern Australia, and Tasmania experienced rates of 1.70, 1.14, 1.13, and 1.09 per 1,000 respectively. In Queensland, at least one-third of deaths recorded were in the Aboriginal population. In the U.S., about 28% of the population of 105 million became infected, and 500,000 to 850,000 died (0.48 to 0.81 percent of the population). Native American tribes were particularly hard hit. In the Four Corners area, there were 3,293 registered deaths among Native Americans . Entire Inuit and Alaskan Native village communities died in Alaska . In Canada, 50,000 died. In Brazil, 300,000 died, including president Rodrigues Alves . In the UK, as many as 250,000 died; in France, more than 400,000. In Ghana , the influenza epidemic killed at least 100,000 people. Tafari Makonnen (the future Haile Selassie , Emperor of Ethiopia ) was one of the first Ethiopians who contracted influenza but survived. Many of his subjects did not; estimates for fatalities in the capital city, Addis Ababa , range from 5,000 to 10,000, or higher. The death toll in Russia has been estimated at 450,000, though the epidemiologists who suggested this number called it a "shot in the dark". If it is correct, Russia lost roughly 0.4% of its population, meaning it suffered the lowest influenza-related mortality in Europe. Another study considers this number unlikely, given that the country was in the grip of a civil war , and the infrastructure of daily life had broken down; the study suggests that Russia's death toll was closer to 2%, or 2.7 million people. Even in areas where mortality was low, so many adults were incapacitated that much of everyday life was hampered. Some communities closed all stores or required customers to leave orders outside. There were reports that healthcare workers could not tend the sick nor the gravediggers bury the dead because they too were ill. Mass graves were dug by steam shovel and bodies buried without coffins in many places. Bristol Bay , a region of Alaska populated by indigenous people , suffered a death rate of 40 percent of the total population, with some villages entirely disappearing. Nenana, Alaska , managed to avoid the extent of the pandemic between 1918 and 1919, but the flu at last reached the town in spring 1920. Reports suggested that during the first two weeks of May, the majority of the town's population became infected; 10% of the population were estimated to have died, most of whom were Alaska Natives. Several Pacific island territories were hit particularly hard. The pandemic reached them from New Zealand, which was too slow to implement measures to prevent ships, such as Talune , carrying the flu from leaving its ports. From New Zealand, the flu reached Tonga (killing 8% of the population), Nauru (16%), and Fiji (5%, 9,000 people). Worst affected was Western Samoa, formerly German Samoa , which had been occupied by New Zealand in 1914. 90% of the population was infected; 30% of adult men, 22% of adult women, and 10% of children died. By contrast, Governor John Martin Poyer prevented the flu from reaching neighboring American Samoa by imposing a blockade. The disease spread fastest through the higher social classes among the indigenous peoples, because of the custom of gathering oral tradition from chiefs on their deathbeds; many community elders were infected through this process. In Iran , the mortality was very high: according to an estimate, between 902,400 and 2,431,000, or 8% to 22% of the total population died. The country was going through the Persian famine of 1917–1919 concurrently. In Ireland , during the worst 12 months, the Spanish flu accounted for one-third of all deaths. In South Africa it is estimated that about 300,000 people amounting to 6% of the population died within six weeks. Government actions in the early stages of the virus' arrival in the country in September 1918 are believed to have unintentionally accelerated its spread throughout the country. Almost a quarter of the working population of Kimberley , consisting of workers in the diamond mines, died. In British Somaliland , one official estimated that 7% of the native population died. This huge death toll resulted from an extremely high infection rate of up to 50% and the extreme severity of the symptoms, suspected to be caused by cytokine storms . In the Pacific, American Samoa and the French colony of New Caledonia succeeded in preventing even a single death from influenza through effective quarantines . However, the outbreak was delayed into 1926 for American Samoa and 1921 for New Caledonia as the quarantine period ended. On American Samoa, at least 25% of the island residents were clinically attacked and 0.1% died, and on New Caledonia, there was widespread illness and 0.1% population died. Australia also managed to avoid the first two waves with a quarantine. Iceland protected a third of its population from exposure by blocking the main road of the island. By the end of the pandemic, the isolated island of Marajó , in Brazil's Amazon River Delta had not reported an outbreak. Saint Helena also reported no deaths. Estimates for the death toll in China have varied widely, a range which reflects the lack of centralized collection of health data at the time due to the Warlord period . China may have experienced a relatively mild flu season in 1918 compared to other areas of the world. However, some reports from its interior suggest that mortality rates from influenza were perhaps higher in at least a few locations in China in 1918. At the very least, there is little evidence that China as a whole was seriously affected by the flu compared to other countries in the world. The first estimate of the Chinese death toll was made in 1991 by Patterson and Pyle, which estimated a toll of between 5 and 9 million. However, this 1991 study was criticized by later studies due to flawed methodology, and newer studies have published estimates of a far lower mortality rate in China. For instance, Iijima in 1998 estimates the death toll in China to be between 1 and 1.28 million based on data available from Chinese port cities. The lower estimates of the Chinese death toll are based on the low mortality rates that were found in Chinese port cities (for example, Hong Kong) and on the assumption that poor communications prevented the flu from penetrating the interior of China. However, some contemporary newspaper and post office reports, as well as reports from missionary doctors, suggest that the flu did penetrate the Chinese interior and that influenza was severe in at least some locations in the countryside of China. Although medical records from China's interior are lacking, extensive medical data were recorded in Chinese port cities, such as then British -controlled Hong Kong, Canton , Peking , Harbin and Shanghai . These data were collected by the Chinese Maritime Customs Service , which was largely staffed by non-Chinese foreigners, such as the British, French, and other European colonial officials in China. As a whole, data from China's port cities show low mortality rates compared to other cities in Asia. For example, the British authorities at Hong Kong and Canton reported a mortality rate from influenza at a rate of 0.25% and 0.32%, much lower than the reported mortality rate of other cities in Asia, such as Calcutta or Bombay, where influenza was much more devastating. Similarly, in the city of Shanghai – which had a population of over 2 million in 1918 – there were only 266 recorded deaths from influenza among the Chinese population in 1918. If extrapolated from the extensive data recorded from Chinese cities, the suggested mortality rate from influenza in China as a whole in 1918 was likely lower than 1% – much lower than the world average (which was around 3–5%). In contrast, Japan and Taiwan had reported a mortality rate from influenza around 0.45% and 0.69% respectively, higher than the mortality rate collected from data in Chinese port cities, such as Hong Kong (0.25%), Canton (0.32%), and Shanghai. However, it is noted that the influenza mortality rate in Hong Kong and Canton are under-recorded, because only the deaths that occurred in colony hospitals were counted. Similarly, in Shanghai, these statistics are limited to that area of the city under the control of the health section of the Shanghai International Settlement, and the actual death toll in Shanghai was much higher. The medical records from China's interior indicate that, compared to cities, rural communities have substantially higher mortality rate. A published influenza survey in Houlu County, Hebei Province, found that the case fatality rate was 9.77% and 0.79% of county population died from influenza in October and November 1918. Even in areas where mortality was low, so many adults were incapacitated that much of everyday life was hampered. Some communities closed all stores or required customers to leave orders outside. There were reports that healthcare workers could not tend the sick nor the gravediggers bury the dead because they too were ill. Mass graves were dug by steam shovel and bodies buried without coffins in many places. Bristol Bay , a region of Alaska populated by indigenous people , suffered a death rate of 40 percent of the total population, with some villages entirely disappearing. Nenana, Alaska , managed to avoid the extent of the pandemic between 1918 and 1919, but the flu at last reached the town in spring 1920. Reports suggested that during the first two weeks of May, the majority of the town's population became infected; 10% of the population were estimated to have died, most of whom were Alaska Natives. Several Pacific island territories were hit particularly hard. The pandemic reached them from New Zealand, which was too slow to implement measures to prevent ships, such as Talune , carrying the flu from leaving its ports. From New Zealand, the flu reached Tonga (killing 8% of the population), Nauru (16%), and Fiji (5%, 9,000 people). Worst affected was Western Samoa, formerly German Samoa , which had been occupied by New Zealand in 1914. 90% of the population was infected; 30% of adult men, 22% of adult women, and 10% of children died. By contrast, Governor John Martin Poyer prevented the flu from reaching neighboring American Samoa by imposing a blockade. The disease spread fastest through the higher social classes among the indigenous peoples, because of the custom of gathering oral tradition from chiefs on their deathbeds; many community elders were infected through this process. In Iran , the mortality was very high: according to an estimate, between 902,400 and 2,431,000, or 8% to 22% of the total population died. The country was going through the Persian famine of 1917–1919 concurrently. In Ireland , during the worst 12 months, the Spanish flu accounted for one-third of all deaths. In South Africa it is estimated that about 300,000 people amounting to 6% of the population died within six weeks. Government actions in the early stages of the virus' arrival in the country in September 1918 are believed to have unintentionally accelerated its spread throughout the country. Almost a quarter of the working population of Kimberley , consisting of workers in the diamond mines, died. In British Somaliland , one official estimated that 7% of the native population died. This huge death toll resulted from an extremely high infection rate of up to 50% and the extreme severity of the symptoms, suspected to be caused by cytokine storms . In the Pacific, American Samoa and the French colony of New Caledonia succeeded in preventing even a single death from influenza through effective quarantines . However, the outbreak was delayed into 1926 for American Samoa and 1921 for New Caledonia as the quarantine period ended. On American Samoa, at least 25% of the island residents were clinically attacked and 0.1% died, and on New Caledonia, there was widespread illness and 0.1% population died. Australia also managed to avoid the first two waves with a quarantine. Iceland protected a third of its population from exposure by blocking the main road of the island. By the end of the pandemic, the isolated island of Marajó , in Brazil's Amazon River Delta had not reported an outbreak. Saint Helena also reported no deaths. Estimates for the death toll in China have varied widely, a range which reflects the lack of centralized collection of health data at the time due to the Warlord period . China may have experienced a relatively mild flu season in 1918 compared to other areas of the world. However, some reports from its interior suggest that mortality rates from influenza were perhaps higher in at least a few locations in China in 1918. At the very least, there is little evidence that China as a whole was seriously affected by the flu compared to other countries in the world. The first estimate of the Chinese death toll was made in 1991 by Patterson and Pyle, which estimated a toll of between 5 and 9 million. However, this 1991 study was criticized by later studies due to flawed methodology, and newer studies have published estimates of a far lower mortality rate in China. For instance, Iijima in 1998 estimates the death toll in China to be between 1 and 1.28 million based on data available from Chinese port cities. The lower estimates of the Chinese death toll are based on the low mortality rates that were found in Chinese port cities (for example, Hong Kong) and on the assumption that poor communications prevented the flu from penetrating the interior of China. However, some contemporary newspaper and post office reports, as well as reports from missionary doctors, suggest that the flu did penetrate the Chinese interior and that influenza was severe in at least some locations in the countryside of China. Although medical records from China's interior are lacking, extensive medical data were recorded in Chinese port cities, such as then British -controlled Hong Kong, Canton , Peking , Harbin and Shanghai . These data were collected by the Chinese Maritime Customs Service , which was largely staffed by non-Chinese foreigners, such as the British, French, and other European colonial officials in China. As a whole, data from China's port cities show low mortality rates compared to other cities in Asia. For example, the British authorities at Hong Kong and Canton reported a mortality rate from influenza at a rate of 0.25% and 0.32%, much lower than the reported mortality rate of other cities in Asia, such as Calcutta or Bombay, where influenza was much more devastating. Similarly, in the city of Shanghai – which had a population of over 2 million in 1918 – there were only 266 recorded deaths from influenza among the Chinese population in 1918. If extrapolated from the extensive data recorded from Chinese cities, the suggested mortality rate from influenza in China as a whole in 1918 was likely lower than 1% – much lower than the world average (which was around 3–5%). In contrast, Japan and Taiwan had reported a mortality rate from influenza around 0.45% and 0.69% respectively, higher than the mortality rate collected from data in Chinese port cities, such as Hong Kong (0.25%), Canton (0.32%), and Shanghai. However, it is noted that the influenza mortality rate in Hong Kong and Canton are under-recorded, because only the deaths that occurred in colony hospitals were counted. Similarly, in Shanghai, these statistics are limited to that area of the city under the control of the health section of the Shanghai International Settlement, and the actual death toll in Shanghai was much higher. The medical records from China's interior indicate that, compared to cities, rural communities have substantially higher mortality rate. A published influenza survey in Houlu County, Hebei Province, found that the case fatality rate was 9.77% and 0.79% of county population died from influenza in October and November 1918. The pandemic mostly killed young adults. In 1918–1919, 99% of pandemic influenza deaths in the U.S. occurred in people under 65, and nearly half of deaths were in young adults 20 to 40 years old. In 1920, the mortality rate among people under 65 had decreased sixfold to half the mortality rate of people over 65, but 92% of deaths still occurred in people under 65. This is unusual since influenza is typically most deadly to weak individuals, such as infants under age two, adults over age 70, and the immunocompromised . In 1918, older adults may have had partial protection caused by exposure to the 1889–1890 flu pandemic, known as the "Russian flu". According to historian John M. Barry, the most vulnerable of all – "those most likely, of the most likely", to die – were pregnant women. He reported that in thirteen studies of hospitalized women in the pandemic, the death rate ranged from 23% to 71%. Of the pregnant women who survived childbirth, over one-quarter (26%) lost the child. Another oddity was that the outbreak was widespread in the summer and autumn (in the Northern Hemisphere); influenza is usually worse in winter. There were also geographic patterns to the disease's fatality. Some parts of Asia had 30 times higher death rates than some parts of Europe, and generally, Africa and Asia had higher rates, while Europe and North America had lower ones. There was also great variation within continents, with three times higher mortality in Hungary and Spain compared to Denmark, two to three times higher chance of death in Sub-Saharan Africa compared to North Africa, and possibly up to ten times higher rates between the extremes of Asia. Cities were affected worse than rural areas. There were also differences between cities, which might have reflected exposure to the milder first wave giving immunity, as well as the introduction of social distancing measures. Another major pattern was the differences between social classes. In Oslo , death rates were inversely correlated with apartment size, as the poorer people living in smaller apartments died at a higher rate. Social status was also reflected in the higher mortality among immigrant communities, with Italian Americans , a recently arrived group at the time, were nearly twice as likely to die compared to the average Americans. These disparities reflected worse diets, crowded living conditions, and problems accessing healthcare. Paradoxically, however, African Americans were relatively spared by the pandemic. More men than women were killed by the flu, as they were more likely to go out and be exposed, while women would tend to stay at home . For the same reason men also were more likely to have pre-existing tuberculosis , which severely worsened the chances of recovery. However, in India the opposite was true, potentially because Indian women were neglected with poorer nutrition, and were expected to care for the sick. A study conducted by He et al . (2011) used a mechanistic modeling approach to study the three waves of the 1918 influenza pandemic. They examined the factors that underlie variability in temporal patterns and their correlation to patterns of mortality and morbidity. Their analysis suggests that temporal variations in transmission rate provide the best explanation, and the variation in transmission required to generate these three waves is within biologically plausible values. Another study by He et al . (2013) used a simple epidemic model incorporating three factors to infer the cause of the three waves of the 1918 influenza pandemic. These factors were school opening and closing, temperature changes throughout the outbreak, and human behavioral changes in response to the outbreak. Their modeling results showed that all three factors are important, but human behavioral responses showed the most significant effects. Academic Andrew Price-Smith has made the argument that the virus helped tip the balance of power in the latter days of the war towards the Allied cause. He provides data that the viral waves hit the Central Powers before the Allied powers and that both morbidity and mortality in Germany and Austria were considerably higher than in Britain and France. A 2006 Lancet study corroborates higher excess mortality rates in Germany (0.76%) and Austria (1.61%) compared to Britain (0.34%) and France (0.75%). Kenneth Kahn at Oxford University Computing Services writes that "Many researchers have suggested that the conditions of the war significantly aided the spread of the disease. And others have argued that the course of the war (and subsequent peace treaty) was influenced by the pandemic." Kahn has developed a model that can be used on home computers to test these theories. Many businesses in the entertainment and service industries suffered losses in revenue, while the healthcare industry reported profit gains. Historian Nancy Bristow has argued that the pandemic, when combined with the increasing number of women attending college, contributed to the success of women in the field of nursing. This was due in part to the failure of medical doctors, who were predominantly men, to contain and prevent the illness. Nursing staff, who were mainly women, celebrated the success of their patient care and did not associate the spread of the disease with their work. A 2020 study found that U.S. cities that implemented early and extensive non-medical measures (quarantine, etc.) suffered no additional adverse economic effects due to implementing those measures. However, the validity of this study has been questioned because of the coincidence of WWI and other problems with data reliability. A 2006 study in the Journal of Political Economy found that "cohorts in utero during the pandemic displayed reduced educational attainment, increased rates of physical disability, lower income, lower socioeconomic status, and higher transfer payments received compared with other birth cohorts." A 2018 study found that the pandemic reduced educational attainment in populations. The flu has also been linked to the outbreak of encephalitis lethargica in the 1920s. Survivors faced an elevated mortality risk. Some survivors did not fully recover from physiological conditions resulting from infection. Academic Andrew Price-Smith has made the argument that the virus helped tip the balance of power in the latter days of the war towards the Allied cause. He provides data that the viral waves hit the Central Powers before the Allied powers and that both morbidity and mortality in Germany and Austria were considerably higher than in Britain and France. A 2006 Lancet study corroborates higher excess mortality rates in Germany (0.76%) and Austria (1.61%) compared to Britain (0.34%) and France (0.75%). Kenneth Kahn at Oxford University Computing Services writes that "Many researchers have suggested that the conditions of the war significantly aided the spread of the disease. And others have argued that the course of the war (and subsequent peace treaty) was influenced by the pandemic." Kahn has developed a model that can be used on home computers to test these theories. Many businesses in the entertainment and service industries suffered losses in revenue, while the healthcare industry reported profit gains. Historian Nancy Bristow has argued that the pandemic, when combined with the increasing number of women attending college, contributed to the success of women in the field of nursing. This was due in part to the failure of medical doctors, who were predominantly men, to contain and prevent the illness. Nursing staff, who were mainly women, celebrated the success of their patient care and did not associate the spread of the disease with their work. A 2020 study found that U.S. cities that implemented early and extensive non-medical measures (quarantine, etc.) suffered no additional adverse economic effects due to implementing those measures. However, the validity of this study has been questioned because of the coincidence of WWI and other problems with data reliability. A 2006 study in the Journal of Political Economy found that "cohorts in utero during the pandemic displayed reduced educational attainment, increased rates of physical disability, lower income, lower socioeconomic status, and higher transfer payments received compared with other birth cohorts." A 2018 study found that the pandemic reduced educational attainment in populations. The flu has also been linked to the outbreak of encephalitis lethargica in the 1920s. Survivors faced an elevated mortality risk. Some survivors did not fully recover from physiological conditions resulting from infection. Despite the high morbidity and mortality rates that resulted from the epidemic, the Spanish flu began to fade from public awareness over the decades until the arrival of news about bird flu and other pandemics in the 1990s and 2000s. This has led some historians to label the Spanish flu a "forgotten pandemic". However, this label has been challenged by the historian Guy Beiner , who has charted a complex history of social and cultural forgetting, demonstrating how the pandemic was overshadowed by the commemoration of the First World War and mostly neglected in mainstream historiography, yet was remembered in private and local traditions across the globe. There are various theories of why the Spanish flu was "forgotten". The rapid pace of the pandemic, which killed most of its victims in the United States within less than nine months, resulted in limited media coverage. The general population was familiar with patterns of pandemic disease in the late 19th and early 20th centuries: typhoid, yellow fever , diphtheria , and cholera all occurred near the same time. These outbreaks probably lessened the significance of the influenza pandemic for the public. In some areas, the flu was not reported on, the only mention being that of advertisements for medicines claiming to cure it. Additionally, the outbreak coincided with the deaths and media focus on the First World War. Another explanation involves the age group affected by the disease. The majority of fatalities, from both the war and the epidemic, were among young adults. The high number of war-related deaths of young adults may have overshadowed the deaths caused by flu. When people read the obituaries, they saw the war or postwar deaths and the deaths from the influenza side by side. Particularly in Europe, where the war's toll was high, the flu may not have had a tremendous psychological impact or may have seemed an extension of the war's tragedies. The duration of the pandemic and the war could have also played a role. The war, however, had initially been expected to end quickly but lasted for four years by the time the pandemic struck. Despite the toll of the pandemic, it was never a large theme in American literature. Alfred Crosby suspects that it may be due to the fact that it occurred after World War I, which was the most important event in that generation's lives. Katherine Anne Porter 's 1939 novella Pale Horse, Pale Rider is one of the most well-known fictional accounts of the pandemic. The 2006 novel The Last Town on Earth focuses on a town which attempts to limit the spread of the flu by preventing people from entering or leaving. The Pull of the Stars is a 2020 novel by Emma Donoghue set in Dublin during the Spanish flu. Its final draft was submitted in March 2020, and publishers fast-tracked publication because of the then ongoing COVID-19 pandemic . The Spanish flu killed a much lower percentage of the world's population than the Black Death , which lasted for many more years. The recent COVID-19 pandemic is estimated to have killed 17.5 - 31.4 million. Despite the toll of the pandemic, it was never a large theme in American literature. Alfred Crosby suspects that it may be due to the fact that it occurred after World War I, which was the most important event in that generation's lives. Katherine Anne Porter 's 1939 novella Pale Horse, Pale Rider is one of the most well-known fictional accounts of the pandemic. The 2006 novel The Last Town on Earth focuses on a town which attempts to limit the spread of the flu by preventing people from entering or leaving. The Pull of the Stars is a 2020 novel by Emma Donoghue set in Dublin during the Spanish flu. Its final draft was submitted in March 2020, and publishers fast-tracked publication because of the then ongoing COVID-19 pandemic . The Spanish flu killed a much lower percentage of the world's population than the Black Death , which lasted for many more years. The recent COVID-19 pandemic is estimated to have killed 17.5 - 31.4 million. The origin of the Spanish flu pandemic, and the relationship between the near-simultaneous outbreaks in humans and swine, have been controversial. One hypothesis is that the virus strain originated at Fort Riley, Kansas, in viruses in poultry and swine which the fort bred for food; the soldiers were then sent from Fort Riley around the world, where they spread the disease. Similarities between a reconstruction of the virus and avian viruses, combined with the human pandemic preceding the first reports of influenza in swine, led researchers to conclude the influenza virus jumped directly from birds to humans, and swine caught the disease from humans. Others have disagreed, and more recent research has suggested the strain may have originated in a nonhuman, mammalian species. An estimated date for its appearance in mammalian hosts has been put at the period 1882–1913. This ancestor virus diverged about 1913–1915 into two clades (or biological groups each descended from a common ancestor), which gave rise to the classical swine and human H1N1 influenza lineages. The last common ancestor of human strains dates between February 1917 and April 1918. Because pigs are more readily infected with avian influenza viruses than are humans, they were suggested as the original recipients of the virus, passing the virus to humans sometime between 1913 and 1918. An effort to recreate the Spanish flu strain (a subtype of avian strain H1N1) was a collaboration among the Armed Forces Institute of Pathology , the USDA ARS Southeast Poultry Research Laboratory, and Mount Sinai School of Medicine in New York City. The effort resulted in the announcement (on 5 October 2005) that the group had successfully determined the virus' genetic sequence , using historic tissue samples recovered by pathologist Johan Hultin from an Inuit female flu victim buried in the Alaskan permafrost and samples preserved from American soldiers Roscoe Vaughan and James Downs. On 18 January 2007, Kobasa et al. (2007) reported that monkeys ( Macaca fascicularis ) infected with the recreated flu strain exhibited classic symptoms of the 1918 pandemic, and died from cytokine storms – an overreaction of the immune system. This may explain why the Spanish flu had its surprising effect on younger, healthier people, as a person with a stronger immune system would potentially have a stronger overreaction. On 16 September 2008, the body of British politician and diplomat Sir Mark Sykes was exhumed to study the RNA of the flu virus in efforts to understand the genetic structure of modern H5N1 bird flu. Sykes had been buried in 1919 in a lead coffin which scientists hoped had helped preserve the virus. The coffin was found to be split and the cadaver badly decomposed; nonetheless, samples of lung and brain tissue were taken. In December 2008, research by Yoshihiro Kawaoka of the University of Wisconsin linked the presence of three specific genes (termed PA, PB1, and PB2) and a nucleoprotein derived from Spanish flu samples to the ability of the flu virus to invade the lungs and cause pneumonia. The combination triggered similar symptoms in animal testing. In June 2010, a team at the Mount Sinai School of Medicine reported the 2009 flu pandemic vaccine provided some cross-protection against the Spanish flu pandemic strain. One of the few things known for certain about influenza in 1918 and for some years after was that it was, except in the laboratory, exclusively a disease of human beings. In 2013, the AIR Worldwide Research and Modeling Group "characterized the historic 1918 pandemic and estimated the effects of a similar pandemic occurring today using the AIR Pandemic Flu Model". In the model, "a modern-day 'Spanish flu' event would result in additional life insurance losses of between US$15.3–27.8 billion in the United States alone", with 188,000–337,000 deaths in the United States. In 2018, Michael Worobey, an evolutionary biology professor at the University of Arizona who is examining the history of the 1918 pandemic, revealed that he obtained tissue slides created by William Rolland, a physician who reported on a respiratory illness likely to be the virus while a pathologist in the British military during World War One. Rolland had authored an article in the Lancet during 1917 about a respiratory illness outbreak beginning in 1916 in Étaples, France. Worobey traced recent references to that article to family members who had retained slides that Rolland had prepared during that time. Worobey extracted tissue from the slides to potentially reveal more about the origin of the pathogen. In 2021 an investigation used the virus sequence to obtain the Hemagglutinin (HA) antigen and observe the adaptive immunity in 32 survivors of the 1918 flu pandemic, all of them presented seroreactivity and 7 of 8 further tested presented memory B cells able to produce antibodies that bound to the HA antigen highlighting the ability of the immunological memory many decades after.The high mortality rate of the influenza pandemic is one aspect that sets the pandemic apart from other disease outbreaks. Another factor is the higher mortality rate of men compared with women. Men with an underlying condition were at significantly more risk. Tuberculosis was one of the deadliest diseases in the 1900s, and killed more men than women. But with the spread of influenza disease, the cases of tuberculosis cases in men decreased. Many scholars have noted that tuberculosis increased the mortality rate of influenza in males, decreasing their life expectancy. During the 1900s tuberculosis was more common in males than females, but studies show that when influenza spread the tuberculosis mortality rate among females changed. The death rate of tuberculosis in females increased significantly and would continue to decline until post-pandemic. Death rates were particularly high in those aged 20–35. The only comparable disease to this was the Black Death , or bubonic plague , in the 1300s. As other studies have shown, tuberculosis and influenza had comorbidities and one affected the other. The ages of males dying of the flu show that tuberculosis was a factor, and as males primarily had this disease at the time of the pandemic, they had a higher mortality rate. Life expectancy dropped in males during the pandemic but then increased two years after the pandemic. One major cause of the spread of influenza was social behavior. Men had more social variation and were mobile more than women due to their work. Even though there was a higher mortality rate in males, each region showed different results, due to such factors as nutritional deficiency . In Newfoundland , the pandemic spread was highly variable. Influenza did not discriminate who was infected, indeed it attacked the socioeconomic status of people. Although social variability allowed the disease to move quickly geographically, it tended to spread faster and affect men more than women due to labor and social contact. Newfoundland's leading cause of death before the pandemic was tuberculosis and this is known to be a severe underlying condition for people and increases the |mortality rate when infected by the influenza disease. There was diverse labor in Newfoundland, men and women had various occupations that involved day-to-day interaction. But, fishing had a major role in the economy and so males were more mobile than females and had more contact with other parts of the world. The spread of the pandemic is known to have begun in the spring of 1918, but Newfoundland did not see the deadly wave until June or July, which aligns with the high demand for employment in the fishery. The majority of men were working along the coast during the summer and it was typical for entire families to move to Newfoundland and work. Studies show a much higher mortality rate in males compared with females. But, during the first, second, and third waves of the pandemic, the mortality shifted. During the first wave, men had a higher mortality rate, but the mortality rate of females increased and was higher during the second and third waves. The female population was larger in certain regions of Newfoundland and therefore had a bigger impact on the death rate. Records indicate the most deaths during the first wave of the pandemic were among young men in their 20s, which reflects the age of enlistment in the war. The mobility of young men during 1918 was linked to the spread of influenza and the biggest wave of the epidemic. In late 1917 and throughout 1918, thousands of male troops gathered at the Halifax port before heading to Europe. Any soldier that was ill and could not depart was added to the population of Halifax , which increased the case rate of influenza among men during the war . To determine the cause of the death during the pandemic, war scientists used the Commonwealth War Graves Commission (CWGC), which reported under 2 million men and women died during the wars, with a record of those who died from 1917 to 1918. The movement of soldiers during this time and the transportation from United States between Canada likely had a significant effect on the spread of the pandemic. One major cause of the spread of influenza was social behavior. Men had more social variation and were mobile more than women due to their work. Even though there was a higher mortality rate in males, each region showed different results, due to such factors as nutritional deficiency . In Newfoundland , the pandemic spread was highly variable. Influenza did not discriminate who was infected, indeed it attacked the socioeconomic status of people. Although social variability allowed the disease to move quickly geographically, it tended to spread faster and affect men more than women due to labor and social contact. Newfoundland's leading cause of death before the pandemic was tuberculosis and this is known to be a severe underlying condition for people and increases the |mortality rate when infected by the influenza disease. There was diverse labor in Newfoundland, men and women had various occupations that involved day-to-day interaction. But, fishing had a major role in the economy and so males were more mobile than females and had more contact with other parts of the world. The spread of the pandemic is known to have begun in the spring of 1918, but Newfoundland did not see the deadly wave until June or July, which aligns with the high demand for employment in the fishery. The majority of men were working along the coast during the summer and it was typical for entire families to move to Newfoundland and work. Studies show a much higher mortality rate in males compared with females. But, during the first, second, and third waves of the pandemic, the mortality shifted. During the first wave, men had a higher mortality rate, but the mortality rate of females increased and was higher during the second and third waves. The female population was larger in certain regions of Newfoundland and therefore had a bigger impact on the death rate. Records indicate the most deaths during the first wave of the pandemic were among young men in their 20s, which reflects the age of enlistment in the war. The mobility of young men during 1918 was linked to the spread of influenza and the biggest wave of the epidemic. In late 1917 and throughout 1918, thousands of male troops gathered at the Halifax port before heading to Europe. Any soldier that was ill and could not depart was added to the population of Halifax , which increased the case rate of influenza among men during the war . To determine the cause of the death during the pandemic, war scientists used the Commonwealth War Graves Commission (CWGC), which reported under 2 million men and women died during the wars, with a record of those who died from 1917 to 1918. The movement of soldiers during this time and the transportation from United States between Canada likely had a significant effect on the spread of the pandemic. Records indicate the most deaths during the first wave of the pandemic were among young men in their 20s, which reflects the age of enlistment in the war. The mobility of young men during 1918 was linked to the spread of influenza and the biggest wave of the epidemic. In late 1917 and throughout 1918, thousands of male troops gathered at the Halifax port before heading to Europe. Any soldier that was ill and could not depart was added to the population of Halifax , which increased the case rate of influenza among men during the war . To determine the cause of the death during the pandemic, war scientists used the Commonwealth War Graves Commission (CWGC), which reported under 2 million men and women died during the wars, with a record of those who died from 1917 to 1918. The movement of soldiers during this time and the transportation from United States between Canada likely had a significant effect on the spread of the pandemic.

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Avian influenza

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Influenza A virus subtype H10N7

Influenza A virus subtype H10N7 (A/H10N7) is a subtype of the species Influenza A virus (sometimes called bird flu virus). H10N7 was first reported in humans in Egypt in 2004. It caused illness in two one-year-old infants, and residents of Ismailia, Egypt; one child's father, and a poultry merchant. The first reported H10N7 outbreak in the US occurred in Minnesota on two turkey farms in 1979 and on a third in 1980. "The clinical signs ranged from severe, with a mortality rate as high as 31%, to subclinical. Antigenically indistinguishable viruses were isolated from healthy mallards on a pond adjacent to the turkey farms". The Influenza A (H10N7) virus was also held responsible for an increased mortality of harbour seals ( Phoca vitulina ) in Europe in 2014. First cases were reported in spring 2014 in Sweden and subsequently spread to Denmark. Within a few months the virus spread to the Wadden Sea area of Germany and the Netherlands causing the death of about 10% of the local harbour seal population.

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Avian influenza

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Influenza treatment

Treatments for influenza include a range of medications and therapies that are used in response to disease influenza . Treatments may either directly target the influenza virus itself; or instead they may just offer relief to symptoms of the disease, while the body's own immune system works to recover from infection. The main classes of antiviral drugs used against influenza are neuraminidase inhibitors , such as zanamivir and oseltamivir , polymerase acidic endonuclease inhibitors such as baloxavir marboxil , or inhibitors of the viral M2 protein , such as amantadine and rimantadine . These drugs can reduce the severity of symptoms if taken soon after infection and can also be taken to decrease the risk of infection. However, virus strains have emerged that show drug resistance to some classes of drug.The United States authority on disease prevention, the Centers for Disease Control and Prevention (CDC), recommends that people with influenza infections: Stay at home Get plenty of rest Drink a lot of liquids Do not smoke or drink alcohol Consider over-the-counter medications to relieve flu symptoms Consult a physician early on for best possible treatment Remain alert for emergency warning signs Warning signs are symptoms that indicate that the disease is becoming serious and needs immediate medical attention. These include: [ citation needed ] Difficulty breathing or shortness of breath Pain or pressure in the chest or abdomen Dizziness Confusion Severe or persistent vomiting In children other warning signs include irritability, failing to wake up and interact, rapid breathing, and a blueish skin color. Another warning sign in children is if the flu symptoms appear to resolve, but then reappear with fever and a bad cough. Antiviral drugs directly target the viruses responsible for influenza infections. Generally, anti-viral drugs work optimally when taken within a few days of the onset of symptoms. Certain drugs are used prophylactically , that is they are used in uninfected individuals to guard against infection. [ medical citation needed ] Four licensed influenza antiviral agents are available in the United States: zanamivir , oseltamivir phosphate , peramivir , and baloxavir marboxil . They are available through prescription only. In Russia and China a drug called arbidol is also used as a treatment. Testing of the drug has predominantly occurred in these countries and, although no clinical trials have been published demonstrating this is an effective drug, some data suggest that this could be a useful treatment for influenza. Interferons are cellular signalling factors produced in response to viral infection. Research into the use of interferons to combat influenza began in the 1960s in the Soviet Union , culminating in a trial of 14,000 subjects at the height of the Hong Kong Flu of 1969, in which those treated prophylactically with interferon were more than 50% less likely to suffer symptoms, though evidence of latent infection was present. In these early studies leukocytes were collected from donated blood and exposed to a high dose of Newcastle disease , causing them to release interferons. Although interferon therapies became widespread in the Soviet Union, the method was doubted in the United States after high doses of interferon proved ineffective in trials. Though the 1969 study used 256 units of interferon, subsequent studies used up to 8.4 million units. It has since been proposed that activity of interferon is highest at low concentrations. Phase III trials in Australia are planned for 2010, and initial trials are planned in the U.S. for late 2009. Interferons have also been investigated as adjuvants to enhance to effectiveness of influenza vaccines . This work was based on experiments in mice that suggested that type I interferons could enhance the effectiveness of influenza vaccines in mice. However, a clinical trial in 2008 found that oral dosing of elderly patients with interferon-alpha actually reduced their immune response to an influenza vaccine. Viferon is a suppository of (non- pegylated ) interferon alpha -2b, ascorbic acid (vitamin C), and tocopherol (vitamin E) which was reported in two small studies to be as effective as arbidol. Another interferon alfa-2b medicine, "Grippferon", nasal drops, is used for treatment and emergency prevention of Influenza and cold. Its manufacturers have appealed to the WHO to consider its use against avian influenza and H1N1 Influenza 09 (Human Swine Flu), stating that it was used successfully in Russia for eight years, but that "the medical profession in Europe and the USA is not informed about this medicine". Interferons are cellular signalling factors produced in response to viral infection. Research into the use of interferons to combat influenza began in the 1960s in the Soviet Union , culminating in a trial of 14,000 subjects at the height of the Hong Kong Flu of 1969, in which those treated prophylactically with interferon were more than 50% less likely to suffer symptoms, though evidence of latent infection was present. In these early studies leukocytes were collected from donated blood and exposed to a high dose of Newcastle disease , causing them to release interferons. Although interferon therapies became widespread in the Soviet Union, the method was doubted in the United States after high doses of interferon proved ineffective in trials. Though the 1969 study used 256 units of interferon, subsequent studies used up to 8.4 million units. It has since been proposed that activity of interferon is highest at low concentrations. Phase III trials in Australia are planned for 2010, and initial trials are planned in the U.S. for late 2009. Interferons have also been investigated as adjuvants to enhance to effectiveness of influenza vaccines . This work was based on experiments in mice that suggested that type I interferons could enhance the effectiveness of influenza vaccines in mice. However, a clinical trial in 2008 found that oral dosing of elderly patients with interferon-alpha actually reduced their immune response to an influenza vaccine. Viferon is a suppository of (non- pegylated ) interferon alpha -2b, ascorbic acid (vitamin C), and tocopherol (vitamin E) which was reported in two small studies to be as effective as arbidol. Another interferon alfa-2b medicine, "Grippferon", nasal drops, is used for treatment and emergency prevention of Influenza and cold. Its manufacturers have appealed to the WHO to consider its use against avian influenza and H1N1 Influenza 09 (Human Swine Flu), stating that it was used successfully in Russia for eight years, but that "the medical profession in Europe and the USA is not informed about this medicine". Influenza viruses can show resistance to anti-viral drugs. Like the development of bacterial antibiotic resistance , this can result from over-use of these drugs. For example, a study published in the June 2009 Issue of Nature Biotechnology emphasized the urgent need for augmentation of oseltamivir (Tamiflu) stockpiles with additional antiviral drugs including zanamivir (Relenza) based on an evaluation of the performance of these drugs in the scenario that the 2009 H1N1 'Swine Flu' neuraminidase (NA) were to acquire the tamiflu-resistance (His274Tyr) mutation which is currently widespread in seasonal H1N1 strains. Yet another example is in the case of the amantadines treatment may lead to the rapid production of resistant viruses, and over-use of these drugs has probably contributed to the spread of resistance. In particular, this high-level of resistance may be due to the easy availability of amantadines as part of over-the-counter cold remedies in countries such as China and Russia, and their use to prevent outbreaks of influenza in farmed poultry. On the other hand, a few strains resistant to neuraminidase inhibitors have emerged and circulated in the absence of much use of the drugs involved, and the frequency with which drug resistant strains appears shows little correlation with the level of use of these drugs. However, laboratory studies have shown that it is possible for the use of sub-optimal doses of these drugs as a prophylactic measure might contribute to the development of drug resistance. During the United States 2005–2006 influenza season, increasing incidence of drug resistance by strain H3N2 to amantadine and rimantadine led the CDC to recommend oseltamivir as a prophylactic drug, and the use of either oseltamivir or zanamivir as treatment. Antiviral drugs are prescription-only medication in the United States. Readily available over-the-counter medications do not directly affect the disease, but they do provide relief from influenza symptoms, as illustrated in the table below. Children and teenagers with flu symptoms (particularly fever) should avoid taking aspirin as taking aspirin in the presence of influenza infection (especially Influenzavirus B ) can lead to Reye syndrome , a rare but potentially fatal disease of the brain. Several generic prescription medications might prove useful to treat a potential H5N1 avian flu outbreak, including statins , fibrates , and chloroquine . Malnutrition can reduce the ability of the body to resist infections and is a common cause of immunodeficiency in the developing world. For instance, in a study in Ecuador , micronutrient deficiencies were found to be common in the elderly, especially for vitamin C , vitamin D , vitamin B-6 , vitamin B-12 , folic acid , and zinc , and these are thought to weaken the immune system or cause anemia and thus place people at greater risk of respiratory infections such as influenza. Seasonal variation in sunlight exposure, which is required for vitamin D synthesis within the body, has been proposed as one of the factors accounting for the seasonality of influenza. A meta-analysis of 13 studies indicated some support for adjunctive vitamin D therapy for influenza, but called for more rigorous clinical trials to settle the issue conclusively. A recent review discussing herbal and alternative medicines in influenza treatment details evidence suggesting that N-acetylcysteine , elderberry , or a combination of Eleutherococcus senticosus and Andrographis paniculata may help to shorten the course of influenza infection. The article cites more limited evidence including animal or in vitro studies to suggest possible benefit from vitamin C, DHEA , high lactoferrin whey protein , Echinacea spp., Panax quinquefolium , Larix occidentalis arabinogalactans , elenolic acid (a constituent of olive leaf extract ), Astragalus membranaceus , and Isatis tinctoria or Isatis indigotica . Another review assessed the quality of evidence for alternative influenza treatments, it concluded that there was "no compelling evidence" that any of these treatments were effective and that the available data on these products is particularly weak, with trials in this area suffering from many shortcomings, such as being small and poorly-designed and not testing for adverse effects. The activity of N-acetylcysteine (NAC) against influenza was first suggested in 1966. In 1997 a randomized clinical trial found that volunteers taking 1.2 grams of N-acetylcysteine daily for six months were as likely as those taking placebo to be infected by influenza, but only 25% of them experienced clinical symptoms, as contrasted with 67% of the control group . The authors concluded that resistance to flu symptoms was associated with a shift in cell mediated immunity from anergy toward normoergy , as measured by the degree of skin reactivity to seven common antigens such as tetanus and Candida albicans . Several animal studies found that in a mouse model of lethal infection with a high dose of influenza, oral supplementation with one gram of N-acetylcysteine per kilogram of body weight daily increased the rate of survival, either when administered alone or in combination with the antiviral drugs ribavirin or oseltamivir. NAC was shown to block or reduce cytopathic effects in influenza-infected macrophages, to reduce DNA fragmentation ( apoptosis ) in equine influenza-infected canine kidney cells, and to reduce RANTES production in cultured airway cells in response to influenza virus by 18%. The compound has been proposed for treatment of influenza. A few news reports have suggested the use of an elderberry ( Sambucus nigra ) extract as a potential preventative against the 2009 flu pandemic . The preparation has been reported to reduce the duration of influenza symptoms by raising levels of cytokines. However, the use of the preparation has been described as "imprudent" when an influenza strain causes death in healthy adults by cytokine storm leading to primary viral pneumonia. The manufacturer cites a lack of evidence for cytokine-related risks, but labels the product only as an antioxidant and food supplement . The mixture of Eleutherococcus senticosus ("Siberian ginseng") and Andrographis paniculata , sold under the trade name Kan Jang, was reported in the Journal of Herbal Pharmacotherapy to outperform amantadine in reducing influenza-related sick time and complications in a Volgograd pilot study of 71 patients in 2003. Prior to this, an extract of Eleutherococcus senticosus was shown to inhibit replication of RNA but not DNA viruses in vitro . Among nine Chinese medicinal herbs tested, Andrographis paniculata was shown to be most effective in inhibiting RANTES secretion by H1N1 influenza infected cells in cell culture , with an IC 50 for the ethanol extract of 1.2 milligrams per liter. High dietary intake of green tea (specifically, catechins and theanine that is found in tea products) has been correlated with reduced risk of contracting influenza, as well as having an antiviral effect upon types A and B. Specifically, the high levels of epigallocatechin gallate, epicatechin gallate, and epigallocatechin present in green tea were found to inhibit influenza virus replication. Additionally, topical application has been suggested to possibly act as a mild disinfectant. Regular dietary intake of green tea has been associated with stronger immune response to infection, through the enhancement of T-Cell function. The activity of N-acetylcysteine (NAC) against influenza was first suggested in 1966. In 1997 a randomized clinical trial found that volunteers taking 1.2 grams of N-acetylcysteine daily for six months were as likely as those taking placebo to be infected by influenza, but only 25% of them experienced clinical symptoms, as contrasted with 67% of the control group . The authors concluded that resistance to flu symptoms was associated with a shift in cell mediated immunity from anergy toward normoergy , as measured by the degree of skin reactivity to seven common antigens such as tetanus and Candida albicans . Several animal studies found that in a mouse model of lethal infection with a high dose of influenza, oral supplementation with one gram of N-acetylcysteine per kilogram of body weight daily increased the rate of survival, either when administered alone or in combination with the antiviral drugs ribavirin or oseltamivir. NAC was shown to block or reduce cytopathic effects in influenza-infected macrophages, to reduce DNA fragmentation ( apoptosis ) in equine influenza-infected canine kidney cells, and to reduce RANTES production in cultured airway cells in response to influenza virus by 18%. The compound has been proposed for treatment of influenza. A few news reports have suggested the use of an elderberry ( Sambucus nigra ) extract as a potential preventative against the 2009 flu pandemic . The preparation has been reported to reduce the duration of influenza symptoms by raising levels of cytokines. However, the use of the preparation has been described as "imprudent" when an influenza strain causes death in healthy adults by cytokine storm leading to primary viral pneumonia. The manufacturer cites a lack of evidence for cytokine-related risks, but labels the product only as an antioxidant and food supplement . The mixture of Eleutherococcus senticosus ("Siberian ginseng") and Andrographis paniculata , sold under the trade name Kan Jang, was reported in the Journal of Herbal Pharmacotherapy to outperform amantadine in reducing influenza-related sick time and complications in a Volgograd pilot study of 71 patients in 2003. Prior to this, an extract of Eleutherococcus senticosus was shown to inhibit replication of RNA but not DNA viruses in vitro . Among nine Chinese medicinal herbs tested, Andrographis paniculata was shown to be most effective in inhibiting RANTES secretion by H1N1 influenza infected cells in cell culture , with an IC 50 for the ethanol extract of 1.2 milligrams per liter. High dietary intake of green tea (specifically, catechins and theanine that is found in tea products) has been correlated with reduced risk of contracting influenza, as well as having an antiviral effect upon types A and B. Specifically, the high levels of epigallocatechin gallate, epicatechin gallate, and epigallocatechin present in green tea were found to inhibit influenza virus replication. Additionally, topical application has been suggested to possibly act as a mild disinfectant. Regular dietary intake of green tea has been associated with stronger immune response to infection, through the enhancement of T-Cell function. An alternative to vaccination used in the 1918 flu pandemic was the direct transfusion of blood, plasma, or serum from recovered patients. Though medical experiments of the era lacked some procedural refinements, eight publications from 1918 to 1925 reported that the treatment could approximately halve the mortality in hospitalized severe cases with an average case-fatality rate of 37% when untreated. Bovine colostrum might also serve as a source of antibodies for some applications. Human T lymphocytes can be expanded in vitro using beads holding specific antigens to activate the cells and stimulate growth. Clonal populations of CD8+ cytotoxic T cells have been grown which carry T cell receptors specific to influenza. These work much like antibodies but are permanently bound to these cells. (See cellular immunity ) . High concentrations of N-acetylcysteine have been used to enhance growth of these cells. This method is still in early research. An alternative to vaccination used in the 1918 flu pandemic was the direct transfusion of blood, plasma, or serum from recovered patients. Though medical experiments of the era lacked some procedural refinements, eight publications from 1918 to 1925 reported that the treatment could approximately halve the mortality in hospitalized severe cases with an average case-fatality rate of 37% when untreated. Bovine colostrum might also serve as a source of antibodies for some applications. Human T lymphocytes can be expanded in vitro using beads holding specific antigens to activate the cells and stimulate growth. Clonal populations of CD8+ cytotoxic T cells have been grown which carry T cell receptors specific to influenza. These work much like antibodies but are permanently bound to these cells. (See cellular immunity ) . High concentrations of N-acetylcysteine have been used to enhance growth of these cells. This method is still in early research.

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Avian influenza

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Poultry disease

Poultry diseases occur in poultry , which are domesticated birds kept for their meat, eggs or feathers. Poultry species include the chicken , turkey , duck , goose and ostrich .

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Avian influenza

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Influenza A virus subtype H5N3

H5N3 is a subtype of the species Influenza A virus (sometimes called the bird flu virus).H5N3 was identified in Quebec in August 2005 and in Sweden in October 2005. H5N3 virus was identified at a farm in La Garnache , France in late January 2009. Ninety birds were found dead between 29 January 2009 and 31 January 2009. The remaining stock of 4,932 birds was culled on 1 February 2009. In Germany, in December 2013, 102 ostriches and 28 chickens in a farm in Blumberg were slaughtered due to suspicion of infection with avian influenza. Samples showed that the birds were infected with the H5N3 virus.

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Avian influenza

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Swine influenza

Swine influenza is an infection caused by any of several types of swine influenza viruses . Swine influenza virus ( SIV ) or swine-origin influenza virus ( S-OIV ) refers to any strain of the influenza family of viruses that is endemic in pigs . As of 2009, identified SIV strains include influenza C and the subtypes of influenza A known as H1N1 , H1N2 , H2N1, H3N1 , H3N2 , and H2N3 . The swine influenza virus is common throughout pig populations worldwide. Transmission of the virus from pigs to humans is rare and does not always lead to human illness, often resulting only in the production of antibodies in the blood. If transmission causes human illness, it is called a zoonotic swine flu. People with regular exposure to pigs are at increased risk of swine flu infections. Around the mid-20th century, the identification of influenza subtypes was made possible, allowing accurate diagnosis of transmission to humans. Since then, only 50 such transmissions have been confirmed. These strains of swine flu rarely pass from human to human. Symptoms of zoonotic swine flu in humans are similar to those of influenza and influenza-like illness and include chills , fever , sore throat , muscle pains , severe headache , coughing , weakness , shortness of breath, and general discomfort . It is estimated that, in the 2009 flu pandemic , 11–21% of the then global population (of about 6.8 billion), equivalent to around 700 million to 1.4 billion people, contracted the illness—more, in absolute terms, than the Spanish flu pandemic . [ citation needed ] There were 18,449 confirmed fatalities. However, in a 2012 study, the CDC estimated more than 284,000 possible fatalities worldwide, with numbers ranging from 150,000 to 575,000. In August 2010, the World Health Organization declared the swine flu pandemic officially over. Subsequent cases of swine flu were reported in India in 2015, with over 31,156 positive test cases and 1,841 deaths .In pigs, a swine influenza infection produces fever , lethargy , discharge from the nose or eyes, sneezing , coughing , difficulty breathing , eye redness or inflammation, and decreased appetite. In some cases, the infection can cause miscarriage . However, infected pigs may not exhibit any symptoms. Although mortality is usually low (around 1–4%), the virus can cause weight loss and poor growth , in turn causing economic loss to farmers. Infected pigs can lose up to 12 pounds of body weight over a three- to four-week period. Influenza A is responsible for infecting swine and was first identified in 1918. Because both avian and mammalian influenza viruses can bind to receptors in pigs, pigs have often been seen as "mixing vessels", facilitating the evolution of strains that can be passed on to other mammals, such as humans. Direct transmission of a swine flu virus from pigs to humans is possible ( zoonotic swine flu). Fifty cases are known to have occurred since the first report in medical literature in 1958, which have resulted in a total of six deaths. Of these six people, one was pregnant, one had leukemia , one had Hodgkin's lymphoma , and two were known to be previously healthy. No medical history was reported for the remaining case The true rate of infection may be higher, as most cases only cause a very mild disease and may never be reported or diagnosed. According to the United States Centers for Disease Control and Prevention (CDC), in humans the symptoms of the 2009 "swine flu" H1N1 virus are similar to influenza and influenza-like illness . Symptoms include fever , cough , sore throat , watery eyes, body aches, shortness of breath, headache , weight loss, chills , sneezing, runny nose, coughing, dizziness, abdominal pain, lack of appetite, and fatigue . During the 2009 outbreak, an elevated percentage of patients reporting diarrhea and vomiting . Because these symptoms are not specific to swine flu, a differential diagnosis of probable swine flu requires not only symptoms, but also a high likelihood of swine flu due to the person's recent and past medical history. For example, during the 2009 swine flu outbreak in the United States , the CDC advised physicians to "consider swine influenza infection in the differential diagnosis of patients with acute febrile respiratory illness who have either been in contact with persons with confirmed swine flu, or who were in one of the five U.S. states that have reported swine flu cases or in Mexico during the seven days preceding their illness onset." A diagnosis of confirmed swine flu requires laboratory testing of a respiratory sample (a simple nose and throat swab). The most common cause of death is respiratory failure . Other causes of death are pneumonia (leading to sepsis ), high fever (leading to neurological problems), dehydration (from excessive vomiting and diarrhea ), electrolyte imbalance and kidney failure . Fatalities are more likely in young children and the elderly.Direct transmission of a swine flu virus from pigs to humans is possible ( zoonotic swine flu). Fifty cases are known to have occurred since the first report in medical literature in 1958, which have resulted in a total of six deaths. Of these six people, one was pregnant, one had leukemia , one had Hodgkin's lymphoma , and two were known to be previously healthy. No medical history was reported for the remaining case The true rate of infection may be higher, as most cases only cause a very mild disease and may never be reported or diagnosed. According to the United States Centers for Disease Control and Prevention (CDC), in humans the symptoms of the 2009 "swine flu" H1N1 virus are similar to influenza and influenza-like illness . Symptoms include fever , cough , sore throat , watery eyes, body aches, shortness of breath, headache , weight loss, chills , sneezing, runny nose, coughing, dizziness, abdominal pain, lack of appetite, and fatigue . During the 2009 outbreak, an elevated percentage of patients reporting diarrhea and vomiting . Because these symptoms are not specific to swine flu, a differential diagnosis of probable swine flu requires not only symptoms, but also a high likelihood of swine flu due to the person's recent and past medical history. For example, during the 2009 swine flu outbreak in the United States , the CDC advised physicians to "consider swine influenza infection in the differential diagnosis of patients with acute febrile respiratory illness who have either been in contact with persons with confirmed swine flu, or who were in one of the five U.S. states that have reported swine flu cases or in Mexico during the seven days preceding their illness onset." A diagnosis of confirmed swine flu requires laboratory testing of a respiratory sample (a simple nose and throat swab). The most common cause of death is respiratory failure . Other causes of death are pneumonia (leading to sepsis ), high fever (leading to neurological problems), dehydration (from excessive vomiting and diarrhea ), electrolyte imbalance and kidney failure . Fatalities are more likely in young children and the elderly.Influenza is common in pigs. About half of breeding pigs in the USA have been exposed to the virus. Antibodies to the virus are also common in pigs in other countries. The main route of transmission is through direct contact between infected and uninfected animals. These close contacts are particularly common during animal transport. Intensive farming may also increase the risk of transmission, as the pigs are raised in very close proximity to each other. Direct transfer of the virus probably occurs though pigs touching noses or through dried mucus. Airborne transmission through the aerosols produced by pigs coughing or sneezing are also an important means of infection. The virus usually spreads quickly through a herd, infecting all the pigs within just a few days. Transmission may also occur through wild animals, such as wild boar , which can spread the disease between farms. People who work with poultry and swine, especially those with intense exposures, are at increased risk of zoonotic infection with influenza virus endemic in these animals, and constitute a population of human hosts in which zoonosis and reassortment can co-occur. Vaccination of these workers against influenza and surveillance for new influenza strains among this population may therefore be an important public health measure. Transmission of influenza from swine to humans who work with swine was documented in a small surveillance study performed in 2004 at the University of Iowa. This study, among others, forms the basis of a recommendation that people whose jobs involve handling poultry and swine be the focus of increased public health surveillance. Other professions at particular risk of infection are veterinarians and meat processing workers, although the risk of infection for both of these groups is lower than that of farm workers. Pigs are unusual because they can be infected with influenza strains that usually infect three different species: pigs, birds, and humans. Within pigs, influenza viruses may exchange genes and produce novel strains. Avian influenza virus H3N2 is endemic in pigs in China and has been detected in pigs in Vietnam, increasing fears of the emergence of new variant strains. H3N2 evolved from H2N2 by antigenic shift . In August 2004, researchers in China found H5N1 in pigs. These H5N1 infections may be common. In a survey of 10 apparently healthy pigs housed near poultry farms in West Java , where avian flu had broken out, five of the pig samples contained the H5N1 virus. The Indonesian government found similar results in the same region, though additional tests of 150 pigs outside the area were negative. The influenza virion is roughly spherical. It is an enveloped virus; the outer layer is a lipid membrane which is taken from the host cell in which the virus multiplies. Inserted into the lipid membrane are glycoprotein "spikes" of hemagglutinin (HA) and neuraminidase (NA). The combination of HA and NA proteins determine the subtype of influenza virus (A/H1N1, for example). HA and NA are important in the immune response against the virus, and antibodies against these spikes may protect against infection. The antiviral drugs Relenza and Tamiflu target NA by inhibiting neuraminidase and preventing the release of viruses from host cells. Also embedded in the lipid membrane is the M2 protein , which is the target of the antiviral adamantanes amantadine and rimantadine . Of the three genera of influenza viruses that cause human flu , two also cause influenza in pigs, with influenza A being common in pigs and influenza C being rare. Influenza B has not been reported in pigs. Within influenza A and influenza C, the strains found in pigs and humans are largely distinct, although because of reassortment there have been transfers of genes among strains crossing swine, avian, and human species boundaries. Influenza viruses infect both humans and pigs, but do not infect birds. Transmission between pigs and humans have occurred in the past. For example, influenza C caused small outbreaks of a mild form of influenza amongst children in Japan and California. As a result of the limited host range and lack of genetic diversity in influenza C, this form of influenza does not cause pandemics in humans. Swine influenza is caused by influenza A subtypes H1N1 , H1N2 , H2N3 , H3N1 , and H3N2 . In pigs, four influenza A virus subtypes (H1N1, H1N2, H3N2 and H7N9) are the most common strains worldwide. In the United States , the H1N1 subtype was exclusively prevalent among swine populations before 1998. Since late August 1998, H3N2 subtypes have been isolated from pigs. As of 2004, H3N2 virus isolates in US swine and turkey stocks were triple reassortants , containing genes from human (HA, NA, and PB1), swine (NS, NP, and M), and avian (PB2 and PA) lineages. In August 2012, the Center for Disease Control and Prevention confirmed 145 human cases (113 in Indiana, 30 in Ohio, one in Hawaii and one in Illinois) of H3N2v since July 2012. The death of a 61-year-old Madison County, Ohio woman is the first in the USA associated with a new swine flu strain. She contracted the illness after having contact with hogs at the Ross County Fair. Influenza is common in pigs. About half of breeding pigs in the USA have been exposed to the virus. Antibodies to the virus are also common in pigs in other countries. The main route of transmission is through direct contact between infected and uninfected animals. These close contacts are particularly common during animal transport. Intensive farming may also increase the risk of transmission, as the pigs are raised in very close proximity to each other. Direct transfer of the virus probably occurs though pigs touching noses or through dried mucus. Airborne transmission through the aerosols produced by pigs coughing or sneezing are also an important means of infection. The virus usually spreads quickly through a herd, infecting all the pigs within just a few days. Transmission may also occur through wild animals, such as wild boar , which can spread the disease between farms. People who work with poultry and swine, especially those with intense exposures, are at increased risk of zoonotic infection with influenza virus endemic in these animals, and constitute a population of human hosts in which zoonosis and reassortment can co-occur. Vaccination of these workers against influenza and surveillance for new influenza strains among this population may therefore be an important public health measure. Transmission of influenza from swine to humans who work with swine was documented in a small surveillance study performed in 2004 at the University of Iowa. This study, among others, forms the basis of a recommendation that people whose jobs involve handling poultry and swine be the focus of increased public health surveillance. Other professions at particular risk of infection are veterinarians and meat processing workers, although the risk of infection for both of these groups is lower than that of farm workers. Pigs are unusual because they can be infected with influenza strains that usually infect three different species: pigs, birds, and humans. Within pigs, influenza viruses may exchange genes and produce novel strains. Avian influenza virus H3N2 is endemic in pigs in China and has been detected in pigs in Vietnam, increasing fears of the emergence of new variant strains. H3N2 evolved from H2N2 by antigenic shift . In August 2004, researchers in China found H5N1 in pigs. These H5N1 infections may be common. In a survey of 10 apparently healthy pigs housed near poultry farms in West Java , where avian flu had broken out, five of the pig samples contained the H5N1 virus. The Indonesian government found similar results in the same region, though additional tests of 150 pigs outside the area were negative. Influenza is common in pigs. About half of breeding pigs in the USA have been exposed to the virus. Antibodies to the virus are also common in pigs in other countries. The main route of transmission is through direct contact between infected and uninfected animals. These close contacts are particularly common during animal transport. Intensive farming may also increase the risk of transmission, as the pigs are raised in very close proximity to each other. Direct transfer of the virus probably occurs though pigs touching noses or through dried mucus. Airborne transmission through the aerosols produced by pigs coughing or sneezing are also an important means of infection. The virus usually spreads quickly through a herd, infecting all the pigs within just a few days. Transmission may also occur through wild animals, such as wild boar , which can spread the disease between farms. People who work with poultry and swine, especially those with intense exposures, are at increased risk of zoonotic infection with influenza virus endemic in these animals, and constitute a population of human hosts in which zoonosis and reassortment can co-occur. Vaccination of these workers against influenza and surveillance for new influenza strains among this population may therefore be an important public health measure. Transmission of influenza from swine to humans who work with swine was documented in a small surveillance study performed in 2004 at the University of Iowa. This study, among others, forms the basis of a recommendation that people whose jobs involve handling poultry and swine be the focus of increased public health surveillance. Other professions at particular risk of infection are veterinarians and meat processing workers, although the risk of infection for both of these groups is lower than that of farm workers. Pigs are unusual because they can be infected with influenza strains that usually infect three different species: pigs, birds, and humans. Within pigs, influenza viruses may exchange genes and produce novel strains. Avian influenza virus H3N2 is endemic in pigs in China and has been detected in pigs in Vietnam, increasing fears of the emergence of new variant strains. H3N2 evolved from H2N2 by antigenic shift . In August 2004, researchers in China found H5N1 in pigs. These H5N1 infections may be common. In a survey of 10 apparently healthy pigs housed near poultry farms in West Java , where avian flu had broken out, five of the pig samples contained the H5N1 virus. The Indonesian government found similar results in the same region, though additional tests of 150 pigs outside the area were negative. The influenza virion is roughly spherical. It is an enveloped virus; the outer layer is a lipid membrane which is taken from the host cell in which the virus multiplies. Inserted into the lipid membrane are glycoprotein "spikes" of hemagglutinin (HA) and neuraminidase (NA). The combination of HA and NA proteins determine the subtype of influenza virus (A/H1N1, for example). HA and NA are important in the immune response against the virus, and antibodies against these spikes may protect against infection. The antiviral drugs Relenza and Tamiflu target NA by inhibiting neuraminidase and preventing the release of viruses from host cells. Also embedded in the lipid membrane is the M2 protein , which is the target of the antiviral adamantanes amantadine and rimantadine . Of the three genera of influenza viruses that cause human flu , two also cause influenza in pigs, with influenza A being common in pigs and influenza C being rare. Influenza B has not been reported in pigs. Within influenza A and influenza C, the strains found in pigs and humans are largely distinct, although because of reassortment there have been transfers of genes among strains crossing swine, avian, and human species boundaries. Influenza viruses infect both humans and pigs, but do not infect birds. Transmission between pigs and humans have occurred in the past. For example, influenza C caused small outbreaks of a mild form of influenza amongst children in Japan and California. As a result of the limited host range and lack of genetic diversity in influenza C, this form of influenza does not cause pandemics in humans. Swine influenza is caused by influenza A subtypes H1N1 , H1N2 , H2N3 , H3N1 , and H3N2 . In pigs, four influenza A virus subtypes (H1N1, H1N2, H3N2 and H7N9) are the most common strains worldwide. In the United States , the H1N1 subtype was exclusively prevalent among swine populations before 1998. Since late August 1998, H3N2 subtypes have been isolated from pigs. As of 2004, H3N2 virus isolates in US swine and turkey stocks were triple reassortants , containing genes from human (HA, NA, and PB1), swine (NS, NP, and M), and avian (PB2 and PA) lineages. In August 2012, the Center for Disease Control and Prevention confirmed 145 human cases (113 in Indiana, 30 in Ohio, one in Hawaii and one in Illinois) of H3N2v since July 2012. The death of a 61-year-old Madison County, Ohio woman is the first in the USA associated with a new swine flu strain. She contracted the illness after having contact with hogs at the Ross County Fair. Of the three genera of influenza viruses that cause human flu , two also cause influenza in pigs, with influenza A being common in pigs and influenza C being rare. Influenza B has not been reported in pigs. Within influenza A and influenza C, the strains found in pigs and humans are largely distinct, although because of reassortment there have been transfers of genes among strains crossing swine, avian, and human species boundaries.Influenza viruses infect both humans and pigs, but do not infect birds. Transmission between pigs and humans have occurred in the past. For example, influenza C caused small outbreaks of a mild form of influenza amongst children in Japan and California. As a result of the limited host range and lack of genetic diversity in influenza C, this form of influenza does not cause pandemics in humans. Swine influenza is caused by influenza A subtypes H1N1 , H1N2 , H2N3 , H3N1 , and H3N2 . In pigs, four influenza A virus subtypes (H1N1, H1N2, H3N2 and H7N9) are the most common strains worldwide. In the United States , the H1N1 subtype was exclusively prevalent among swine populations before 1998. Since late August 1998, H3N2 subtypes have been isolated from pigs. As of 2004, H3N2 virus isolates in US swine and turkey stocks were triple reassortants , containing genes from human (HA, NA, and PB1), swine (NS, NP, and M), and avian (PB2 and PA) lineages. In August 2012, the Center for Disease Control and Prevention confirmed 145 human cases (113 in Indiana, 30 in Ohio, one in Hawaii and one in Illinois) of H3N2v since July 2012. The death of a 61-year-old Madison County, Ohio woman is the first in the USA associated with a new swine flu strain. She contracted the illness after having contact with hogs at the Ross County Fair. The CDC recommends real-time PCR as the method of choice for diagnosing H1N1. The oral or nasal fluid collection and RNA virus-preserving filter-paper card is commercially available. This method allows a specific diagnosis of novel influenza (H1N1) as opposed to seasonal influenza . Near-patient point-of-care tests are in development. Prevention of swine influenza has three components: prevention in pigs, prevention of transmission to humans, and prevention of its spread among humans. Proper handwashing techniques can prevent the virus from spreading. Individuals can prevent infection by not touching the eyes, nose, or mouth, distancing from others who display symptoms of the cold or flu, and avoiding contact with others when displaying symptoms. Methods of preventing the spread of influenza among swine include facility management, herd management, and vaccination ( ATCvet code: QI09AA03 ( WHO ) ). Because much of the illness and death associated with swine flu involves secondary infection by other pathogens, control strategies that rely on vaccination may be insufficient. Control of swine influenza by vaccination has become more difficult in recent decades, as the evolution of the virus has resulted in inconsistent responses to traditional vaccines. Standard commercial swine flu vaccines are effective in controlling the infection when the virus strains match enough to have significant cross-protection, and custom (autogenous) vaccines made from the specific viruses isolated are created and used in the more difficult cases. Present vaccination strategies for SIV control and prevention in swine farms typically include the use of one of several bivalent SIV vaccines commercially available in the United States. Of the 97 recent H3N2 isolates examined, only 41 isolates had strong serologic cross-reactions with antiserum to three commercial SIV vaccines. Since the protective ability of influenza vaccines depends primarily on the closeness of the match between the vaccine virus and the epidemic virus, the presence of nonreactive H3N2 SIV variants suggests current commercial vaccines might not effectively protect pigs from infection with a majority of H3N2 viruses. The United States Department of Agriculture researchers say while pig vaccination keeps pigs from getting sick, it does not block infection or shedding of the virus. Facility management includes using disinfectants and ambient temperature to control viruses in the environment. They are unlikely to survive outside living cells for more than two weeks, except in cold (but above freezing) conditions, and are readily inactivated by disinfectants. Herd management includes not adding pigs carrying influenza to herds that have not been exposed to the virus. The virus survives in healthy carrier pigs for up to three months and can be recovered from them between outbreaks. Carrier pigs are usually responsible for the introduction of SIV into previously uninfected herds and countries, so new animals should be quarantined . After an outbreak, as immunity in exposed pigs wanes, new outbreaks of the same strain can occur. Swine can be infected by both avian and human flu strains of influenza, and therefore are hosts where the antigenic shifts can occur that create new influenza strains. The transmission from swine to humans is believed to occur mainly in swine farms, where farmers are in close contact with live pigs. Although strains of swine influenza are usually not able to infect humans, it may occasionally happen, so farmers and veterinarians are encouraged to use face masks when dealing with infected animals. The use of vaccines on swine to prevent their infection is a major method of limiting swine-to-human transmission. Risk factors that may contribute to the swine-to-human transmission include smoking and, especially, not wearing gloves when working with sick animals, thereby increasing the likelihood of subsequent hand-to-eye, hand-to-nose, or hand-to-mouth transmission. Influenza spreads between humans when infected people cough or sneeze, then other people breathe in the virus or touch something with the virus on it and then touch their own face. The CDC warned against touching mucosal membranes such as the eyes, nose, or mouth during the 2009 H1N1 pandemic, as these are common entry points for flu viruses. Swine flu cannot be spread by pork products, since the virus is not transmitted through food. The swine flu in humans is most contagious during the first five days of the illness, although some people, most commonly children, can remain contagious for up to ten days. Diagnosis can be made by sending a specimen, collected during the first five days, for analysis. Recommendations to prevent the spread of the virus among humans include using standard infection control , which includes frequent washing of hands with soap and water or with alcohol-based hand sanitizers , especially after being out in public. Chance of transmission is also reduced by disinfecting household surfaces, which can be done effectively with a diluted chlorine bleach solution. Influenza can spread in coughs or sneezes, but an increasing body of evidence shows small droplets containing the virus can linger on tabletops, telephones, and other surfaces and be transferred via the fingers to the eyes, nose, or mouth. Alcohol-based gel or foam hand sanitizers work well to destroy viruses and bacteria. Anyone with flu-like symptoms, such as a sudden fever, cough, or muscle aches, should stay away from work or public transportation and should contact a doctor for advice. Social distancing can be another infection control tactic. Individuals should avoid other people who might be infected or if infected themselves isolate from others for the duration of the infection. During active outbreaks, avoiding large gatherings, increasing physical distance in public places, or if possible remaining at home as much as is feasible can prevent further spread of disease. Public health and other responsible authorities have action plans which may request or require social distancing actions, depending on the severity of the outbreak. [ citation needed ] Vaccines are available for different kinds of swine flu. The U.S. Food and Drug Administration (FDA) approved the new swine flu vaccine for use in the United States on September 15, 2009. Studies by the National Institutes of Health show a single dose creates enough antibodies to protect against the virus within about 10 days. In the aftermath of the 2009 pandemic, several studies were conducted to see which population groups were most likely to have received an influenza vaccine. These studies demonstrated that caucasians are much more likely to be vaccinated for seasonal influenza and for the H1N1 strain than African Americans. This could be due to several factors. Historically, there has been mistrust of vaccines and of the medical community from African Americans. [ citation needed ] Many African Americans do not believe vaccines or doctors to be effective. This mistrust stems from the exploitation of the African American communities during studies like the Tuskegee study . Additionally, vaccines are typically administered in clinics, hospitals, or doctor's offices. Many people of lower socioeconomic status are less likely to receive vaccinations because they do not have health insurance. [ citation needed ] Although there is no formal national surveillance system in the United States to determine what viruses are circulating in pigs, an informal surveillance network in the United States is part of a world surveillance network. Methods of preventing the spread of influenza among swine include facility management, herd management, and vaccination ( ATCvet code: QI09AA03 ( WHO ) ). Because much of the illness and death associated with swine flu involves secondary infection by other pathogens, control strategies that rely on vaccination may be insufficient. Control of swine influenza by vaccination has become more difficult in recent decades, as the evolution of the virus has resulted in inconsistent responses to traditional vaccines. Standard commercial swine flu vaccines are effective in controlling the infection when the virus strains match enough to have significant cross-protection, and custom (autogenous) vaccines made from the specific viruses isolated are created and used in the more difficult cases. Present vaccination strategies for SIV control and prevention in swine farms typically include the use of one of several bivalent SIV vaccines commercially available in the United States. Of the 97 recent H3N2 isolates examined, only 41 isolates had strong serologic cross-reactions with antiserum to three commercial SIV vaccines. Since the protective ability of influenza vaccines depends primarily on the closeness of the match between the vaccine virus and the epidemic virus, the presence of nonreactive H3N2 SIV variants suggests current commercial vaccines might not effectively protect pigs from infection with a majority of H3N2 viruses. The United States Department of Agriculture researchers say while pig vaccination keeps pigs from getting sick, it does not block infection or shedding of the virus. Facility management includes using disinfectants and ambient temperature to control viruses in the environment. They are unlikely to survive outside living cells for more than two weeks, except in cold (but above freezing) conditions, and are readily inactivated by disinfectants. Herd management includes not adding pigs carrying influenza to herds that have not been exposed to the virus. The virus survives in healthy carrier pigs for up to three months and can be recovered from them between outbreaks. Carrier pigs are usually responsible for the introduction of SIV into previously uninfected herds and countries, so new animals should be quarantined . After an outbreak, as immunity in exposed pigs wanes, new outbreaks of the same strain can occur. Swine can be infected by both avian and human flu strains of influenza, and therefore are hosts where the antigenic shifts can occur that create new influenza strains. The transmission from swine to humans is believed to occur mainly in swine farms, where farmers are in close contact with live pigs. Although strains of swine influenza are usually not able to infect humans, it may occasionally happen, so farmers and veterinarians are encouraged to use face masks when dealing with infected animals. The use of vaccines on swine to prevent their infection is a major method of limiting swine-to-human transmission. Risk factors that may contribute to the swine-to-human transmission include smoking and, especially, not wearing gloves when working with sick animals, thereby increasing the likelihood of subsequent hand-to-eye, hand-to-nose, or hand-to-mouth transmission. Influenza spreads between humans when infected people cough or sneeze, then other people breathe in the virus or touch something with the virus on it and then touch their own face. The CDC warned against touching mucosal membranes such as the eyes, nose, or mouth during the 2009 H1N1 pandemic, as these are common entry points for flu viruses. Swine flu cannot be spread by pork products, since the virus is not transmitted through food. The swine flu in humans is most contagious during the first five days of the illness, although some people, most commonly children, can remain contagious for up to ten days. Diagnosis can be made by sending a specimen, collected during the first five days, for analysis. Recommendations to prevent the spread of the virus among humans include using standard infection control , which includes frequent washing of hands with soap and water or with alcohol-based hand sanitizers , especially after being out in public. Chance of transmission is also reduced by disinfecting household surfaces, which can be done effectively with a diluted chlorine bleach solution. Influenza can spread in coughs or sneezes, but an increasing body of evidence shows small droplets containing the virus can linger on tabletops, telephones, and other surfaces and be transferred via the fingers to the eyes, nose, or mouth. Alcohol-based gel or foam hand sanitizers work well to destroy viruses and bacteria. Anyone with flu-like symptoms, such as a sudden fever, cough, or muscle aches, should stay away from work or public transportation and should contact a doctor for advice. Social distancing can be another infection control tactic. Individuals should avoid other people who might be infected or if infected themselves isolate from others for the duration of the infection. During active outbreaks, avoiding large gatherings, increasing physical distance in public places, or if possible remaining at home as much as is feasible can prevent further spread of disease. Public health and other responsible authorities have action plans which may request or require social distancing actions, depending on the severity of the outbreak. [ citation needed ] Vaccines are available for different kinds of swine flu. The U.S. Food and Drug Administration (FDA) approved the new swine flu vaccine for use in the United States on September 15, 2009. Studies by the National Institutes of Health show a single dose creates enough antibodies to protect against the virus within about 10 days. In the aftermath of the 2009 pandemic, several studies were conducted to see which population groups were most likely to have received an influenza vaccine. These studies demonstrated that caucasians are much more likely to be vaccinated for seasonal influenza and for the H1N1 strain than African Americans. This could be due to several factors. Historically, there has been mistrust of vaccines and of the medical community from African Americans. [ citation needed ] Many African Americans do not believe vaccines or doctors to be effective. This mistrust stems from the exploitation of the African American communities during studies like the Tuskegee study . Additionally, vaccines are typically administered in clinics, hospitals, or doctor's offices. Many people of lower socioeconomic status are less likely to receive vaccinations because they do not have health insurance. [ citation needed ]Vaccines are available for different kinds of swine flu. The U.S. Food and Drug Administration (FDA) approved the new swine flu vaccine for use in the United States on September 15, 2009. Studies by the National Institutes of Health show a single dose creates enough antibodies to protect against the virus within about 10 days. In the aftermath of the 2009 pandemic, several studies were conducted to see which population groups were most likely to have received an influenza vaccine. These studies demonstrated that caucasians are much more likely to be vaccinated for seasonal influenza and for the H1N1 strain than African Americans. This could be due to several factors. Historically, there has been mistrust of vaccines and of the medical community from African Americans. [ citation needed ] Many African Americans do not believe vaccines or doctors to be effective. This mistrust stems from the exploitation of the African American communities during studies like the Tuskegee study . Additionally, vaccines are typically administered in clinics, hospitals, or doctor's offices. Many people of lower socioeconomic status are less likely to receive vaccinations because they do not have health insurance. [ citation needed ]Although there is no formal national surveillance system in the United States to determine what viruses are circulating in pigs, an informal surveillance network in the United States is part of a world surveillance network. As swine influenza is rarely fatal to pigs, little treatment beyond rest and supportive care is required. Instead, veterinary efforts are focused on preventing the spread of the virus throughout the farm or to other farms. Vaccination and animal management techniques are most important in these efforts. Antibiotics are also used to treat the disease, which, although they have no effect against the influenza virus, do help prevent bacterial pneumonia and other secondary infections in influenza-weakened herds. In Europe the avian-like H1N1 and the human-like H3N2 and H1N2 are the most common influenza subtypes in swine, of which avian-like H1N1 is the most frequent. Since 2009 another subtype, pdmH1N1(2009), emerged globally and also in European pig population. The prevalence varies from country to country but all of the subtypes are continuously circulating in swine herds. In the EU region whole-virus vaccines are available which are inactivated and adjuvanted. Vaccination of sows is common practice and reveals also a benefit to young pigs by prolonging the maternally level of antibodies. Several commercial vaccines are available including a trivalent one being used in sow vaccination and a vaccine against pdmH1N1(2009). In vaccinated sows multiplication of viruses and virus shedding are significantly reduced. [ citation needed ] If a human becomes sick with swine flu, antiviral drugs can make the illness milder and make the patient feel better faster. They may also prevent serious flu complications. For treatment, antiviral drugs work best if started soon after getting sick (within two days of symptoms). Beside antivirals, supportive care at home or in a hospital focuses on controlling fevers, relieving pain and maintaining fluid balance, as well as identifying and treating any secondary infections or other medical problems. The U.S. Centers for Disease Control and Prevention recommends the use of oseltamivir (Tamiflu) or zanamivir (Relenza) for the treatment and/or prevention of infection with swine influenza viruses; however, the majority of people infected with the virus make a full recovery without requiring medical attention or antiviral drugs. The virus isolated in the 2009 outbreak have been found resistant to amantadine and rimantadine . As swine influenza is rarely fatal to pigs, little treatment beyond rest and supportive care is required. Instead, veterinary efforts are focused on preventing the spread of the virus throughout the farm or to other farms. Vaccination and animal management techniques are most important in these efforts. Antibiotics are also used to treat the disease, which, although they have no effect against the influenza virus, do help prevent bacterial pneumonia and other secondary infections in influenza-weakened herds. In Europe the avian-like H1N1 and the human-like H3N2 and H1N2 are the most common influenza subtypes in swine, of which avian-like H1N1 is the most frequent. Since 2009 another subtype, pdmH1N1(2009), emerged globally and also in European pig population. The prevalence varies from country to country but all of the subtypes are continuously circulating in swine herds. In the EU region whole-virus vaccines are available which are inactivated and adjuvanted. Vaccination of sows is common practice and reveals also a benefit to young pigs by prolonging the maternally level of antibodies. Several commercial vaccines are available including a trivalent one being used in sow vaccination and a vaccine against pdmH1N1(2009). In vaccinated sows multiplication of viruses and virus shedding are significantly reduced. [ citation needed ]If a human becomes sick with swine flu, antiviral drugs can make the illness milder and make the patient feel better faster. They may also prevent serious flu complications. For treatment, antiviral drugs work best if started soon after getting sick (within two days of symptoms). Beside antivirals, supportive care at home or in a hospital focuses on controlling fevers, relieving pain and maintaining fluid balance, as well as identifying and treating any secondary infections or other medical problems. The U.S. Centers for Disease Control and Prevention recommends the use of oseltamivir (Tamiflu) or zanamivir (Relenza) for the treatment and/or prevention of infection with swine influenza viruses; however, the majority of people infected with the virus make a full recovery without requiring medical attention or antiviral drugs. The virus isolated in the 2009 outbreak have been found resistant to amantadine and rimantadine . Swine influenza was first proposed to be a disease related to human flu during the 1918 flu pandemic , when pigs became ill at the same time as humans. The first identification of an influenza virus as a cause of disease in pigs occurred about ten years later, in 1930. For the following 60 years, swine influenza strains were almost exclusively H1N1. Then, between 1997 and 2002, new strains of three different subtypes and five different genotypes emerged as causes of influenza among pigs in North America. In 1997–1998, H3N2 strains emerged. These strains, which include genes derived by reassortment from human, swine and avian viruses, have become a major cause of swine influenza in North America. Reassortment between H1N1 and H3N2 produced H1N2 . In 1999 in Canada, a strain of H4N6 crossed the species barrier from birds to pigs, but was contained on a single farm. The H1N1 form of swine flu is one of the descendants of the strain that caused the 1918 flu pandemic . As well as persisting in pigs, the descendants of the 1918 virus have also circulated in humans through the 20th century, contributing to the normal seasonal epidemics of influenza. However, direct transmission from pigs to humans is rare, with only 12 recorded cases in the U.S. since 2005. Nevertheless, the retention of influenza strains in pigs after these strains have disappeared from the human population might make pigs a reservoir where influenza viruses could persist, later emerging to reinfect humans once human immunity to these strains has waned. Swine flu has been reported numerous times as a zoonosis in humans, usually with limited distribution, rarely with a widespread distribution. Outbreaks in swine are common and cause significant economic losses in industry, primarily by causing stunting and extended time to market. For example, this disease costs the British meat industry about £65 million every year. The 1918 flu pandemic in humans was associated with H1N1 and influenza appearing in pigs; this may reflect a zoonosis either from swine to humans, or from humans to swine. Although it is not certain in which direction the virus was transferred, some evidence suggests that in this case pigs caught the disease from humans. For instance, swine influenza was only noted as a new disease of pigs in 1918 after the first large outbreaks of influenza amongst people. Although a recent phylogenetic analysis of more recent strains of influenza in humans, birds, and other animals including swine suggests the 1918 outbreak in humans followed a reassortment event within a mammal, the exact origin of the 1918 strain remains elusive. It is estimated that anywhere from 50 to 100 million people were killed worldwide. The swine flu was initially seen in the US in April 2009, where the strain of the particular virus was a mixture from 3 types of strains. Six of the genes are very similar to the H1N2 influenza virus that was found in pigs around 2000. On February 5, 1976, a United States army recruit at Fort Dix said he felt tired and weak. He died the next day, and four of his fellow soldiers were later hospitalized. Two weeks after his death, health officials announced the cause of death was a new strain of swine flu. The strain, a variant of H1N1, is known as A/New Jersey/1976 (H1N1) . It was detected only from January 19 to February 9 and did not spread beyond Fort Dix. This new strain appeared to be closely related to the strain involved in the 1918 flu pandemic. Moreover, the ensuing increased surveillance uncovered another strain in circulation in the U.S.: A/Victoria/75 (H3N2) , which spread simultaneously, also caused illness, and persisted until March. Alarmed public health officials decided action must be taken to head off another major pandemic, and urged President Gerald Ford that every person in the U.S. be vaccinated for the disease. The vaccination program was plagued by delays and public relations problems. On October 1, 1976, immunizations began, and three senior citizens died soon after receiving their injections. This resulted in a media outcry that linked these deaths to the immunizations, despite the lack of any proof the vaccine was the cause. According to science writer Patrick Di Justo, however, by the time the truth was known—that the deaths were not proven to be related to the vaccine—it was too late. "The government had long feared mass panic about swine flu—now they feared mass panic about the swine flu vaccinations." This became a strong setback to the program. There were reports of Guillain–Barré syndrome (GBS), a paralyzing neuromuscular disorder, affecting some people who had received swine flu immunizations. Although whether a link exists is still not clear, this syndrome may be a side effect of influenza vaccines. As a result, Di Justo writes, "the public refused to trust a government-operated health program that killed old people and crippled young people." In total, 48,161,019 Americans, or just over 22% of the population, had been immunized by the time the National Influenza Immunization Program was effectively halted on December 16, 1976. Overall, there were 1098 cases of GBS recorded nationwide by CDC surveillance, 532 of which occurred after vaccination and 543 before vaccination. About one to two cases per 100,000 people of GBS occur every year, whether or not people have been vaccinated. The vaccination program seems to have increased this normal risk of developing GBS by about to one extra case per 100,000 vaccinations. Recompensation charges were filed for over 4,000 cases of severe vaccination damage, including 25 deaths, totaling US$3.5 billion, by 1979. The CDC stated most studies on modern influenza vaccines have seen no link with GBS, Although one review gives an incidence of about one case per million vaccinations, a large study in China, reported in the New England Journal of Medicine , covering close to 100 million doses of H1N1 flu vaccine, found only 11 cases of GBS, which is lower than the normal rate of the disease in China: "The risk-benefit ratio, which is what vaccines and everything in medicine is about, is overwhelmingly in favor of vaccination." In September 1988, a swine flu virus killed one woman and infected others. A 32-year-old woman, Barbara Ann Wieners, was eight months pregnant when she and her husband, Ed, became ill after visiting the hog barn at a county fair in Walworth County, Wisconsin . Barbara died eight days later, after developing pneumonia. The only pathogen identified was an H1N1 strain of swine influenza virus. Doctors were able to induce labor and deliver a healthy daughter before she died. Her husband recovered from his symptoms. Influenza-like illness (ILI) was reportedly widespread among the pigs exhibited at the fair. Of the 25 swine exhibitors aged 9 to 19 at the fair, 19 tested positive for antibodies to SIV, but no serious illnesses were seen. The virus was able to spread between people, since one to three health care personnel who had cared for the pregnant woman developed mild, influenza-like illnesses, and antibody tests suggested they had been infected with swine flu, but there was no community outbreak. In 1998, swine flu was found in pigs in four U.S. states. Within a year, it had spread through pig populations across the United States. Scientists found this virus had originated in pigs as a recombinant form of flu strains from birds and humans. This outbreak confirmed that pigs can serve as a crucible where novel influenza viruses emerge as a result of the reassortment of genes from different strains. Genetic components of these 1998 triple-hybrid strains would later form six out of the eight viral gene segments in the 2009 flu outbreak. On August 20, 2007, Department of Agriculture officers investigated the outbreak of swine flu in Nueva Ecija and central Luzon , Philippines. The mortality rate is less than 10% for swine flu, unless there are complications like hog cholera . On July 27, 2007, the Philippine National Meat Inspection Service (NMIS) raised a hog cholera "red alert" warning over Metro Manila and five regions of Luzon after the disease spread to backyard pig farms in Bulacan and Pampanga , even if they tested negative for the swine flu virus. Since November 2009, 14 deaths as a result of swine flu in Northern Ireland have been reported. The majority of the deceased were reported to have pre-existing health conditions which had lowered their immunity. This closely corresponds to the 19 patients who had died in the year prior due to swine flu, where 18 of the 19 were determined to have lowered immune systems. Because of this, many mothers who have just given birth are strongly encouraged to get a flu shot because their immune systems are vulnerable. Also, studies have shown that people between the ages of 15 and 44 have the highest rate of infection. Although most people now recover, having any conditions that lower one's immune system increases the risk of having the flu become potentially lethal. In Northern Ireland now, approximately 56% of all people under 65 who are entitled to the vaccine have gotten the shot, and the outbreak is said to be under control. Swine flu outbreaks were reported in India in late 2014 and early 2015. As of March 19, 2015 the disease has affected 31,151 people and claimed over 1,841 lives. The largest number of reported cases and deaths due to the disease occurred in the western part of India including states like Delhi , Madhya Pradesh , Rajasthan , and Gujarat Andhra Pradesh Researchers of MIT have claimed that the swine flu has mutated in India to a more virulent version with changes in Hemagglutinin protein, contradicting earlier research by Indian researchers. There was another outbreak in India in 2017. The states of Maharashtra and Gujarat were the worst affected. Gujarat high court has given Gujarat government instructions to control deaths by swine flu. 1,090 people died of swine flu in India in 2019 until August 31, 2019. Swine flu outbreaks were reported in Nepal in the spring of 2015. Up to April 21, 2015, the disease had claimed 26 lives in the most severely affected district, Jajarkot in Northwest Nepal. Cases were also detected in the districts of Kathmandu , Morang , Kaski , and Chitwan . As of 22 April 2015 the Nepal Ministry of Health reported that 2,498 people had been treated in Jajarkot, of whom 552 were believed to have swine flu, and acknowledged that the government's response had been inadequate. The Jajarkot outbreak had just been declared an emergency when the April 2015 Nepal earthquake struck on 25 April 2015, diverting all medical and emergency resources to quake-related rescue and recovery. [ citation needed ] Seven cases of swine flu were reported in Punjab province of Pakistan , mainly in the city of Multan , in January 2017. Cases of swine flu were also reported in Lahore and Faisalabad . As of March 16, 2017, over a hundred confirmed cases of swine flu and at least six deaths were reported in the Maldivian capital of Malé and some other islands. Makeshift flu clinics were opened in Malé. Schools in the capital were closed, prison visitations suspended, several events cancelled, and all non-essential travel to other islands outside the capital was advised against by the HPA. An influenza vaccination program focusing on pregnant women was initiated thereafter. An official visit by Saudi King Salman bin Abdulaziz Al Saud to the Maldives during his Asian tour was also cancelled last minute amidst fears over the outbreak of swine flu. G4 EA H1N1 , also known as the G4 swine flu virus (G4) is a swine influenza virus strain discovered in China. The virus is a variant genotype 4 (G4) Eurasian avian-like (EA) H1N1 virus that mainly affects pigs, but there is some evidence of it infecting people. A peer-reviewed paper from the Proceedings of the National Academy of Sciences ( PNAS ) stated that "G4 EA H1N1 viruses possess all the essential hallmarks of being highly adapted to infect humans ... Controlling the prevailing G4 EA H1N1 viruses in pigs and close monitoring of swine working populations should be promptly implemented." Michael Ryan, executive director of the World Health Organization (WHO) Health Emergencies Program , stated in July 2020 that this strain of influenza virus was not new and had been under surveillance since 2011. Almost 30,000 swine had been monitored via nasal swabs between 2011 and 2018. While other variants of the virus have appeared and diminished, the study claimed the G4 variant has sharply increased since 2016 to become the predominant strain. The Chinese Ministry of Agriculture and Rural Affairs rebutted the study, saying that the media had interpreted the study "in an exaggerated and nonfactual way" and that the number of pigs sampled was too small to demonstrate G4 had become the dominant strain. Between 2016 and 2018, a serum surveillance program screened 338 swine production workers in China for exposure (presence of antibodies ) to G4 EA H1N1 and found 35 (10.4%) positive. Among another 230 people screened who did not work in the swine industry, 10 (4.4%) were serum positive for antibodies indicating exposure. Two cases of infection caused by the G4 variant have been documented as of July 2020, with no confirmed cases of human-to-human transmission . Health officials (including Anthony Fauci ) say the virus should be monitored, particularly among those in close contact with pigs, but it is not an immediate threat. There are no reported cases or evidence of the virus outside of China as of July 2020. Swine influenza was first proposed to be a disease related to human flu during the 1918 flu pandemic , when pigs became ill at the same time as humans. The first identification of an influenza virus as a cause of disease in pigs occurred about ten years later, in 1930. For the following 60 years, swine influenza strains were almost exclusively H1N1. Then, between 1997 and 2002, new strains of three different subtypes and five different genotypes emerged as causes of influenza among pigs in North America. In 1997–1998, H3N2 strains emerged. These strains, which include genes derived by reassortment from human, swine and avian viruses, have become a major cause of swine influenza in North America. Reassortment between H1N1 and H3N2 produced H1N2 . In 1999 in Canada, a strain of H4N6 crossed the species barrier from birds to pigs, but was contained on a single farm. The H1N1 form of swine flu is one of the descendants of the strain that caused the 1918 flu pandemic . As well as persisting in pigs, the descendants of the 1918 virus have also circulated in humans through the 20th century, contributing to the normal seasonal epidemics of influenza. However, direct transmission from pigs to humans is rare, with only 12 recorded cases in the U.S. since 2005. Nevertheless, the retention of influenza strains in pigs after these strains have disappeared from the human population might make pigs a reservoir where influenza viruses could persist, later emerging to reinfect humans once human immunity to these strains has waned. Swine flu has been reported numerous times as a zoonosis in humans, usually with limited distribution, rarely with a widespread distribution. Outbreaks in swine are common and cause significant economic losses in industry, primarily by causing stunting and extended time to market. For example, this disease costs the British meat industry about £65 million every year. The 1918 flu pandemic in humans was associated with H1N1 and influenza appearing in pigs; this may reflect a zoonosis either from swine to humans, or from humans to swine. Although it is not certain in which direction the virus was transferred, some evidence suggests that in this case pigs caught the disease from humans. For instance, swine influenza was only noted as a new disease of pigs in 1918 after the first large outbreaks of influenza amongst people. Although a recent phylogenetic analysis of more recent strains of influenza in humans, birds, and other animals including swine suggests the 1918 outbreak in humans followed a reassortment event within a mammal, the exact origin of the 1918 strain remains elusive. It is estimated that anywhere from 50 to 100 million people were killed worldwide. The swine flu was initially seen in the US in April 2009, where the strain of the particular virus was a mixture from 3 types of strains. Six of the genes are very similar to the H1N2 influenza virus that was found in pigs around 2000. The 1918 flu pandemic in humans was associated with H1N1 and influenza appearing in pigs; this may reflect a zoonosis either from swine to humans, or from humans to swine. Although it is not certain in which direction the virus was transferred, some evidence suggests that in this case pigs caught the disease from humans. For instance, swine influenza was only noted as a new disease of pigs in 1918 after the first large outbreaks of influenza amongst people. Although a recent phylogenetic analysis of more recent strains of influenza in humans, birds, and other animals including swine suggests the 1918 outbreak in humans followed a reassortment event within a mammal, the exact origin of the 1918 strain remains elusive. It is estimated that anywhere from 50 to 100 million people were killed worldwide. The swine flu was initially seen in the US in April 2009, where the strain of the particular virus was a mixture from 3 types of strains. Six of the genes are very similar to the H1N2 influenza virus that was found in pigs around 2000. On February 5, 1976, a United States army recruit at Fort Dix said he felt tired and weak. He died the next day, and four of his fellow soldiers were later hospitalized. Two weeks after his death, health officials announced the cause of death was a new strain of swine flu. The strain, a variant of H1N1, is known as A/New Jersey/1976 (H1N1) . It was detected only from January 19 to February 9 and did not spread beyond Fort Dix. This new strain appeared to be closely related to the strain involved in the 1918 flu pandemic. Moreover, the ensuing increased surveillance uncovered another strain in circulation in the U.S.: A/Victoria/75 (H3N2) , which spread simultaneously, also caused illness, and persisted until March. Alarmed public health officials decided action must be taken to head off another major pandemic, and urged President Gerald Ford that every person in the U.S. be vaccinated for the disease. The vaccination program was plagued by delays and public relations problems. On October 1, 1976, immunizations began, and three senior citizens died soon after receiving their injections. This resulted in a media outcry that linked these deaths to the immunizations, despite the lack of any proof the vaccine was the cause. According to science writer Patrick Di Justo, however, by the time the truth was known—that the deaths were not proven to be related to the vaccine—it was too late. "The government had long feared mass panic about swine flu—now they feared mass panic about the swine flu vaccinations." This became a strong setback to the program. There were reports of Guillain–Barré syndrome (GBS), a paralyzing neuromuscular disorder, affecting some people who had received swine flu immunizations. Although whether a link exists is still not clear, this syndrome may be a side effect of influenza vaccines. As a result, Di Justo writes, "the public refused to trust a government-operated health program that killed old people and crippled young people." In total, 48,161,019 Americans, or just over 22% of the population, had been immunized by the time the National Influenza Immunization Program was effectively halted on December 16, 1976. Overall, there were 1098 cases of GBS recorded nationwide by CDC surveillance, 532 of which occurred after vaccination and 543 before vaccination. About one to two cases per 100,000 people of GBS occur every year, whether or not people have been vaccinated. The vaccination program seems to have increased this normal risk of developing GBS by about to one extra case per 100,000 vaccinations. Recompensation charges were filed for over 4,000 cases of severe vaccination damage, including 25 deaths, totaling US$3.5 billion, by 1979. The CDC stated most studies on modern influenza vaccines have seen no link with GBS, Although one review gives an incidence of about one case per million vaccinations, a large study in China, reported in the New England Journal of Medicine , covering close to 100 million doses of H1N1 flu vaccine, found only 11 cases of GBS, which is lower than the normal rate of the disease in China: "The risk-benefit ratio, which is what vaccines and everything in medicine is about, is overwhelmingly in favor of vaccination." In September 1988, a swine flu virus killed one woman and infected others. A 32-year-old woman, Barbara Ann Wieners, was eight months pregnant when she and her husband, Ed, became ill after visiting the hog barn at a county fair in Walworth County, Wisconsin . Barbara died eight days later, after developing pneumonia. The only pathogen identified was an H1N1 strain of swine influenza virus. Doctors were able to induce labor and deliver a healthy daughter before she died. Her husband recovered from his symptoms. Influenza-like illness (ILI) was reportedly widespread among the pigs exhibited at the fair. Of the 25 swine exhibitors aged 9 to 19 at the fair, 19 tested positive for antibodies to SIV, but no serious illnesses were seen. The virus was able to spread between people, since one to three health care personnel who had cared for the pregnant woman developed mild, influenza-like illnesses, and antibody tests suggested they had been infected with swine flu, but there was no community outbreak. In 1998, swine flu was found in pigs in four U.S. states. Within a year, it had spread through pig populations across the United States. Scientists found this virus had originated in pigs as a recombinant form of flu strains from birds and humans. This outbreak confirmed that pigs can serve as a crucible where novel influenza viruses emerge as a result of the reassortment of genes from different strains. Genetic components of these 1998 triple-hybrid strains would later form six out of the eight viral gene segments in the 2009 flu outbreak. On August 20, 2007, Department of Agriculture officers investigated the outbreak of swine flu in Nueva Ecija and central Luzon , Philippines. The mortality rate is less than 10% for swine flu, unless there are complications like hog cholera . On July 27, 2007, the Philippine National Meat Inspection Service (NMIS) raised a hog cholera "red alert" warning over Metro Manila and five regions of Luzon after the disease spread to backyard pig farms in Bulacan and Pampanga , even if they tested negative for the swine flu virus. Since November 2009, 14 deaths as a result of swine flu in Northern Ireland have been reported. The majority of the deceased were reported to have pre-existing health conditions which had lowered their immunity. This closely corresponds to the 19 patients who had died in the year prior due to swine flu, where 18 of the 19 were determined to have lowered immune systems. Because of this, many mothers who have just given birth are strongly encouraged to get a flu shot because their immune systems are vulnerable. Also, studies have shown that people between the ages of 15 and 44 have the highest rate of infection. Although most people now recover, having any conditions that lower one's immune system increases the risk of having the flu become potentially lethal. In Northern Ireland now, approximately 56% of all people under 65 who are entitled to the vaccine have gotten the shot, and the outbreak is said to be under control. Swine flu outbreaks were reported in India in late 2014 and early 2015. As of March 19, 2015 the disease has affected 31,151 people and claimed over 1,841 lives. The largest number of reported cases and deaths due to the disease occurred in the western part of India including states like Delhi , Madhya Pradesh , Rajasthan , and Gujarat Andhra Pradesh Researchers of MIT have claimed that the swine flu has mutated in India to a more virulent version with changes in Hemagglutinin protein, contradicting earlier research by Indian researchers. There was another outbreak in India in 2017. The states of Maharashtra and Gujarat were the worst affected. Gujarat high court has given Gujarat government instructions to control deaths by swine flu. 1,090 people died of swine flu in India in 2019 until August 31, 2019. Swine flu outbreaks were reported in Nepal in the spring of 2015. Up to April 21, 2015, the disease had claimed 26 lives in the most severely affected district, Jajarkot in Northwest Nepal. Cases were also detected in the districts of Kathmandu , Morang , Kaski , and Chitwan . As of 22 April 2015 the Nepal Ministry of Health reported that 2,498 people had been treated in Jajarkot, of whom 552 were believed to have swine flu, and acknowledged that the government's response had been inadequate. The Jajarkot outbreak had just been declared an emergency when the April 2015 Nepal earthquake struck on 25 April 2015, diverting all medical and emergency resources to quake-related rescue and recovery. [ citation needed ] Seven cases of swine flu were reported in Punjab province of Pakistan , mainly in the city of Multan , in January 2017. Cases of swine flu were also reported in Lahore and Faisalabad . As of March 16, 2017, over a hundred confirmed cases of swine flu and at least six deaths were reported in the Maldivian capital of Malé and some other islands. Makeshift flu clinics were opened in Malé. Schools in the capital were closed, prison visitations suspended, several events cancelled, and all non-essential travel to other islands outside the capital was advised against by the HPA. An influenza vaccination program focusing on pregnant women was initiated thereafter. An official visit by Saudi King Salman bin Abdulaziz Al Saud to the Maldives during his Asian tour was also cancelled last minute amidst fears over the outbreak of swine flu.On February 5, 1976, a United States army recruit at Fort Dix said he felt tired and weak. He died the next day, and four of his fellow soldiers were later hospitalized. Two weeks after his death, health officials announced the cause of death was a new strain of swine flu. The strain, a variant of H1N1, is known as A/New Jersey/1976 (H1N1) . It was detected only from January 19 to February 9 and did not spread beyond Fort Dix. This new strain appeared to be closely related to the strain involved in the 1918 flu pandemic. Moreover, the ensuing increased surveillance uncovered another strain in circulation in the U.S.: A/Victoria/75 (H3N2) , which spread simultaneously, also caused illness, and persisted until March. Alarmed public health officials decided action must be taken to head off another major pandemic, and urged President Gerald Ford that every person in the U.S. be vaccinated for the disease. The vaccination program was plagued by delays and public relations problems. On October 1, 1976, immunizations began, and three senior citizens died soon after receiving their injections. This resulted in a media outcry that linked these deaths to the immunizations, despite the lack of any proof the vaccine was the cause. According to science writer Patrick Di Justo, however, by the time the truth was known—that the deaths were not proven to be related to the vaccine—it was too late. "The government had long feared mass panic about swine flu—now they feared mass panic about the swine flu vaccinations." This became a strong setback to the program. There were reports of Guillain–Barré syndrome (GBS), a paralyzing neuromuscular disorder, affecting some people who had received swine flu immunizations. Although whether a link exists is still not clear, this syndrome may be a side effect of influenza vaccines. As a result, Di Justo writes, "the public refused to trust a government-operated health program that killed old people and crippled young people." In total, 48,161,019 Americans, or just over 22% of the population, had been immunized by the time the National Influenza Immunization Program was effectively halted on December 16, 1976. Overall, there were 1098 cases of GBS recorded nationwide by CDC surveillance, 532 of which occurred after vaccination and 543 before vaccination. About one to two cases per 100,000 people of GBS occur every year, whether or not people have been vaccinated. The vaccination program seems to have increased this normal risk of developing GBS by about to one extra case per 100,000 vaccinations. Recompensation charges were filed for over 4,000 cases of severe vaccination damage, including 25 deaths, totaling US$3.5 billion, by 1979. The CDC stated most studies on modern influenza vaccines have seen no link with GBS, Although one review gives an incidence of about one case per million vaccinations, a large study in China, reported in the New England Journal of Medicine , covering close to 100 million doses of H1N1 flu vaccine, found only 11 cases of GBS, which is lower than the normal rate of the disease in China: "The risk-benefit ratio, which is what vaccines and everything in medicine is about, is overwhelmingly in favor of vaccination." In September 1988, a swine flu virus killed one woman and infected others. A 32-year-old woman, Barbara Ann Wieners, was eight months pregnant when she and her husband, Ed, became ill after visiting the hog barn at a county fair in Walworth County, Wisconsin . Barbara died eight days later, after developing pneumonia. The only pathogen identified was an H1N1 strain of swine influenza virus. Doctors were able to induce labor and deliver a healthy daughter before she died. Her husband recovered from his symptoms. Influenza-like illness (ILI) was reportedly widespread among the pigs exhibited at the fair. Of the 25 swine exhibitors aged 9 to 19 at the fair, 19 tested positive for antibodies to SIV, but no serious illnesses were seen. The virus was able to spread between people, since one to three health care personnel who had cared for the pregnant woman developed mild, influenza-like illnesses, and antibody tests suggested they had been infected with swine flu, but there was no community outbreak. In 1998, swine flu was found in pigs in four U.S. states. Within a year, it had spread through pig populations across the United States. Scientists found this virus had originated in pigs as a recombinant form of flu strains from birds and humans. This outbreak confirmed that pigs can serve as a crucible where novel influenza viruses emerge as a result of the reassortment of genes from different strains. Genetic components of these 1998 triple-hybrid strains would later form six out of the eight viral gene segments in the 2009 flu outbreak. On August 20, 2007, Department of Agriculture officers investigated the outbreak of swine flu in Nueva Ecija and central Luzon , Philippines. The mortality rate is less than 10% for swine flu, unless there are complications like hog cholera . On July 27, 2007, the Philippine National Meat Inspection Service (NMIS) raised a hog cholera "red alert" warning over Metro Manila and five regions of Luzon after the disease spread to backyard pig farms in Bulacan and Pampanga , even if they tested negative for the swine flu virus. Since November 2009, 14 deaths as a result of swine flu in Northern Ireland have been reported. The majority of the deceased were reported to have pre-existing health conditions which had lowered their immunity. This closely corresponds to the 19 patients who had died in the year prior due to swine flu, where 18 of the 19 were determined to have lowered immune systems. Because of this, many mothers who have just given birth are strongly encouraged to get a flu shot because their immune systems are vulnerable. Also, studies have shown that people between the ages of 15 and 44 have the highest rate of infection. Although most people now recover, having any conditions that lower one's immune system increases the risk of having the flu become potentially lethal. In Northern Ireland now, approximately 56% of all people under 65 who are entitled to the vaccine have gotten the shot, and the outbreak is said to be under control. Swine flu outbreaks were reported in India in late 2014 and early 2015. As of March 19, 2015 the disease has affected 31,151 people and claimed over 1,841 lives. The largest number of reported cases and deaths due to the disease occurred in the western part of India including states like Delhi , Madhya Pradesh , Rajasthan , and Gujarat Andhra Pradesh Researchers of MIT have claimed that the swine flu has mutated in India to a more virulent version with changes in Hemagglutinin protein, contradicting earlier research by Indian researchers. There was another outbreak in India in 2017. The states of Maharashtra and Gujarat were the worst affected. Gujarat high court has given Gujarat government instructions to control deaths by swine flu. 1,090 people died of swine flu in India in 2019 until August 31, 2019. Swine flu outbreaks were reported in Nepal in the spring of 2015. Up to April 21, 2015, the disease had claimed 26 lives in the most severely affected district, Jajarkot in Northwest Nepal. Cases were also detected in the districts of Kathmandu , Morang , Kaski , and Chitwan . As of 22 April 2015 the Nepal Ministry of Health reported that 2,498 people had been treated in Jajarkot, of whom 552 were believed to have swine flu, and acknowledged that the government's response had been inadequate. The Jajarkot outbreak had just been declared an emergency when the April 2015 Nepal earthquake struck on 25 April 2015, diverting all medical and emergency resources to quake-related rescue and recovery. [ citation needed ]Seven cases of swine flu were reported in Punjab province of Pakistan , mainly in the city of Multan , in January 2017. Cases of swine flu were also reported in Lahore and Faisalabad . As of March 16, 2017, over a hundred confirmed cases of swine flu and at least six deaths were reported in the Maldivian capital of Malé and some other islands. Makeshift flu clinics were opened in Malé. Schools in the capital were closed, prison visitations suspended, several events cancelled, and all non-essential travel to other islands outside the capital was advised against by the HPA. An influenza vaccination program focusing on pregnant women was initiated thereafter. An official visit by Saudi King Salman bin Abdulaziz Al Saud to the Maldives during his Asian tour was also cancelled last minute amidst fears over the outbreak of swine flu.G4 EA H1N1 , also known as the G4 swine flu virus (G4) is a swine influenza virus strain discovered in China. The virus is a variant genotype 4 (G4) Eurasian avian-like (EA) H1N1 virus that mainly affects pigs, but there is some evidence of it infecting people. A peer-reviewed paper from the Proceedings of the National Academy of Sciences ( PNAS ) stated that "G4 EA H1N1 viruses possess all the essential hallmarks of being highly adapted to infect humans ... Controlling the prevailing G4 EA H1N1 viruses in pigs and close monitoring of swine working populations should be promptly implemented." Michael Ryan, executive director of the World Health Organization (WHO) Health Emergencies Program , stated in July 2020 that this strain of influenza virus was not new and had been under surveillance since 2011. Almost 30,000 swine had been monitored via nasal swabs between 2011 and 2018. While other variants of the virus have appeared and diminished, the study claimed the G4 variant has sharply increased since 2016 to become the predominant strain. The Chinese Ministry of Agriculture and Rural Affairs rebutted the study, saying that the media had interpreted the study "in an exaggerated and nonfactual way" and that the number of pigs sampled was too small to demonstrate G4 had become the dominant strain. Between 2016 and 2018, a serum surveillance program screened 338 swine production workers in China for exposure (presence of antibodies ) to G4 EA H1N1 and found 35 (10.4%) positive. Among another 230 people screened who did not work in the swine industry, 10 (4.4%) were serum positive for antibodies indicating exposure. Two cases of infection caused by the G4 variant have been documented as of July 2020, with no confirmed cases of human-to-human transmission . Health officials (including Anthony Fauci ) say the virus should be monitored, particularly among those in close contact with pigs, but it is not an immediate threat. There are no reported cases or evidence of the virus outside of China as of July 2020.

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Avian influenza

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Global spread of H5N1 in 2005

The global spread of (highly pathogenic) H5N1 in birds is considered a significant pandemic threat. While prior H5N1 strains have been known, they were significantly different from the current H5N1 strain on a genetic level, making the global spread of this new strain unprecedented. The current H5N1 strain is a fast-mutating , highly pathogenic avian influenza virus (HPAI) found in multiple bird species. It is both epizootic (an epidemic in non-humans) and panzootic (a disease affecting animals of many species especially over a wide area). Unless otherwise indicated, "H5N1" in this article refers to the recent highly pathogenic strain of H5N1. In January 2005 an outbreak of avian influenza affected thirty three out of sixty four cities and provinces in Vietnam , leading to the forced killing of nearly 1.2 million poultry. Up to 140 million birds are believed to have died or been killed because of the outbreak. In April 2005 an unprecedented die-off began of over 6,000 migratory birds at Qinghai Lake in central China over three months. This strain of H5N1 is the same strain as is spread west by migratory birds over at least the next ten months. In August 2005 H5N1 spread to Kazakhstan , Mongolia and Russia . On September 30, 2005, David Nabarro , the newly appointed Senior United Nations System Coordinator for Avian and Human Influenza, warned the world that an outbreak of avian influenza could kill 5 to 150 million people. David Nabarro later stated that as the virus had spread to migratory birds, an outbreak could start in Africa or the Middle East . Later in 2005 H5N1 spread to Turkey , Romania , Croatia and Kuwait . Notes:August 3, 2005 August 11, 2005 August 22, 2005September 30, 2005October 13, 2005 October 15, 2005 October 19, 2005 October 26, 2005 October 31, 2005November 12, 2005December 30, 2005 "China confirms its third human death from bird flu. That brings the death toll [...] to 74, comprising 14 victims in Thailand, four in Cambodia, 11 in Indonesia, 42 in Vietnam and three in China."

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Avian influenza

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Human mortality from H5N1

The thin line represents average mortality of recent cases. The thicker line represents mortality averaged over all cases. According to WHO: " Assessment of mortality rates and the time intervals between symptom onset and hospitalization and between symptom onset and death suggests that the illness pattern has not changed substantially during the three years. " Human mortality from H5N1 or the human fatality ratio from H5N1 or the case-fatality rate of H5N1 is the ratio of the number of confirmed human deaths resulting from confirmed cases of transmission and infection of H5N1 to the number of those confirmed cases. For example, if there are 100 confirmed cases of humans infected with H5N1 and 50 die, then there is a 50% human fatality ratio (or mortality rate). H5N1 flu is a concern due to the global spread of H5N1 that constitutes a pandemic threat. The majority of H5N1 flu cases have been reported in southeast and east Asia. The case-fatality rate is central to pandemic planning. Estimates of case-fatality (CF) rates for past influenza pandemics have ranged from to 2-3% for the 1918 pandemic to about 0.6% for the 1957 pandemic to 0.2% for the 1968 pandemic . As of 2008, the official World Health Organization estimate for the case-fatality rate for the outbreak of H5N1 avian influenza was approximately 60%. Public health officials in Ontario, Canada argue that the true case-fatality rate could be lower, pointing to studies suggesting it could be 14-33%, and warned that it was unlikely to be as low as the 0.1–0.4% rate that was built into many pandemic plans. H5N1 infections in humans are generally caused by bird to human transmission of the virus. Until May 2006, the WHO estimate of the number of human to human transmissions had been "two or three cases". On May 24, 2006, Dr. Julie L. Gerberding, director of the United States Centers for Disease Control and Prevention in Atlanta , estimated that there had been "at least three." On May 30, Maria Cheng, a WHO spokeswoman, said there were "probably about half a dozen," but that no one "has got a solid number." The cases of suspected human to human transmission that continue to be found have been isolated and contained, and include transmission among members of a family in Sumatra, Indonesia in June 2006 as well as earlier and later instances arising in other countries. However, no pandemic strain of H5N1 has yet been found. The key point is that, at present, "the virus is not spreading efficiently or sustainably among humans." H5N1 vaccines for chickens exist and are sometimes used, although there are many difficulties that make it especially difficult to decide whether vaccination will do more harm than good. In the U.S. H5N1 pre-pandemic vaccines exist in quantities sufficient to inoculate a few million people and might be useful for priming to "boost the immune response to a different H5N1 vaccine tailor-made years later to thwart an emerging pandemic". Japan has inoculated 6,000 health care workers with a pre-pandemic vaccine, and is planning how to proceed with widespread vaccinations, particularly workers who would provide utilities during an outbreak. Switzerland is also considering preemptive vaccination to protect the general public. H5N1 pandemic vaccines and the technologies to rapidly create them are in the H5N1 clinical trials stage but cannot be verified as useful until after a pandemic strain emerges. Efforts to identify the changes that might result in a human-communicable strain have resulted in laboratory-generated H5N1 with substantially greater affinity for human cellular receptors after a change of just two of the H5 surface proteins. Significantly, mouse antibodies were 10 times less potent against the mutants than against the pre-mutated viruses. A graphic exhibiting total cases and mortality incidence is kept current by the WHO at https://web.archive.org/web/20080827215244/http://www.wpro.who.int/NR/rdonlyres/7549914F-5C83-4418-8C20-007ADCC07C61/0/s3.jpg and complements the country-specific information shown below. Country-specific totals of cases and deaths kept current by the WHO may be viewed by clicking through the links provided at Global influenza virological surveillance and the map links provided here Map Gallery Search Results Global influenza virological surveillance (in the Global Health Observatory)A strain of H5N1 killed chickens in 1959 in Scotland and turkeys in 1991 in England . This strain was "highly pathogenic" (deadly to birds) but caused neither illness nor death in humans. "The precursor of the H5N1 influenza virus that spread to humans in 1997 was first detected in Guangdong , China , in 1996, when it caused a moderate number of deaths in geese and attracted very little attention." In 1997, in Hong Kong , 18 humans were infected and 6 died in the first known case of H5N1 infecting humans. H5N1 had evolved from a zero mortality rate to a 33% mortality rate. The first report, in the current wave of HPAI A(H5N1) outbreaks, was of an outbreak that began December 10, 2003 in the Republic of Korea and continued for fourteen weeks. This strain caused asymptomatic infections in humans and may have died out, like the 1959 strain, so that its low mortality level would have little value for predicting the mortality rate of a pandemic evolving from existing HPAI A(H5N1) strains. The apparently extinct strain that caused human deaths from H5N1 in the Northern part of Vietnam in 2003, 2004 and 2005 also had a much lower case mortality rate than the currently existing strains. Changes are occurring in H5N1 that are increasing its pathogenicity in mammals. From inception through 2007, the total number of WHO -confirmed cases was 349, with 216 of those fatalities (as reported by the U.N. on January 15, 2008, confirming earlier deaths) reflecting a 62% fatality rate among WHO -confirmed cases through 2007. These overall figures fail to bring forward fluctuations that have appeared from year to year and in particular geographic areas. In 2005, when a markedly less-lethal strain in Northern Vietnam was responsible for most of the cases reported worldwide, only 42 of 97 people confirmed by the WHO to be infected with H5N1 died — a 43% fatality rate. In 2006, the case fatality ratio was higher among the WHO -confirmed cases, with 79 deaths among 114 confirmed cases. — or 69%. In 2007, 59 of the 86 WHO-confirmed cases ended in death, again a 69% fatality rate. And 24 of the first 31 cases of 2008 (to April 30, 2008) have been fatal, or 77%. The higher total case fatality ratio after the end of 2005 may reflect the widespread circulation in Vietnam of a less-lethal clade of H5N1 in 2005, which was subsequently brought under control. The change was nonetheless interpreted by some as indicating that the virus itself was becoming more deadly over time. In fact, when less-virulent strains die off, the surviving strains are the more virulent. Such difficulties in interpretation underscore that the global case fatality ratio can serve as but a crude and imperfect summary of the current complex situation with its many contributing factors, and not a clear or reliable predictive tool. If and when an influenza pandemic arises from one of the currently circulating pre-pandemic strains of Asian lineage HPAI A(H5N1) , the mortality rates for the resulting human adapted pandemic strain cannot be predicted with any confidence. [ citation needed ]The global case fatality ratio looks only to the official tally of cases confirmed by the WHO . It takes no account of other cases, such as those appearing in press reports. Nor does it reflect any estimate of the global extent of mild, asymptomatic, or other cases which are undiagnosed, unreported by national governments to the WHO , or for any reason cannot be confirmed by the WHO . While the WHO 's case count is clearly the most authoritative, these unavoidable limitations result in an unknown number of cases being omitted from it. The problem of overlooked but genuine cases is emphasized by occasional reports in which later serology reveals antibodies to the H5N1 infection in the blood of persons who were never known to have bird flu, and who then are confirmed by the WHO only retroactively as "cases." Press reports of such cases, often poultry handlers, have appeared in various countries. The largest number of asymptomatic cases was confirmed in 2006 among Korean workers who had assisted in massive culls of H5N1-infected poultry. This relatively benign Korean strain of H5N1 has died out, and the remaining strains of H5N1 have a higher case fatality rate in humans. Unconfirmed cases have a potentially huge impact on the case fatality ratio. This mathematical impact is well understood by epidemiologists, and is easy to see in theory. For example, if for each confirmed case reported by the WHO we assume that there has been another mild and unreported case, the actual global number of cases would be double the current number of WHO -confirmed cases. The fatality ratio for H5N1 infections would then be calculated as the same number of deaths, but divided by a doubled number for total cases, resulting in a hypothetical death ratio of half the currently reported fatality ratio. Such a result would indicate to epidemiologists that the world was confronting an H5N1 virus that is less-lethal than currently assumed, although possibly one that was more contagious and difficult to track. A case-fatality ratio based on an accurate and all-inclusive count of cases would be invaluable, but unfortunately it is impossible to attain. The ability to diagnose every case of H5N1 as it arises does not exist. A few small reported studies have attempted to gather preliminary data on this crucial statistic, by carrying out systematic blood testing of neighbors and contacts of fatal cases in villages where there had been confirmed H5N1 fatalities. In most cases, this testing failed to turn up any overlooked mild cases, though in at least one study mild overlooked cases were identified. These methodical studies of contacts provide significant evidence that the high death rate among confirmed cases in the villages where these studies were carried out cannot be simply attributed to a wholesale failure to detect mild cases. Unfortunately, these studies are likely to remain too few and sketchy to define the complex situation worldwide regarding the lethality of the varying H5N1 clades. The testing and reporting necessary for mass serology studies to determine the incidence of overlooked cases for each existing clade and strain of H5N1 worldwide would be prohibitively costly. [ citation needed ] Hence the precise allocation of infections by the various H5N1 clades across the spectrum including lethal, serious, mild, and asymptomatic cases is likely to remain unknown in both humans and the hundreds of other species it can infect. Scientists are very concerned about what we do know about H5N1 ; but even more concerned about the vast amount of important data that we don't know about H5N1 and its future mutations. [ citation needed ]Review of patient ages and outcomes reveals that H5N1 attacks are especially lethal in pre-adults and young adults, while older victims tend to have milder attacks and to survive. This is consistent with the frequent development of a cytokine storm in the affected. Few persons over 50 years of age seem to have become infected by H5N1, and very few have died following an H5N1 attack. Instead, the age-fatality curve of H5N1 influenza attacks in humans resembles that of the 1918 Spanish pandemic flu, and is the opposite of the mortality curve of seasonal flu strains, since seasonal influenza preferentially kills the elderly and does not kill by cytokine storm . An additional factor which may be active is that H1N1 was the predominant human flu circulating from 1918 until 1957 when the H2N2 strain emerged. Hence those over 50 years old have had the opportunity to be exposed to H1N1, and to develop some immune response to the N1 group contained in that human form of flu. Likewise, annual flu vaccination includes inoculation against a type-A human H1N1 flu, leading to the possibility that the annual flu shot or Flumist inoculation might confer some immunity against H5N1 bird flu infection, and indeed testing the blood of volunteers to look for immune response to H5N1 found that some blood samples showed immunity, but more of the blood samples of persons who had received the flu shot showed an immune response. Another factor complicating any attempt to predict lethality of an eventual pandemic strain is the variability of the resistance of human victims to the pathogen. Many people with the current H5N1 influenza have been blood relatives (but rarely spouses) of other victims. Though this observation seemed to suggest that a familial genetic susceptibility might have played a role in human infection, a study by researchers at the Harvard School of public health noted no significant familial pattern of infection. Clearly, those whose immune systems are best able to fight off the virus are the most likely to survive a pandemic. Those with impairment of the needed immune function, whether from familial genetics or from AIDS, have poorer chances. Moreover, the health care system is generally expected to be overwhelmed throughout a pandemic. Persons needing access to medical care, whether for influenza or for unrelated serious maladies, are unlikely to receive the accustomed care, and without it their survival chances will be reduced. [ citation needed ]Although the actual rate of mortality during a pandemic is unknowable in advance, it is pressing to predict the possible ranges for that lethality responsibly in advance. The pre-pandemic case fatality ratio of over 50% provides a grim backdrop for the fact that the currently circulating H5N1 strains have certain genetic similarities with the Spanish Influenza pandemic virus. In that pandemic, 50 million to 100 million people worldwide were killed during about a year in 1918 and 1919. The highly lethal second and third waves of the 1918 Spanish flu evolved through time into a less virulent and more transmissible human form. Although the overall fatality rate for the Spanish flu is estimated to have been 10% to 20% of the population, [ citation needed ] the lethal waves of the Spanish flu are not reported to have emerged with anything like the over-50% case fatality ratio observed to date in human H5N1 infection. Studies indicating that an H5N1 pandemic may be more pathogenic than was the Spanish flu include a mouse study in which the H5N1 virus elicited significantly higher levels of pro-inflammatory cytokines in the lungs. A human H5N1 pandemic might emerge with initial lethality resembling that over-50% case fatality now observed in pre-pandemic H5N1 human cases, rather than with the still-high 1-2% seen with the Spanish flu or with the lower rates seen in the two more recent influenza pandemics. As a WHO working group noted, Determinants of virulence and transmissibility. The U.S. CDC presents a similarly sobering conclusion authored by Robert G. Webster et al.: Although some mammalian adaptations have been noted, H5N1 remains better adapted for infecting birds than mammalian hosts, which is why the disease it causes is called a bird flu . No pandemic strain of H5N1 has yet been found. The precise nature and extent of the genetic alterations that might change one of the currently circulating avian influenza strains into a human flu strain cannot be known in advance. While many of the current H5N1 strains circulating in birds can generate a dangerous cytokine storm in healthy adult humans, the ultimate pandemic strain might arise from a less-lethal strain, or its current level of lethality might be lost in the adaptation to a human host. If H5N1 mutates so that it can jump from human to human, while maintaining a relatively high level of mortality, how many people could die? Risk communication analysts Peter M. Sandman and Jody Lanard give a round-up of the various estimates: Worldwide mortality estimates range all the way from 2-7.4 million deaths (the "conservatively low" pandemic influenza calculation of a flu modeling expert at the U.S. Centers for Disease Control and Prevention) to 1000 million deaths (the bird flu pandemic prediction of one Russian virologist). The estimates of most H5N1 experts range less widely but still widely. In an H5N1 pandemic, the experts guess that somewhere between a quarter of us and half of us would get sick, and somewhere between one percent and five percent of those who got sick would die — the young and hale as well as the old and frail. If it's a quarter and one percent, that's 16 million dead; if it's a half and five percent, it's 160 million dead. Either way it's a big number. The renowned virus expert Robert G. Webster provided perhaps the most extreme estimate when he acknowledged in March 2006 that H5N1 has the theoretical capacity to mutate into a form that could kill one half of the human population, stating, "Society just can't accept the idea that 50 percent of the population could die. And I think we have to face that possibility". H5N1 may cause more than one influenza pandemic as it is expected to continue mutating in birds regardless of whether humans develop herd immunity to a future pandemic strain. Influenza pandemics from its genetic offspring may include influenza A virus subtypes other than H5N1. While genetic analysis of the H5N1 virus shows that influenza pandemics from its genetic offspring can easily be far more lethal than the Spanish flu pandemic, planning for a future influenza pandemic is based on what can be done and there is no higher Pandemic Severity Index level than a Category 5 pandemic which, roughly speaking, is any pandemic as bad the Spanish flu or worse; and for which all intervention measures are to be used. There "is evidence of at least three independent virulence factors connected with three different genes . It is highly unlikely that all of the high-virulence alleles will simultaneously mutate and disappear if and when the haemagglutinin gene changes so as to make the haemagglutinin molecule better adapted for the human-type (alpha-2,6-linked) receptor (which is a necessary prerequisite in order that a pandemic with H5N1 virus may start). It is more probable that evolutionary adaptation of the haemagglutinin of H5N1 viruses to the human-type receptor will happen without any simultaneous change in those other genetic properties that now are important for explaining the exceptionally high virulence of certain strains of avian-adapted H5N1 influenza virus. The change of the haemagglutinin molecule from avian adaptation to human adaptation must be expected to act as an additional virulence factor because it will enhance the total number of cells that can be infected (per host organism), increase the total rate of virus replication and potentiate the effects of the other virulence factors already present." The H5N1 genes work together in ways we don't yet understand. Influenza research is continuing. The genetic factors that make H5N1 so deadly are only partly understood. Known factors involve the surface antigen encoding gene segments H ( hemagglutinin ) and N ( neuraminidase ) genes (causing it to be H5N1 for example), as well as the matrix M2 gene, and the polymerase genes. A change of just two genes identified in laboratory testing appears to substantially increase the affinity of H5N1 for binding with human cell surface receptors. Neuraminidase is an antigenic glycoprotein enzyme found on the surface of the influenza viruses . It helps the release of progeny viruses from infected cells. Flu drugs Tamiflu and Relenza work by inhibiting some strains of neuraminidase . They were developed based on N2 and N9. "In the N1 form of the protein, a small segment called the 150-loop is inverted, creating a hollow pocket that does not exist in the N2 and N9 proteins. [...] When the researchers looked at how existing drugs interacted with the N1 protein, they found that, in the presence of neuraminidase inhibitors, the loop changed its conformation to one similar to that in the N2 and N9 proteins." The amino acid substitution (Ser31Asn) in the M2 gene in some H5N1 genotypes is associated with amantadine resistance which increases lethality. However the pathogenicity of H5N1/97 was related to the nonstructural (NS) gene. NS codes for two nonstructural proteins (NS1 and NEP). The NS1 gene of the highly pathogenic avian H5N1 viruses circulating in poultry and waterfowl in Southeast Asia is believed to be responsible for an enhanced proinflammatory cytokine response (especially TNFa) induced by these viruses in human macrophages. H5N1 NS1 is characterized by a single amino acid change at position 92. By changing the amino acid from glutamic acid to aspartic acid, researchers were able to abrogate the effect of the H5N1 NS1. This single amino acid change in the NS1 gene greatly increased the pathogenicity of the H5N1 influenza virus. This is one genetic factor in why H5N1 is so deadly. [ citation needed ] Polymerase encoding gene segments are also implicated in why H5N1 is so deadly. PA genes code for the PA protein, which is a critical component of the viral polymerase. The PB1 gene codes for the PB1 protein and the PB1-F2 protein. The PB1-F2 protein probably contributes to viral pathogenicity and might have an important role in determining the severity of pandemic influenza. Until H5N1, all known avian influenza viruses had a Glu at position 627, while all human influenza viruses had a lysine. Recently, some 75% of H5N1 human virus isolates identified in Vietnam had a mutation consisting of Lysine at residue 627 in the PB2 protein; a change believed associated with high levels of virulence. Areas of research to identify the likelihood of rapid or slow evolution to human contagion, or for predicting the greater or lesser likelihood of a rather lethal human-adapted influenza include: [ citation needed ] bird species susceptibility bird migration paths cell-based vaccine development adjuvant testing human vaccine clinical trials bird vaccine testing and use computer simulations of pandemic spread patterns (e.g. will grounding flights help?) detailed shape and gene code analysis of each of the RNA strands for as many flu virus strains as possible and making them available on a database for study wild bird testing for flu viruses testing humans for asymptomatic H5N1 infection training exercises in case of a pandemic Computer simulations and direct gene manipulation have yielded inconclusive results. Scientific advances may attenuate probable lethality. The genetic lethality potential of the initial flu pandemic strain is only one important factor in determining the ultimate outcome in number of human lives lost. Another factor that grows potentially more important with the passage of time is human preparation. For example, no influenza vaccine specific to H5N1 could be produced when it emerged in Hong Kong in 1997, because it was lethal to eggs. Reverse DNA techniques have since made a vaccine possible, and several H5N1 vaccines have been tested and are in production in at least limited quantities. Vaccine development and production facilities are being ramped up, and possible pre-pandemic vaccines are being produced and studied. If a human pandemic does not emerge in the next few years, its eventual emergence may become almost a non-event if a very-effective pre-pandemic vaccine has prepared the population with sufficient herd immunity to blunt its lethality. Indeed, if there is sufficient immunity to stop it at the source, it will not become pandemic. [ citation needed ] As long as the likelihood of protecting the population continues to rise with the passage of time, that likelihood becomes an increasingly important factor in predicting the loss of lives and the amount of economic dislocation that will ultimately occur. In light of human potential to develop herd immunity via vaccination in advance of a pandemic strain, the time that it allows us to do so before it evolves may become as crucial or more crucial to the measure of damage it causes than its own lethality and contagiousness. [ citation needed ] Among the more attractive alternatives available for reducing mortality is vaccine stockpiling and prepandemic vaccination. "Human H5N1 vaccines are currently available and can induce heterotypic immunity. WHO and governments should give urgent consideration to the use of these vaccines for the priming of individuals or communities who would be at greatest risk of infection if an H5N1 influenza pandemic were to emerge." Death associated with influenza A viruses "is usually mediated by superinfection with bacteria, mainly Streptococcus pneumoniae.", suggesting that lethality may be reduced by vaccination against pneumonia. Among others, the Secretary of the United States Department of Health and Human Services (HHS) has repeatedly pointed out the key role of preparation in reducing pandemic mortality, including as examples research in cell- and DNA-based vaccines, as well as stockpiling available vaccines and antivirals and increasing vaccine manufacturing capacity. H5N1 may cause more than one influenza pandemic as it is expected to continue mutating in birds regardless of whether humans develop herd immunity to a future pandemic strain. Influenza pandemics from its genetic offspring may include influenza A virus subtypes other than H5N1. While genetic analysis of the H5N1 virus shows that influenza pandemics from its genetic offspring can easily be far more lethal than the Spanish flu pandemic, planning for a future influenza pandemic is based on what can be done and there is no higher Pandemic Severity Index level than a Category 5 pandemic which, roughly speaking, is any pandemic as bad the Spanish flu or worse; and for which all intervention measures are to be used. There "is evidence of at least three independent virulence factors connected with three different genes . It is highly unlikely that all of the high-virulence alleles will simultaneously mutate and disappear if and when the haemagglutinin gene changes so as to make the haemagglutinin molecule better adapted for the human-type (alpha-2,6-linked) receptor (which is a necessary prerequisite in order that a pandemic with H5N1 virus may start). It is more probable that evolutionary adaptation of the haemagglutinin of H5N1 viruses to the human-type receptor will happen without any simultaneous change in those other genetic properties that now are important for explaining the exceptionally high virulence of certain strains of avian-adapted H5N1 influenza virus. The change of the haemagglutinin molecule from avian adaptation to human adaptation must be expected to act as an additional virulence factor because it will enhance the total number of cells that can be infected (per host organism), increase the total rate of virus replication and potentiate the effects of the other virulence factors already present." The H5N1 genes work together in ways we don't yet understand. Influenza research is continuing. The genetic factors that make H5N1 so deadly are only partly understood. Known factors involve the surface antigen encoding gene segments H ( hemagglutinin ) and N ( neuraminidase ) genes (causing it to be H5N1 for example), as well as the matrix M2 gene, and the polymerase genes. A change of just two genes identified in laboratory testing appears to substantially increase the affinity of H5N1 for binding with human cell surface receptors. Neuraminidase is an antigenic glycoprotein enzyme found on the surface of the influenza viruses . It helps the release of progeny viruses from infected cells. Flu drugs Tamiflu and Relenza work by inhibiting some strains of neuraminidase . They were developed based on N2 and N9. "In the N1 form of the protein, a small segment called the 150-loop is inverted, creating a hollow pocket that does not exist in the N2 and N9 proteins. [...] When the researchers looked at how existing drugs interacted with the N1 protein, they found that, in the presence of neuraminidase inhibitors, the loop changed its conformation to one similar to that in the N2 and N9 proteins." The amino acid substitution (Ser31Asn) in the M2 gene in some H5N1 genotypes is associated with amantadine resistance which increases lethality. However the pathogenicity of H5N1/97 was related to the nonstructural (NS) gene. NS codes for two nonstructural proteins (NS1 and NEP). The NS1 gene of the highly pathogenic avian H5N1 viruses circulating in poultry and waterfowl in Southeast Asia is believed to be responsible for an enhanced proinflammatory cytokine response (especially TNFa) induced by these viruses in human macrophages. H5N1 NS1 is characterized by a single amino acid change at position 92. By changing the amino acid from glutamic acid to aspartic acid, researchers were able to abrogate the effect of the H5N1 NS1. This single amino acid change in the NS1 gene greatly increased the pathogenicity of the H5N1 influenza virus. This is one genetic factor in why H5N1 is so deadly. [ citation needed ] Polymerase encoding gene segments are also implicated in why H5N1 is so deadly. PA genes code for the PA protein, which is a critical component of the viral polymerase. The PB1 gene codes for the PB1 protein and the PB1-F2 protein. The PB1-F2 protein probably contributes to viral pathogenicity and might have an important role in determining the severity of pandemic influenza. Until H5N1, all known avian influenza viruses had a Glu at position 627, while all human influenza viruses had a lysine. Recently, some 75% of H5N1 human virus isolates identified in Vietnam had a mutation consisting of Lysine at residue 627 in the PB2 protein; a change believed associated with high levels of virulence.Areas of research to identify the likelihood of rapid or slow evolution to human contagion, or for predicting the greater or lesser likelihood of a rather lethal human-adapted influenza include: [ citation needed ] bird species susceptibility bird migration paths cell-based vaccine development adjuvant testing human vaccine clinical trials bird vaccine testing and use computer simulations of pandemic spread patterns (e.g. will grounding flights help?) detailed shape and gene code analysis of each of the RNA strands for as many flu virus strains as possible and making them available on a database for study wild bird testing for flu viruses testing humans for asymptomatic H5N1 infection training exercises in case of a pandemic Computer simulations and direct gene manipulation have yielded inconclusive results.Scientific advances may attenuate probable lethality. The genetic lethality potential of the initial flu pandemic strain is only one important factor in determining the ultimate outcome in number of human lives lost. Another factor that grows potentially more important with the passage of time is human preparation. For example, no influenza vaccine specific to H5N1 could be produced when it emerged in Hong Kong in 1997, because it was lethal to eggs. Reverse DNA techniques have since made a vaccine possible, and several H5N1 vaccines have been tested and are in production in at least limited quantities. Vaccine development and production facilities are being ramped up, and possible pre-pandemic vaccines are being produced and studied. If a human pandemic does not emerge in the next few years, its eventual emergence may become almost a non-event if a very-effective pre-pandemic vaccine has prepared the population with sufficient herd immunity to blunt its lethality. Indeed, if there is sufficient immunity to stop it at the source, it will not become pandemic. [ citation needed ] As long as the likelihood of protecting the population continues to rise with the passage of time, that likelihood becomes an increasingly important factor in predicting the loss of lives and the amount of economic dislocation that will ultimately occur. In light of human potential to develop herd immunity via vaccination in advance of a pandemic strain, the time that it allows us to do so before it evolves may become as crucial or more crucial to the measure of damage it causes than its own lethality and contagiousness. [ citation needed ] Among the more attractive alternatives available for reducing mortality is vaccine stockpiling and prepandemic vaccination. "Human H5N1 vaccines are currently available and can induce heterotypic immunity. WHO and governments should give urgent consideration to the use of these vaccines for the priming of individuals or communities who would be at greatest risk of infection if an H5N1 influenza pandemic were to emerge." Death associated with influenza A viruses "is usually mediated by superinfection with bacteria, mainly Streptococcus pneumoniae.", suggesting that lethality may be reduced by vaccination against pneumonia.Among others, the Secretary of the United States Department of Health and Human Services (HHS) has repeatedly pointed out the key role of preparation in reducing pandemic mortality, including as examples research in cell- and DNA-based vaccines, as well as stockpiling available vaccines and antivirals and increasing vaccine manufacturing capacity. Governments and other organizations at many levels and in many places have produced "planning" reports that, among other things, have offered speculation on the mortality rate of an eventual H5N1 pandemic. That speculation has varied widely. One such report stated that "over half a million Americans could die and over 2.3 million could be hospitalized if a moderately severe strain of a pandemic flu virus hits the U.S.". No one knew if "moderately severe" was an accurate guess or not. A report entitled A Killer Flu? projected that, with an assumed (guessed) contraction rate of just 25%, and with a severity rate as low as that of the two lowest severity flu pandemics of the 1900s, a modern influenza A pandemic would cause 180 thousand deaths in the US, while a pandemic equaling the 1918 Spanish flu in level of lethality would cause one million deaths in the US. Again, the report offered no evidence that an emerging H5N1 flu pandemic would be between these figures. The current avian flu, in humans, is fatal in over 50% of confirmed cases. Yet early projections like those above have assumed that such a lethal avian strain would surely lose genes contributing to its lethality in humans as it made the adaptations necessary for ready transmission in the human population. This optimistic assumption cannot be relied on. As the WHO reported in November 2006, initial outbreaks of an H5N1 pandemic could rival the current lethality of over 50%. Further information necessary to make an accurate projection of initial lethality of an H5N1 pandemic does not exist, as no data was collected that could show the pre-pandemic virulence in any potential flu strain until after the last pandemic of the 20th Century. There is no basis for assuming that an H5N1 pandemic will emerge with only the far lower 1-2% lethality rate of the Spanish flu, once assumed to be a worst-case scenario. There exists no reliable prediction of the mortality rate of an H5N1 pandemic, and it would be irresponsible to confine planning to only optimistic assumptions out of step with the currently observed case fatality ratio. [ citation needed ] Although marred by unrealistically low ranges of assumed mortality, the earlier planning reports nevertheless show convincingly that we are not prepared even for a pandemic as severe as the milder pandemics of the past century., let alone the much higher case fatality ratios seen more recently.

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Avian influenza

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Influenza vaccine

none Influenza vaccines , colloquially known as flu shots , are vaccines that protect against infection by influenza viruses . New versions of the vaccines are developed twice a year, as the influenza virus rapidly changes. While their effectiveness varies from year to year, most provide modest to high protection against influenza . Vaccination against influenza began in the 1930s, with large-scale availability in the United States beginning in 1945. Both the World Health Organization and the U.S. Centers for Disease Control and Prevention (CDC) recommend yearly vaccination for nearly all people over the age of six months, especially those at high risk, and the influenza vaccine is now on the WHO's List of Essential Medicines . The European Centre for Disease Prevention and Control (ECDC) also recommends yearly vaccination of high-risk groups, particularly pregnant women, the elderly, children between six months and five years, and those with certain health problems. The vaccines are generally safe, including for people who have severe egg allergies . A common side effect is soreness near the site of injection. Fever occurs in five to ten percent of children vaccinated, and temporary muscle pains or feelings of tiredness may occur. In certain years, the vaccine was linked to an increase in Guillain–Barré syndrome among older people at a rate of about one case per million doses. Influenza vaccines are not recommended in those who have had a severe allergy to previous versions of the vaccine itself. The vaccine comes in inactive and weakened viral forms. The live, weakened vaccine is generally not recommended in pregnant women, children less than two years old, adults older than 50, or people with a weakened immune system . Depending on the type it can be injected into a muscle , sprayed into the nose , or injected into the middle layer of the skin (intradermal). The intradermal vaccine was not available during the 2018–2019 and 2019–2020 influenza seasons. Vaccines are used in both humans and non-humans. Human vaccine is meant unless specifically identified as a veterinary, poultry or livestock vaccine. During the worldwide Spanish flu pandemic of 1918, "Pharmacists tried everything they knew, everything they had ever heard of, from the ancient art of bleeding patients, to administering oxygen , to developing new vaccines and serums (chiefly against what we now call Hemophilus influenzae – a name derived from the fact that it was originally considered the etiological agent – and several types of pneumococci). Only one therapeutic measure, transfusing blood from recovered patients to new victims, showed any hint of success." In 1931, viral growth in embryonated hens' eggs was reported by Ernest William Goodpasture and colleagues at Vanderbilt University . The work was extended to growth of influenza virus by several workers, including Thomas Francis , Jonas Salk , Wilson Smith, and Macfarlane Burnet , leading to the first experimental influenza vaccines. In the 1940s, the US military developed the first approved inactivated vaccines for influenza, which were used during World War II . Hens' eggs continued to be used to produce virus used in influenza vaccines, but manufacturers made improvements in the purity of the virus by developing improved processes to remove egg proteins and to reduce systemic reactivity of the vaccine. In 2012, the US Food and Drug Administration (FDA) approved influenza vaccines made by growing virus in cell cultures and influenza vaccines made from recombinant proteins have been approved, with plant-based influenza vaccines being tested [ when? ] in clinical trials. The egg-based technology for producing influenza vaccine was created in the 1950s. In the US swine flu scare of 1976 , President Gerald Ford was confronted with a potential swine flu pandemic. The vaccination program was rushed, yet plagued by delays and public relations problems. Meanwhile, maximum military containment efforts succeeded unexpectedly in confining the new strain to the single army base where it had originated. On that base, a number of soldiers fell severely ill, but only one died. The program was canceled after about 24% of the population had received vaccinations. An excess in deaths of 25 over normal annual levels as well as 400 excess hospitalizations, both from Guillain–Barré syndrome , were estimated to have occurred from the vaccination program itself, demonstrating that the vaccine itself is not free of risks. In the end, however, even the maligned 1976 vaccine may have saved lives. A 2010 study found a significantly enhanced immune response against the 2009 pandemic H1N1 in study participants who had received vaccination against the swine flu in 1976. The 2009 H1N1 "swine flu" outbreak resulted in the rapid approval of pandemic influenza vaccines. Pandemrix was quickly modified to target the circulating strain and by late 2010, 70 million people had received a dose. Eight years later, the BMJ gained access to vaccine pharmacovigilance reports compiled by GSK (GlaxoSmithKline) during the pandemic which the BMJ reported indicated death was 5.39 fold more likely with Pandemrix vs the other pandemic vaccines. A quadrivalent flu vaccine administered by nasal mist was approved by the FDA in March 2012. Fluarix Quadrivalent was approved by the FDA in December 2012. In 2014, the Canadian National Advisory Committee on Immunization (NACI) published a review of quadrivalent influenza vaccines. Starting with the 2018–2019 influenza season most of the regular-dose egg-based flu shots and all the recombinant and cell-grown flu vaccines in the United States are quadrivalent. In the 2019–2020 influenza season all regular-dose flu shots and all recombinant influenza vaccine in the United States are quadrivalent. In November 2019, the FDA approved Fluzone High-Dose Quadrivalent for use in the United States starting with the 2020–2021 influenza season. In February 2020, the FDA approved Fluad Quadrivalent for use in the United States. In July 2020, the FDA approved both Fluad and Fluad Quadrivalent for use in the United States for the 2020–2021 influenza season. The B/Yamagata lineage of influenza B , one of the four lineages targeted by quadrivalent vaccines, might have become extinct in 2020/2021 due to COVID-19 pandemic measures, and there have been no naturally occurring cases confirmed since March 2020. In 2023, the World Health Organization concluded that protection against the Yamagata lineage was no longer necessary in the seasonal flu vaccine, so future vaccines are recommended to be trivalent instead of quadrivalent. For the 2024–2025 Northern Hemisphere influenza season, the FDA recommends removing B/Yamagata from all influenza vaccines. During the worldwide Spanish flu pandemic of 1918, "Pharmacists tried everything they knew, everything they had ever heard of, from the ancient art of bleeding patients, to administering oxygen , to developing new vaccines and serums (chiefly against what we now call Hemophilus influenzae – a name derived from the fact that it was originally considered the etiological agent – and several types of pneumococci). Only one therapeutic measure, transfusing blood from recovered patients to new victims, showed any hint of success." In 1931, viral growth in embryonated hens' eggs was reported by Ernest William Goodpasture and colleagues at Vanderbilt University . The work was extended to growth of influenza virus by several workers, including Thomas Francis , Jonas Salk , Wilson Smith, and Macfarlane Burnet , leading to the first experimental influenza vaccines. In the 1940s, the US military developed the first approved inactivated vaccines for influenza, which were used during World War II . Hens' eggs continued to be used to produce virus used in influenza vaccines, but manufacturers made improvements in the purity of the virus by developing improved processes to remove egg proteins and to reduce systemic reactivity of the vaccine. In 2012, the US Food and Drug Administration (FDA) approved influenza vaccines made by growing virus in cell cultures and influenza vaccines made from recombinant proteins have been approved, with plant-based influenza vaccines being tested [ when? ] in clinical trials. The egg-based technology for producing influenza vaccine was created in the 1950s. In the US swine flu scare of 1976 , President Gerald Ford was confronted with a potential swine flu pandemic. The vaccination program was rushed, yet plagued by delays and public relations problems. Meanwhile, maximum military containment efforts succeeded unexpectedly in confining the new strain to the single army base where it had originated. On that base, a number of soldiers fell severely ill, but only one died. The program was canceled after about 24% of the population had received vaccinations. An excess in deaths of 25 over normal annual levels as well as 400 excess hospitalizations, both from Guillain–Barré syndrome , were estimated to have occurred from the vaccination program itself, demonstrating that the vaccine itself is not free of risks. In the end, however, even the maligned 1976 vaccine may have saved lives. A 2010 study found a significantly enhanced immune response against the 2009 pandemic H1N1 in study participants who had received vaccination against the swine flu in 1976. The 2009 H1N1 "swine flu" outbreak resulted in the rapid approval of pandemic influenza vaccines. Pandemrix was quickly modified to target the circulating strain and by late 2010, 70 million people had received a dose. Eight years later, the BMJ gained access to vaccine pharmacovigilance reports compiled by GSK (GlaxoSmithKline) during the pandemic which the BMJ reported indicated death was 5.39 fold more likely with Pandemrix vs the other pandemic vaccines. A quadrivalent flu vaccine administered by nasal mist was approved by the FDA in March 2012. Fluarix Quadrivalent was approved by the FDA in December 2012. In 2014, the Canadian National Advisory Committee on Immunization (NACI) published a review of quadrivalent influenza vaccines. Starting with the 2018–2019 influenza season most of the regular-dose egg-based flu shots and all the recombinant and cell-grown flu vaccines in the United States are quadrivalent. In the 2019–2020 influenza season all regular-dose flu shots and all recombinant influenza vaccine in the United States are quadrivalent. In November 2019, the FDA approved Fluzone High-Dose Quadrivalent for use in the United States starting with the 2020–2021 influenza season. In February 2020, the FDA approved Fluad Quadrivalent for use in the United States. In July 2020, the FDA approved both Fluad and Fluad Quadrivalent for use in the United States for the 2020–2021 influenza season. The B/Yamagata lineage of influenza B , one of the four lineages targeted by quadrivalent vaccines, might have become extinct in 2020/2021 due to COVID-19 pandemic measures, and there have been no naturally occurring cases confirmed since March 2020. In 2023, the World Health Organization concluded that protection against the Yamagata lineage was no longer necessary in the seasonal flu vaccine, so future vaccines are recommended to be trivalent instead of quadrivalent. For the 2024–2025 Northern Hemisphere influenza season, the FDA recommends removing B/Yamagata from all influenza vaccines. The US Centers for Disease Control and Prevention (CDC) recommends the flu vaccine as the best way to protect people against the flu and prevent its spread. The flu vaccine can also reduce the severity of the flu if a person contracts a strain that the vaccine did not contain. It takes about two weeks following vaccination for protective antibodies to form. A 2012 meta-analysis found that flu vaccination was effective 67 percent of the time; the populations that benefited the most were HIV-positive adults aged 18 to 55 (76 percent), healthy adults aged 18 to 46 (approximately 70 percent), and healthy children aged six months to 24 months (66 percent). The influenza vaccine also appears to protect against myocardial infarction with a benefit of 15–45%. A vaccine is assessed by its efficacy – the extent to which it reduces risk of disease under controlled conditions – and its effectiveness – the observed reduction in risk after the vaccine is put into use. In the case of influenza, effectiveness is expected to be lower than the efficacy because it is measured using the rates of influenza-like illness , which is not always caused by influenza. Studies on the effectiveness of flu vaccines in the real world are difficult; vaccines may be imperfectly matched, virus prevalence varies widely between years, and influenza is often confused with other influenza-like illnesses. However, in most years (16 of the 19 years before 2007), the flu vaccine strains have been a good match for the circulating strains, and even a mismatched vaccine can often provide cross-protection. The virus rapidly changes due to antigenic drift , a slight mutation in the virus that causes a new strain to arise. The effectiveness of seasonal flu vaccines varies significantly, with an estimated average efficacy of 50–60% against symptomatic disease, depending on vaccine strain, age, prior immunity, and immune function, so vaccinated people can still contract influenza. The effectiveness of flu vaccines is considered to be suboptimal, particularly among the elderly, but vaccination is still beneficial in reducing the mortality rate and hospitalization rate due to influenza as well as duration of hospitalization. Vaccination of school-age children has shown to provide indirect protection for other age groups. LAIVs are recommended for children based on superior efficacy, especially for children under 6, and greater immunity against non-vaccine strains when compared to inactivated vaccines. From 2012 to 2015 in New Zealand, vaccine effectiveness against admission to an intensive care unit was 82%. Effectiveness against hospitalized influenza illness in the 2019–2020 United States flu season was 41% overall and 54% in people aged 65 years or older. One review found 31% effectiveness against death among adults. Repeated annual influenza vaccination generally offers consistent year-on-year protection against influenza. There is, however, suggestive evidence that repeated vaccinations may cause a reduction in vaccine effectiveness for certain influenza subtypes; this has no relevance to current recommendations for yearly vaccinations but might influence future vaccination policy. As of 2019 [ update ] , the CDC recommends a yearly vaccine as most studies demonstrate overall effectiveness of annual influenza vaccination. There is not enough evidence to establish significant differences in the effectiveness of different influenza vaccine types , but there are high-dose or adjuvanted products that induce a stronger immune response in the elderly. According to a 2016 study by faculty at the University of New South Wales, getting a flu shot was as effective or better at preventing a heart attack than even quitting smoking. In April 2002, the Advisory Committee on Immunization Practices (ACIP) encouraged that children 6 to 23 months of age be vaccinated annually against influenza. In 2010, ACIP recommended annual influenza vaccination for those 6 months of age and older. Currently the CDC recommends that everyone except infants under the age of six months should receive the seasonal influenza vaccine. Vaccination campaigns usually focus special attention on people who are at high risk of serious complications if they catch the flu, such as pregnant women, children under 59 months, the elderly, and people with chronic illnesses or weakened immune systems , as well as those to whom they are exposed, such as health care workers. As the death rate is also high among infants who catch influenza, the CDC and the WHO recommend that household contacts and caregivers of infants be vaccinated to reduce the risk of passing an influenza infection to the infant. In children, the vaccine appears to decrease the risk of influenza and possibly influenza-like illness . In children under the age of two data are limited. During the 2017–18 flu season, the CDC director indicated that 85 percent of the children who died "likely will not have been vaccinated". In the United States, as of January 2019 [ update ] , the CDC recommend that children aged six through 35 months may receive either 0.25 milliliters or 0.5 milliliters per dose of Fluzone Quadrivalent. There is no preference for one or the other dose volume of Fluzone Quadrivalent for that age group. All persons 36 months of age and older should receive 0.5 milliliters per dose of Fluzone Quadrivalent. As of October 2018 [ update ] , Afluria Quadrivalent is licensed for children six months of age and older in the United States. Children six months through 35 months of age should receive 0.25 milliliters for each dose of Afluria Quadrivalent. All persons 36 months of age and older should receive 0.5 milliliters per dose of Afluria Quadrivalent. As of February 2018 [ update ] , Afluria Tetra is licensed for adults and children five years of age and older in Canada. In 2014, the Canadian National Advisory Committee on Immunization (NACI) published a review of influenza vaccination in healthy 5–18-year-olds, and in 2015, published a review of the use of pediatric Fluad in children 6–72 months of age. In one study, conducted in a tertiary referral center, the rate of influenza vaccination in children was only 31%. Higher rates were found among immuno-suppressed pediatric patients (46%), and in patients with inflammatory bowel disease (50%). In unvaccinated adults, 16% get symptoms similar to the flu, while about 10% of vaccinated adults do. Vaccination decreased confirmed cases of influenza from about 2.4% to 1.1%. No effect on hospitalization was found. In working adults, a review by the Cochrane Collaboration found that vaccination resulted in a modest decrease in both influenza symptoms and working days lost, without affecting transmission or influenza-related complications. In healthy working adults, influenza vaccines can provide moderate protection against virologically confirmed influenza, though such protection is greatly reduced or absent in some seasons. In health care workers, a 2006 review found a net benefit. Of the eighteen studies in this review, only two also assessed the relationship of patient mortality relative to staff influenza vaccine uptake; both found that higher rates of health care worker vaccination correlated with reduced patient deaths. A 2014 review found benefits to patients when health care workers were immunized, as supported by moderate evidence based in part on the observed reduction in all-cause deaths in patients whose health care workers were given immunization compared with comparison patients where the workers were not offered vaccine. Evidence for an effect in adults over 65 is unclear. Systematic reviews examining both randomized controlled and case–control studies found a lack of high-quality evidence. Reviews of case–control studies found effects against laboratory-confirmed influenza, pneumonia , and death among the community-dwelling elderly. The group most vulnerable to non-pandemic flu, the elderly, benefits least from the vaccine. There are multiple reasons behind this steep decline in vaccine efficacy, the most common of which are the declining immunological function and frailty associated with advanced age. In a non-pandemic year, a person in the United States aged 50–64 is nearly ten times more likely to die an influenza-associated death than a younger person, and a person over 65 is more than ten times more likely to die an influenza-associated death than the 50–64 age group. There is a high-dose flu vaccine specifically formulated to provide a stronger immune response. Available evidence indicates that vaccinating the elderly with the high-dose vaccine leads to a stronger immune response against influenza than the regular-dose vaccine. A flu vaccine containing an adjuvant was approved by the US Food and Drug Administration (FDA) in November 2015, for use by adults aged 65 years of age and older. The vaccine is marketed as Fluad in the US and was first available in the 2016–2017 flu season. The vaccine contains the MF59C.1 adjuvant which is an oil-in-water emulsion of squalene oil. It is the first adjuvanted seasonal flu vaccine marketed in the United States. It is not clear if there is a significant benefit for the elderly to use a flu vaccine containing the MF59C.1 adjuvant. Per Advisory Committee on Immunization Practices guidelines, Fluad can be used as an alternative to other influenza vaccines approved for people 65 years and older. Vaccinating health care workers who work with elderly people is recommended in many countries, with the goal of reducing influenza outbreaks in this vulnerable population. While there is no conclusive evidence from randomized clinical trials that vaccinating health care workers helps protect elderly people from influenza, there is tentative evidence of benefit. Fluad Quad was approved for use in Australia in September 2019, Fluad Quadrivalent was approved for use in the United States in February 2020, and Fluad Tetra was approved for use in the European Union in May 2020. As well as protecting mother and child from the effects of an influenza infection, the immunization of pregnant women tends to increase their chances of experiencing a successful full-term pregnancy. The trivalent inactivated influenza vaccine is protective in pregnant women infected with HIV . A vaccine is assessed by its efficacy – the extent to which it reduces risk of disease under controlled conditions – and its effectiveness – the observed reduction in risk after the vaccine is put into use. In the case of influenza, effectiveness is expected to be lower than the efficacy because it is measured using the rates of influenza-like illness , which is not always caused by influenza. Studies on the effectiveness of flu vaccines in the real world are difficult; vaccines may be imperfectly matched, virus prevalence varies widely between years, and influenza is often confused with other influenza-like illnesses. However, in most years (16 of the 19 years before 2007), the flu vaccine strains have been a good match for the circulating strains, and even a mismatched vaccine can often provide cross-protection. The virus rapidly changes due to antigenic drift , a slight mutation in the virus that causes a new strain to arise. The effectiveness of seasonal flu vaccines varies significantly, with an estimated average efficacy of 50–60% against symptomatic disease, depending on vaccine strain, age, prior immunity, and immune function, so vaccinated people can still contract influenza. The effectiveness of flu vaccines is considered to be suboptimal, particularly among the elderly, but vaccination is still beneficial in reducing the mortality rate and hospitalization rate due to influenza as well as duration of hospitalization. Vaccination of school-age children has shown to provide indirect protection for other age groups. LAIVs are recommended for children based on superior efficacy, especially for children under 6, and greater immunity against non-vaccine strains when compared to inactivated vaccines. From 2012 to 2015 in New Zealand, vaccine effectiveness against admission to an intensive care unit was 82%. Effectiveness against hospitalized influenza illness in the 2019–2020 United States flu season was 41% overall and 54% in people aged 65 years or older. One review found 31% effectiveness against death among adults. Repeated annual influenza vaccination generally offers consistent year-on-year protection against influenza. There is, however, suggestive evidence that repeated vaccinations may cause a reduction in vaccine effectiveness for certain influenza subtypes; this has no relevance to current recommendations for yearly vaccinations but might influence future vaccination policy. As of 2019 [ update ] , the CDC recommends a yearly vaccine as most studies demonstrate overall effectiveness of annual influenza vaccination. There is not enough evidence to establish significant differences in the effectiveness of different influenza vaccine types , but there are high-dose or adjuvanted products that induce a stronger immune response in the elderly. According to a 2016 study by faculty at the University of New South Wales, getting a flu shot was as effective or better at preventing a heart attack than even quitting smoking. In April 2002, the Advisory Committee on Immunization Practices (ACIP) encouraged that children 6 to 23 months of age be vaccinated annually against influenza. In 2010, ACIP recommended annual influenza vaccination for those 6 months of age and older. Currently the CDC recommends that everyone except infants under the age of six months should receive the seasonal influenza vaccine. Vaccination campaigns usually focus special attention on people who are at high risk of serious complications if they catch the flu, such as pregnant women, children under 59 months, the elderly, and people with chronic illnesses or weakened immune systems , as well as those to whom they are exposed, such as health care workers. As the death rate is also high among infants who catch influenza, the CDC and the WHO recommend that household contacts and caregivers of infants be vaccinated to reduce the risk of passing an influenza infection to the infant. In children, the vaccine appears to decrease the risk of influenza and possibly influenza-like illness . In children under the age of two data are limited. During the 2017–18 flu season, the CDC director indicated that 85 percent of the children who died "likely will not have been vaccinated". In the United States, as of January 2019 [ update ] , the CDC recommend that children aged six through 35 months may receive either 0.25 milliliters or 0.5 milliliters per dose of Fluzone Quadrivalent. There is no preference for one or the other dose volume of Fluzone Quadrivalent for that age group. All persons 36 months of age and older should receive 0.5 milliliters per dose of Fluzone Quadrivalent. As of October 2018 [ update ] , Afluria Quadrivalent is licensed for children six months of age and older in the United States. Children six months through 35 months of age should receive 0.25 milliliters for each dose of Afluria Quadrivalent. All persons 36 months of age and older should receive 0.5 milliliters per dose of Afluria Quadrivalent. As of February 2018 [ update ] , Afluria Tetra is licensed for adults and children five years of age and older in Canada. In 2014, the Canadian National Advisory Committee on Immunization (NACI) published a review of influenza vaccination in healthy 5–18-year-olds, and in 2015, published a review of the use of pediatric Fluad in children 6–72 months of age. In one study, conducted in a tertiary referral center, the rate of influenza vaccination in children was only 31%. Higher rates were found among immuno-suppressed pediatric patients (46%), and in patients with inflammatory bowel disease (50%). In unvaccinated adults, 16% get symptoms similar to the flu, while about 10% of vaccinated adults do. Vaccination decreased confirmed cases of influenza from about 2.4% to 1.1%. No effect on hospitalization was found. In working adults, a review by the Cochrane Collaboration found that vaccination resulted in a modest decrease in both influenza symptoms and working days lost, without affecting transmission or influenza-related complications. In healthy working adults, influenza vaccines can provide moderate protection against virologically confirmed influenza, though such protection is greatly reduced or absent in some seasons. In health care workers, a 2006 review found a net benefit. Of the eighteen studies in this review, only two also assessed the relationship of patient mortality relative to staff influenza vaccine uptake; both found that higher rates of health care worker vaccination correlated with reduced patient deaths. A 2014 review found benefits to patients when health care workers were immunized, as supported by moderate evidence based in part on the observed reduction in all-cause deaths in patients whose health care workers were given immunization compared with comparison patients where the workers were not offered vaccine. Evidence for an effect in adults over 65 is unclear. Systematic reviews examining both randomized controlled and case–control studies found a lack of high-quality evidence. Reviews of case–control studies found effects against laboratory-confirmed influenza, pneumonia , and death among the community-dwelling elderly. The group most vulnerable to non-pandemic flu, the elderly, benefits least from the vaccine. There are multiple reasons behind this steep decline in vaccine efficacy, the most common of which are the declining immunological function and frailty associated with advanced age. In a non-pandemic year, a person in the United States aged 50–64 is nearly ten times more likely to die an influenza-associated death than a younger person, and a person over 65 is more than ten times more likely to die an influenza-associated death than the 50–64 age group. There is a high-dose flu vaccine specifically formulated to provide a stronger immune response. Available evidence indicates that vaccinating the elderly with the high-dose vaccine leads to a stronger immune response against influenza than the regular-dose vaccine. A flu vaccine containing an adjuvant was approved by the US Food and Drug Administration (FDA) in November 2015, for use by adults aged 65 years of age and older. The vaccine is marketed as Fluad in the US and was first available in the 2016–2017 flu season. The vaccine contains the MF59C.1 adjuvant which is an oil-in-water emulsion of squalene oil. It is the first adjuvanted seasonal flu vaccine marketed in the United States. It is not clear if there is a significant benefit for the elderly to use a flu vaccine containing the MF59C.1 adjuvant. Per Advisory Committee on Immunization Practices guidelines, Fluad can be used as an alternative to other influenza vaccines approved for people 65 years and older. Vaccinating health care workers who work with elderly people is recommended in many countries, with the goal of reducing influenza outbreaks in this vulnerable population. While there is no conclusive evidence from randomized clinical trials that vaccinating health care workers helps protect elderly people from influenza, there is tentative evidence of benefit. Fluad Quad was approved for use in Australia in September 2019, Fluad Quadrivalent was approved for use in the United States in February 2020, and Fluad Tetra was approved for use in the European Union in May 2020. As well as protecting mother and child from the effects of an influenza infection, the immunization of pregnant women tends to increase their chances of experiencing a successful full-term pregnancy. The trivalent inactivated influenza vaccine is protective in pregnant women infected with HIV . Common side effects of vaccination include local injection-site reactions and cold -like symptoms. Fever, malaise , and myalgia are less common. Flu vaccines are contraindicated for people who have experienced a severe allergic reaction in response to a flu vaccine or to any component of the vaccine. LAIVs are not given to children or adolescents with severe immunodeficiency or to those who are using salicylate treatments because of the risk of developing Reye syndrome . LAIVs are also not recommended for children under the age of 2, pregnant women, and adults with immunosuppression. Inactivated flu vaccines cannot cause influenza and are regarded as safe during pregnancy. While side effects of the flu vaccine may occur, they are usually minor, including soreness, redness, and swelling around the point of injection, headache, fever, nausea or fatigue. Side effects of a nasal spray vaccine may include runny nose, wheezing, sore throat, cough, or vomiting. In some people, a flu vaccine may cause serious side effects, including an allergic reaction , but this is rare. Furthermore, the common side effects and risks are mild and temporary when compared to the risks and severe health effects of the annual influenza epidemic. Although Guillain–Barré syndrome had been feared as a complication of vaccination, the CDC states that most studies on modern influenza vaccines have seen no link with Guillain–Barré. Infection with influenza virus itself increases both the risk of death (up to one in ten thousand) and the risk of developing Guillain–Barré syndrome to a far higher level than the highest level of suspected vaccine involvement (approximately ten times higher by 2009 estimates). Although one review gives an incidence of about one case of Guillain–Barré per million vaccinations, a large study in China, covering close to a hundred million doses of vaccine against the 2009 H1N1 "swine" flu found only eleven cases of Guillain–Barré syndrome, (0.1 per million doses) total incidence in persons vaccinated, actually lower than the normal rate of the disease in China, and no other notable side effects. Although most influenza vaccines are produced using egg-based techniques, influenza vaccines are nonetheless still recommended as safe for people with egg allergies , even if severe, as no increased risk of allergic reaction to the egg-based vaccines has been shown for people with egg allergies. Studies examining the safety of influenza vaccines in people with severe egg allergies found that anaphylaxis was very rare, occurring in 1.3 cases per million doses given. Monitoring for symptoms from vaccination is recommended in those with more severe symptoms. A study of nearly 800 children with egg allergy, including over 250 with previous anaphylactic reactions, had zero systemic allergic reactions when given the live attenuated flu vaccine. Vaccines produced using other technologies, notably recombinant vaccines and those based on cell culture rather than egg protein, started to become available from 2012 in the US, and later in Europe and Australia. Several studies have identified an increased incidence of narcolepsy among recipients of the pandemic H1N1 influenza AS03 -adjuvanted vaccine; efforts to identify a mechanism for this suggest that narcolepsy is autoimmune, and that the AS03-adjuvanted H1N1 vaccine may mimic hypocretin , serving as a trigger. Some injection-based flu vaccines intended for adults in the United States contain thiomersal (also known as thimerosal), a mercury -based preservative. Despite some controversy in the media, the World Health Organization 's Global Advisory Committee on Vaccine Safety has concluded that there is no evidence of toxicity from thiomersal in vaccines and no reason on grounds of safety to change to more-expensive single-dose administration. Common side effects of vaccination include local injection-site reactions and cold -like symptoms. Fever, malaise , and myalgia are less common. Flu vaccines are contraindicated for people who have experienced a severe allergic reaction in response to a flu vaccine or to any component of the vaccine. LAIVs are not given to children or adolescents with severe immunodeficiency or to those who are using salicylate treatments because of the risk of developing Reye syndrome . LAIVs are also not recommended for children under the age of 2, pregnant women, and adults with immunosuppression. Inactivated flu vaccines cannot cause influenza and are regarded as safe during pregnancy. While side effects of the flu vaccine may occur, they are usually minor, including soreness, redness, and swelling around the point of injection, headache, fever, nausea or fatigue. Side effects of a nasal spray vaccine may include runny nose, wheezing, sore throat, cough, or vomiting. In some people, a flu vaccine may cause serious side effects, including an allergic reaction , but this is rare. Furthermore, the common side effects and risks are mild and temporary when compared to the risks and severe health effects of the annual influenza epidemic. Although Guillain–Barré syndrome had been feared as a complication of vaccination, the CDC states that most studies on modern influenza vaccines have seen no link with Guillain–Barré. Infection with influenza virus itself increases both the risk of death (up to one in ten thousand) and the risk of developing Guillain–Barré syndrome to a far higher level than the highest level of suspected vaccine involvement (approximately ten times higher by 2009 estimates). Although one review gives an incidence of about one case of Guillain–Barré per million vaccinations, a large study in China, covering close to a hundred million doses of vaccine against the 2009 H1N1 "swine" flu found only eleven cases of Guillain–Barré syndrome, (0.1 per million doses) total incidence in persons vaccinated, actually lower than the normal rate of the disease in China, and no other notable side effects. Although most influenza vaccines are produced using egg-based techniques, influenza vaccines are nonetheless still recommended as safe for people with egg allergies , even if severe, as no increased risk of allergic reaction to the egg-based vaccines has been shown for people with egg allergies. Studies examining the safety of influenza vaccines in people with severe egg allergies found that anaphylaxis was very rare, occurring in 1.3 cases per million doses given. Monitoring for symptoms from vaccination is recommended in those with more severe symptoms. A study of nearly 800 children with egg allergy, including over 250 with previous anaphylactic reactions, had zero systemic allergic reactions when given the live attenuated flu vaccine. Vaccines produced using other technologies, notably recombinant vaccines and those based on cell culture rather than egg protein, started to become available from 2012 in the US, and later in Europe and Australia. Several studies have identified an increased incidence of narcolepsy among recipients of the pandemic H1N1 influenza AS03 -adjuvanted vaccine; efforts to identify a mechanism for this suggest that narcolepsy is autoimmune, and that the AS03-adjuvanted H1N1 vaccine may mimic hypocretin , serving as a trigger. Some injection-based flu vaccines intended for adults in the United States contain thiomersal (also known as thimerosal), a mercury -based preservative. Despite some controversy in the media, the World Health Organization 's Global Advisory Committee on Vaccine Safety has concluded that there is no evidence of toxicity from thiomersal in vaccines and no reason on grounds of safety to change to more-expensive single-dose administration. Seasonal flu vaccines are available either as: [ citation needed ] a trivalent or quadrivalent intramuscular injection (IIV3, IIV4, or RIV4, that is, TIV or QIV), which contains the inactivated form of the virus a nasal spray of live attenuated influenza vaccine (LAIV, Q/LAIV), which contains the live but attenuated (weakened) form of the virus. TIV or QIV induce protection after injection (typically intramuscular, though subcutaneous and intradermal routes can also be protective) based on an immune response to the antigens present on the inactivated virus, while cold-adapted LAIV works by establishing infection in the nasal passages. Various public health organizations, including the World Health Organization (WHO), recommend that yearly influenza vaccination be routinely offered, particularly to people at risk of complications of influenza and those individuals who live with or care for high-risk individuals, including: The flu vaccine is contraindicated for those under six months of age and those with severe, life-threatening allergies to flu vaccine or any ingredient in the vaccine. As of 2016 [ update ] , the World Health Organization (WHO) recommends seasonal influenza vaccination for: First priority: Pregnant women Second priority (in no particular order): Children aged 6–59 months Elderly Individuals with specific chronic medical conditions Health-care workers The National Advisory Committee on Immunization (NACI), the group that advises the Public Health Agency of Canada , recommends that everyone over six months of age be encouraged to receive annual influenza vaccination, and that children between the age of six months and 24 months, and their household contacts, should be considered a high priority for the flu vaccine. Particularly: People at high risk of influenza-related complications or hospitalization, including people who are morbidly obese, healthy pregnant women, children aged 6–59 months, the elderly, aboriginals, and people with one of an itemized list of chronic health conditions People capable of transmitting influenza to those at high risk, including household contacts and health care workers People who provide essential community services Certain poultry workers Live attenuated influenza vaccine (LAIV) was not available in Canada for the 2019–2020 season. The European Centre for Disease Prevention and Control (ECDC) recommends vaccinating the elderly as a priority, with a secondary priority people with chronic medical conditions and health care workers. The influenza vaccination strategy is generally that of protecting vulnerable people, rather than limiting influenza circulation or eliminating human influenza sickness. This is in contrast with the high herd immunity strategies for other infectious diseases such as polio and measles . This is also due in part to the financial and logistics burden associated with the need of an annual injection. In the United States routine influenza vaccination is recommended for all persons aged six months and over. It takes up to two weeks after vaccination for sufficient antibodies to develop in the body. The CDC recommends vaccination before the end of October, although it considers getting a vaccine in December or even later to be still beneficial. The U.S. military also requires a flu shot annually for its active and reserve servicemembers. According to the CDC, the live attenuated virus (LAIV4) (which comes in the form of the nasal spray in the US) should be avoided by some groups. Within its blanket recommendation for general vaccination in the United States, the CDC, which began recommending the influenza vaccine to health care workers in 1981, emphasizes to clinicians the special urgency of vaccination for members of certain vulnerable groups, and their caregivers : The US government requires hospitals to report worker vaccination rates. Some US states and hundreds of US hospitals require health care workers to either get vaccinations or wear masks during flu season. These requirements occasionally engender union lawsuits on narrow collective bargaining grounds, but proponents note that courts have generally endorsed forced vaccination laws affecting the general population during disease outbreaks. Vaccination against influenza is especially considered important for members of high-risk groups who would be likely to have complications from influenza, for example pregnant women and children and teenagers from six months to 18 years of age who are receiving aspirin- or salicylate-containing medications and who might be at risk for experiencing Reye syndrome after influenza virus infection; The CDC indicated that live attenuated influenza vaccine (LAIV), also called the nasal spray vaccine, was not recommended for the 2016–2017 flu season in the United States. Furthermore, the CDC recommends that health care personnel who care for severely immunocompromised persons receive injections (TIV or QIV) rather than LAIV. The Australian Government recommends seasonal flu vaccination for everyone over the age of six months. Australia uses inactivated vaccines . Until 2021, the egg-based vaccine has been the only one available (and continues to be the only free one), but from March 2021 a new cell-based vaccine is available for those who wish to pay for it, and it is expected that this one will become the standard by 2026. The standard flu vaccine is free for the following people: children aged six months to five years; people aged 65 years and over; Aboriginal and Torres Strait Islander people aged six months and over; pregnant women; and anyone over six months of age with medical conditions such as severe asthma, lung disease or heart disease, low immunity or diabetes that can lead to complications from influenza.As of 2016 [ update ] , the World Health Organization (WHO) recommends seasonal influenza vaccination for: First priority: Pregnant women Second priority (in no particular order): Children aged 6–59 months Elderly Individuals with specific chronic medical conditions Health-care workersThe National Advisory Committee on Immunization (NACI), the group that advises the Public Health Agency of Canada , recommends that everyone over six months of age be encouraged to receive annual influenza vaccination, and that children between the age of six months and 24 months, and their household contacts, should be considered a high priority for the flu vaccine. Particularly: People at high risk of influenza-related complications or hospitalization, including people who are morbidly obese, healthy pregnant women, children aged 6–59 months, the elderly, aboriginals, and people with one of an itemized list of chronic health conditions People capable of transmitting influenza to those at high risk, including household contacts and health care workers People who provide essential community services Certain poultry workers Live attenuated influenza vaccine (LAIV) was not available in Canada for the 2019–2020 season. The European Centre for Disease Prevention and Control (ECDC) recommends vaccinating the elderly as a priority, with a secondary priority people with chronic medical conditions and health care workers. The influenza vaccination strategy is generally that of protecting vulnerable people, rather than limiting influenza circulation or eliminating human influenza sickness. This is in contrast with the high herd immunity strategies for other infectious diseases such as polio and measles . This is also due in part to the financial and logistics burden associated with the need of an annual injection. In the United States routine influenza vaccination is recommended for all persons aged six months and over. It takes up to two weeks after vaccination for sufficient antibodies to develop in the body. The CDC recommends vaccination before the end of October, although it considers getting a vaccine in December or even later to be still beneficial. The U.S. military also requires a flu shot annually for its active and reserve servicemembers. According to the CDC, the live attenuated virus (LAIV4) (which comes in the form of the nasal spray in the US) should be avoided by some groups. Within its blanket recommendation for general vaccination in the United States, the CDC, which began recommending the influenza vaccine to health care workers in 1981, emphasizes to clinicians the special urgency of vaccination for members of certain vulnerable groups, and their caregivers : The US government requires hospitals to report worker vaccination rates. Some US states and hundreds of US hospitals require health care workers to either get vaccinations or wear masks during flu season. These requirements occasionally engender union lawsuits on narrow collective bargaining grounds, but proponents note that courts have generally endorsed forced vaccination laws affecting the general population during disease outbreaks. Vaccination against influenza is especially considered important for members of high-risk groups who would be likely to have complications from influenza, for example pregnant women and children and teenagers from six months to 18 years of age who are receiving aspirin- or salicylate-containing medications and who might be at risk for experiencing Reye syndrome after influenza virus infection; The CDC indicated that live attenuated influenza vaccine (LAIV), also called the nasal spray vaccine, was not recommended for the 2016–2017 flu season in the United States. Furthermore, the CDC recommends that health care personnel who care for severely immunocompromised persons receive injections (TIV or QIV) rather than LAIV. The Australian Government recommends seasonal flu vaccination for everyone over the age of six months. Australia uses inactivated vaccines . Until 2021, the egg-based vaccine has been the only one available (and continues to be the only free one), but from March 2021 a new cell-based vaccine is available for those who wish to pay for it, and it is expected that this one will become the standard by 2026. The standard flu vaccine is free for the following people: children aged six months to five years; people aged 65 years and over; Aboriginal and Torres Strait Islander people aged six months and over; pregnant women; and anyone over six months of age with medical conditions such as severe asthma, lung disease or heart disease, low immunity or diabetes that can lead to complications from influenza.Uptake of flu vaccination, both seasonally and during pandemics, is often low. Systematic reviews of pandemic flu vaccination uptake have identified several personal factors that may influence uptake, including gender (higher uptake in men), ethnicity (higher in people from ethnic minorities) and having a chronic illness. Beliefs in the safety and effectiveness of the vaccine are also important. A number of measures have been found to be useful to increase rates of vaccination in those over sixty including: patient reminders using leaflets and letters, postcard reminders, client outreach programs, vaccine home visits, group vaccinations, free vaccinations, physician payment, physician reminders and encouraging physician competition. Frontline health care workers are often recommended to get seasonal and any pandemic flu vaccination. For example, in the UK all health care workers involved in patient care are recommended to receive the seasonal flu vaccine, and were also recommended to be vaccinated against the H1N1/09 (later renamed A(H1N1)pdm09 [note 1] ) swine flu virus during the 2009 pandemic . However, uptake is often low. During the 2009 pandemic, low uptake by healthcare workers was seen in countries including the UK, Italy, Greece, and Hong Kong. In a 2010 survey of United States health care workers, 63.5% reported that they received the flu vaccine during the 2010–11 season, an increase from 61.9% reported the previous season. US Health professionals with direct patient contact had higher vaccination uptake, such as physicians and dentists (84.2%) and nurse practitioners (82.6%). The main reason to vaccinate health care workers is to prevent staff from spreading flu to their patients and to reduce staff absence at a time of high service demand, but the reasons health care workers state for their decisions to accept or decline vaccination may more often be to do with perceived personal benefits. In Victoria (Australia) public hospitals, rates of health care worker vaccination in 2005 ranged from 34% for non-clinical staff to 42% for laboratory staff. One of the reasons for rejecting vaccines was concern over adverse reactions; in one study, 31% of resident physicians at a teaching hospital incorrectly believed Australian vaccines could cause influenza. Uptake of flu vaccination, both seasonally and during pandemics, is often low. Systematic reviews of pandemic flu vaccination uptake have identified several personal factors that may influence uptake, including gender (higher uptake in men), ethnicity (higher in people from ethnic minorities) and having a chronic illness. Beliefs in the safety and effectiveness of the vaccine are also important. A number of measures have been found to be useful to increase rates of vaccination in those over sixty including: patient reminders using leaflets and letters, postcard reminders, client outreach programs, vaccine home visits, group vaccinations, free vaccinations, physician payment, physician reminders and encouraging physician competition. Frontline health care workers are often recommended to get seasonal and any pandemic flu vaccination. For example, in the UK all health care workers involved in patient care are recommended to receive the seasonal flu vaccine, and were also recommended to be vaccinated against the H1N1/09 (later renamed A(H1N1)pdm09 [note 1] ) swine flu virus during the 2009 pandemic . However, uptake is often low. During the 2009 pandemic, low uptake by healthcare workers was seen in countries including the UK, Italy, Greece, and Hong Kong. In a 2010 survey of United States health care workers, 63.5% reported that they received the flu vaccine during the 2010–11 season, an increase from 61.9% reported the previous season. US Health professionals with direct patient contact had higher vaccination uptake, such as physicians and dentists (84.2%) and nurse practitioners (82.6%). The main reason to vaccinate health care workers is to prevent staff from spreading flu to their patients and to reduce staff absence at a time of high service demand, but the reasons health care workers state for their decisions to accept or decline vaccination may more often be to do with perceived personal benefits. In Victoria (Australia) public hospitals, rates of health care worker vaccination in 2005 ranged from 34% for non-clinical staff to 42% for laboratory staff. One of the reasons for rejecting vaccines was concern over adverse reactions; in one study, 31% of resident physicians at a teaching hospital incorrectly believed Australian vaccines could cause influenza. Research continues into the idea of a "universal" influenza vaccine that would not require tailoring to a particular strain, but would be effective against a broad variety of influenza viruses. No vaccine candidates had been announced by November 2007, but as of 2021 [ update ] , there are several universal vaccines candidates, in pre-clinical development and in clinical trials. In a 2007 report, the global capacity of approximately 826 million seasonal influenza vaccine doses (inactivated and live) was double the production of 413 million doses. In an aggressive scenario of producing pandemic influenza vaccines by 2013, only 2.8 billion courses could be produced in a six-month time frame. If all high- and upper-middle-income countries sought vaccines for their entire populations in a pandemic, nearly two billion courses would be required. If China pursued this goal as well, more than three billion courses would be required to serve these populations. Vaccine research and development is ongoing to identify novel vaccine approaches that could produce much greater quantities of vaccine at a price that is affordable to the global population. [ citation needed ] Most flu vaccines are grown by vaccine manufacturers in fertilized chicken eggs. In the Northern hemisphere, the manufacturing process begins following the announcement (typically in February) of the WHO recommended strains for the winter flu season. Three strains (representing an H1N1, an H3N2, and a B strain) of flu are selected and chicken eggs are inoculated separately. These monovalent harvests are then combined to make the trivalent vaccine. As of November 2007 [ update ] , both the conventional injection and the nasal spray are manufactured using chicken eggs. The European Union also approved Optaflu , a vaccine produced by Novartis using vats of animal cells. This technique is expected to be more scalable and avoid problems with eggs, such as allergic reactions and incompatibility with strains that affect avians like chickens. Influenza vaccines are produced in pathogen -free eggs that are eleven or twelve days old. The top of the egg is disinfected by wiping it with alcohol and then the egg is candled to identify a non-veinous area in the allantoic cavity where a small hole is poked to serve as a pressure release. A second hole is made at the top of the egg, where the influenza virus is injected in the allantoic cavity, past the chorioallantoic membrane. The two holes are then sealed with melted paraffin and the inoculated eggs are incubated for 48 hours at 37 degrees Celsius. During incubation time, the virus replicates and newly replicated viruses are released into the allantoic fluid After the 48-hour incubation period, the top of the egg is cracked and the ten milliliters of allantoic fluid is removed, from which about fifteen micrograms of the flu vaccine can be obtained. At this point, the viruses have been weakened or killed and the viral antigen is purified and placed inside vials, syringes, or nasal sprayers. Up to 3 eggs are needed to produce one dose of a trivalent vaccine, and an estimated 600 million eggs are produced each year for flu vaccine production. Methods of vaccine generation that bypass the need for eggs include the construction of influenza virus-like particles (VLP). VLP resemble viruses, but there is no need for inactivation, as they do not include viral coding elements, but merely present antigens in a similar manner to a virion. Some methods of producing VLP include cultures of Spodoptera frugiperda Sf9 insect cells and plant-based vaccine production (e.g., production in Nicotiana benthamiana ). There is evidence that some VLPs elicit antibodies that recognize a broader panel of antigenically distinct viral isolates compared to other vaccines in the hemagglutination-inhibition assay (HIA). A gene-based DNA vaccine, used to prime the immune system after boosting with an inactivated H5N1 vaccine , underwent clinical trials in 2011. On November 20, 2012, Novartis received FDA approval for the first cell-culture vaccine. In 2013, the recombinant influenza vaccine, Flublok, was approved for use in the United States. On September 17, 2020, the Committee for Medicinal Products for Human Use (CHMP) of the European Medicines Agency (EMA) adopted a positive opinion, recommending the granting of a marketing authorization for Supemtek, a quadrivalent influenza vaccine (recombinant, prepared in cell culture). The applicant for this medicinal product is Sanofi Pasteur. Supemtek was approved for medical use in the European Union in November 2020. Australia authorised its first and cell-based vaccine in March 2021, based on an "eternal cell line" of a dog kidney . Because of the way it is produced, it produces better-matched vaccine (to the flu strains). According to the WHO , as of 2019 [ update ] , countries where influenza vaccine is produced include: Australia Brazil Canada China France Germany Hungary India Iran Japan Mexico Netherlands Nicaragua Russian Federation South Korea United Kingdom United States Vietnam In addition, Kazakhstan, Serbia and Thailand had facilities in final stages of establishing production. Most flu vaccines are grown by vaccine manufacturers in fertilized chicken eggs. In the Northern hemisphere, the manufacturing process begins following the announcement (typically in February) of the WHO recommended strains for the winter flu season. Three strains (representing an H1N1, an H3N2, and a B strain) of flu are selected and chicken eggs are inoculated separately. These monovalent harvests are then combined to make the trivalent vaccine. As of November 2007 [ update ] , both the conventional injection and the nasal spray are manufactured using chicken eggs. The European Union also approved Optaflu , a vaccine produced by Novartis using vats of animal cells. This technique is expected to be more scalable and avoid problems with eggs, such as allergic reactions and incompatibility with strains that affect avians like chickens. Influenza vaccines are produced in pathogen -free eggs that are eleven or twelve days old. The top of the egg is disinfected by wiping it with alcohol and then the egg is candled to identify a non-veinous area in the allantoic cavity where a small hole is poked to serve as a pressure release. A second hole is made at the top of the egg, where the influenza virus is injected in the allantoic cavity, past the chorioallantoic membrane. The two holes are then sealed with melted paraffin and the inoculated eggs are incubated for 48 hours at 37 degrees Celsius. During incubation time, the virus replicates and newly replicated viruses are released into the allantoic fluid After the 48-hour incubation period, the top of the egg is cracked and the ten milliliters of allantoic fluid is removed, from which about fifteen micrograms of the flu vaccine can be obtained. At this point, the viruses have been weakened or killed and the viral antigen is purified and placed inside vials, syringes, or nasal sprayers. Up to 3 eggs are needed to produce one dose of a trivalent vaccine, and an estimated 600 million eggs are produced each year for flu vaccine production. Methods of vaccine generation that bypass the need for eggs include the construction of influenza virus-like particles (VLP). VLP resemble viruses, but there is no need for inactivation, as they do not include viral coding elements, but merely present antigens in a similar manner to a virion. Some methods of producing VLP include cultures of Spodoptera frugiperda Sf9 insect cells and plant-based vaccine production (e.g., production in Nicotiana benthamiana ). There is evidence that some VLPs elicit antibodies that recognize a broader panel of antigenically distinct viral isolates compared to other vaccines in the hemagglutination-inhibition assay (HIA). A gene-based DNA vaccine, used to prime the immune system after boosting with an inactivated H5N1 vaccine , underwent clinical trials in 2011. On November 20, 2012, Novartis received FDA approval for the first cell-culture vaccine. In 2013, the recombinant influenza vaccine, Flublok, was approved for use in the United States. On September 17, 2020, the Committee for Medicinal Products for Human Use (CHMP) of the European Medicines Agency (EMA) adopted a positive opinion, recommending the granting of a marketing authorization for Supemtek, a quadrivalent influenza vaccine (recombinant, prepared in cell culture). The applicant for this medicinal product is Sanofi Pasteur. Supemtek was approved for medical use in the European Union in November 2020. Australia authorised its first and cell-based vaccine in March 2021, based on an "eternal cell line" of a dog kidney . Because of the way it is produced, it produces better-matched vaccine (to the flu strains). According to the WHO , as of 2019 [ update ] , countries where influenza vaccine is produced include: Australia Brazil Canada China France Germany Hungary India Iran Japan Mexico Netherlands Nicaragua Russian Federation South Korea United Kingdom United States Vietnam In addition, Kazakhstan, Serbia and Thailand had facilities in final stages of establishing production. The cost-effectiveness of seasonal influenza vaccination has been widely evaluated for different groups and in different settings. In the elderly (over 65), the majority of published studies have found that vaccination is cost saving, with the cost savings associated with influenza vaccination (e.g. prevented health care visits) outweighing the cost of vaccination. In older adults (aged 50–64 years), several published studies have found that influenza vaccination is likely to be cost-effective, however the results of these studies were often found to be dependent on key assumptions used in the economic evaluations. The uncertainty in influenza cost-effectiveness models can partially be explained by the complexities involved in estimating the disease burden, as well as the seasonal variability in the circulating strains and the match of the vaccine. In healthy working adults (aged 18–49 years), a 2012 review found that vaccination was generally not cost-saving, with the suitability for funding being dependent on the willingness to pay to obtain the associated health benefits. In children, the majority of studies have found that influenza vaccination was cost-effective, however many of the studies included (indirect) productivity gains, which may not be given the same weight in all settings. Several studies have attempted to predict the cost-effectiveness of interventions (including prepandemic vaccination) to help protect against a future pandemic, however estimating the cost-effectiveness has been complicated by uncertainty as to the severity of a potential future pandemic and the efficacy of measures against it. Influenza research includes molecular virology , molecular evolution , pathogenesis , host immune responses , genomics , and epidemiology . These help in developing influenza countermeasures such as vaccines , therapies and diagnostic tools. Improved influenza countermeasures require basic research on how viruses enter cells, replicate, mutate, evolve into new strains and induce an immune response. The Influenza Genome Sequencing Project is creating a library of influenza sequences that will help researchers' understanding of what makes one strain more lethal than another, what genetic determinants most affect immunogenicity , and how the virus evolves over time. Solutions to limitations in current [ when? ] vaccine methods are being [ when? ] researched. A different approach uses Internet content to estimate the impact of an influenza vaccination campaign. More specifically, researchers have used data from Twitter and Microsoft's Bing search engine , and proposed a statistical framework which, after a series of operations, maps this information to estimates of the influenza-like illness reduction percentage in areas where vaccinations have been performed. The method has been used to quantify the impact of two flu vaccination programmes in England (2013/14 and 2014/15), where school-age children were administered a live attenuated influenza vaccine (LAIV). Notably, the impact estimates were in accordance with estimations from Public Health England based on traditional syndromic surveillance endpoints. The rapid development, production, and distribution of pandemic influenza vaccines could potentially save millions of lives during an influenza pandemic. Due to the short time frame between identification of a pandemic strain and need for vaccination, researchers are looking at novel technologies for vaccine production that could provide better "real-time" access and be produced more affordably, thereby increasing access for people living in low- and moderate-income countries, where an influenza pandemic may likely originate, such as live attenuated (egg-based or cell-based ) technology and recombinant technologies (proteins and virus-like particles). As of July 2009 [ update ] , more than seventy known clinical trials have been completed or are ongoing for pandemic influenza vaccines. In September 2009, the FDA approved four vaccines against the 2009 H1N1 influenza virus (the 2009 pandemic strain), and expected the initial vaccine lots to be available within the following month. In January 2020, the US Food and Drug Administration (FDA) approved Audenz as a vaccine for the H5N1 flu virus. Audenz is a vaccine indicated for active immunization for the prevention of disease caused by the influenza A virus H5N1 subtype contained in the vaccine. Audenz is approved for use in persons six months of age and older at increased risk of exposure to the influenza A virus H5N1 subtype contained in the vaccine. A universal influenza vaccine that would not have to be designed and made for each flu season in each hemisphere would stabilize the supply, avoid error in predicting the season's variants, and protect against escape of the circulating strains by mutation. Such a vaccine has been the subject of research for decades. One approach is to use broadly neutralizing antibodies that, unlike the annual seasonal vaccines used over the first decades of the 21st century that provoke the body to generate an immune response, instead provide a component of the immune response itself. The first neutralizing antibodies were identified in 1993, via experimentation. It was found that the flu neutralizing antibodies bound to the stalk of the Hemagglutinin protein . Antibodies that could bind to the head of those proteins were identified. The highly conserved M2 proton channel was proposed as a potential target for broadly neutralizing antibodies. The challenges for researchers are to identify single antibodies that could neutralize many subtypes of the virus, so that they could be useful in any season, and that target conserved domains that are resistant to antigenic drift . Another approach is to take the conserved domains identified from these projects, and to deliver groups of these antigens to provoke an immune response; various approaches with different antigens, presented different ways (as fusion proteins , mounted on virus-like particles , on non-pathogenic viruses, as DNA, and others), are under development. Efforts have also been undertaken to develop universal vaccines that specifically activate a T-cell response, based on clinical data showing that people with a strong, early T-cell response have better outcomes when infected with influenza and because T-cells respond to conserved epitopes. The challenge for developers is that these epitopes are on internal protein domains that are only mildly immunogenic. Along with the rest of the vaccine field, people working on universal vaccines have experimented with vaccine adjuvants to improve the ability of their vaccines to create a sufficiently powerful and enduring immune response. As of 2019, an oral flu vaccine was in clinical research . The oral vaccine candidate is based on an adenovirus type 5 vector modified to remove genes needed for replication, with an added gene that expresses a small double-stranded RNA hairpin molecule as an adjuvant . In 2020, a Phase II human trial of the pill form of the vaccine showed that it was well tolerated and provided similar immunity to a licensed injectable vaccine. An influenza vaccine and a COVID-19 vaccine may be given safely at the same time. Preliminary research indicates that influenza vaccination does not prevent COVID-19 , but may reduce the incidence and severity of COVID-19 infection. Tom Jefferson , who has led Cochrane Collaboration reviews of flu vaccines, has called clinical evidence concerning flu vaccines "rubbish" and has therefore declared them to be ineffective; he has called for placebo-controlled randomized clinical trials , which most in the field hold as unethical . His views on the efficacy of flu vaccines are rejected by medical institutions including the CDC and the National Institutes of Health , and by key figures in the field like Anthony Fauci . Michael Osterholm , who led the Center for Infectious Disease Research and Policy 2012 review on flu vaccines, recommended getting the vaccine but criticized its promotion, saying, "We have overpromoted and overhyped this vaccine ... it does not protect as promoted. It's all a sales job: it's all public relations." The rapid development, production, and distribution of pandemic influenza vaccines could potentially save millions of lives during an influenza pandemic. Due to the short time frame between identification of a pandemic strain and need for vaccination, researchers are looking at novel technologies for vaccine production that could provide better "real-time" access and be produced more affordably, thereby increasing access for people living in low- and moderate-income countries, where an influenza pandemic may likely originate, such as live attenuated (egg-based or cell-based ) technology and recombinant technologies (proteins and virus-like particles). As of July 2009 [ update ] , more than seventy known clinical trials have been completed or are ongoing for pandemic influenza vaccines. In September 2009, the FDA approved four vaccines against the 2009 H1N1 influenza virus (the 2009 pandemic strain), and expected the initial vaccine lots to be available within the following month. In January 2020, the US Food and Drug Administration (FDA) approved Audenz as a vaccine for the H5N1 flu virus. Audenz is a vaccine indicated for active immunization for the prevention of disease caused by the influenza A virus H5N1 subtype contained in the vaccine. Audenz is approved for use in persons six months of age and older at increased risk of exposure to the influenza A virus H5N1 subtype contained in the vaccine. A universal influenza vaccine that would not have to be designed and made for each flu season in each hemisphere would stabilize the supply, avoid error in predicting the season's variants, and protect against escape of the circulating strains by mutation. Such a vaccine has been the subject of research for decades. One approach is to use broadly neutralizing antibodies that, unlike the annual seasonal vaccines used over the first decades of the 21st century that provoke the body to generate an immune response, instead provide a component of the immune response itself. The first neutralizing antibodies were identified in 1993, via experimentation. It was found that the flu neutralizing antibodies bound to the stalk of the Hemagglutinin protein . Antibodies that could bind to the head of those proteins were identified. The highly conserved M2 proton channel was proposed as a potential target for broadly neutralizing antibodies. The challenges for researchers are to identify single antibodies that could neutralize many subtypes of the virus, so that they could be useful in any season, and that target conserved domains that are resistant to antigenic drift . Another approach is to take the conserved domains identified from these projects, and to deliver groups of these antigens to provoke an immune response; various approaches with different antigens, presented different ways (as fusion proteins , mounted on virus-like particles , on non-pathogenic viruses, as DNA, and others), are under development. Efforts have also been undertaken to develop universal vaccines that specifically activate a T-cell response, based on clinical data showing that people with a strong, early T-cell response have better outcomes when infected with influenza and because T-cells respond to conserved epitopes. The challenge for developers is that these epitopes are on internal protein domains that are only mildly immunogenic. Along with the rest of the vaccine field, people working on universal vaccines have experimented with vaccine adjuvants to improve the ability of their vaccines to create a sufficiently powerful and enduring immune response. As of 2019, an oral flu vaccine was in clinical research . The oral vaccine candidate is based on an adenovirus type 5 vector modified to remove genes needed for replication, with an added gene that expresses a small double-stranded RNA hairpin molecule as an adjuvant . In 2020, a Phase II human trial of the pill form of the vaccine showed that it was well tolerated and provided similar immunity to a licensed injectable vaccine. An influenza vaccine and a COVID-19 vaccine may be given safely at the same time. Preliminary research indicates that influenza vaccination does not prevent COVID-19 , but may reduce the incidence and severity of COVID-19 infection. Tom Jefferson , who has led Cochrane Collaboration reviews of flu vaccines, has called clinical evidence concerning flu vaccines "rubbish" and has therefore declared them to be ineffective; he has called for placebo-controlled randomized clinical trials , which most in the field hold as unethical . His views on the efficacy of flu vaccines are rejected by medical institutions including the CDC and the National Institutes of Health , and by key figures in the field like Anthony Fauci . Michael Osterholm , who led the Center for Infectious Disease Research and Policy 2012 review on flu vaccines, recommended getting the vaccine but criticized its promotion, saying, "We have overpromoted and overhyped this vaccine ... it does not protect as promoted. It's all a sales job: it's all public relations." Veterinary influenza vaccination aims to achieve the following four objectives: Protection from clinical disease Protection from infection with virulent virus Protection from virus excretion Serological differentiation of infected from vaccinated animals (so-called DIVA principle). Horses with horse flu can run a fever, have a dry hacking cough, have a runny nose, and become depressed and reluctant to eat or drink for several days but usually recover in two to three weeks. "Vaccination schedules generally require a primary course of two doses, 3–6 weeks apart, followed by boosters at 6–12 month intervals. It is generally recognized that in many cases such schedules may not maintain protective levels of antibody and more frequent administration is advised in high-risk situations." It is a common requirement at shows in the United Kingdom that horses be vaccinated against equine flu and a vaccination card must be produced; the International Federation for Equestrian Sports (FEI) requires vaccination every six months. Poultry vaccines for bird flu are made inexpensively and are not filtered and purified like human vaccines to remove bits of bacteria or other viruses. They usually contain whole virus, not just hemagglutinin as in most human flu vaccines. Another difference between human and poultry vaccines is that poultry vaccines are adjuvated with mineral oil, which induces a strong immune reaction but can cause inflammation and abscesses. "Chicken vaccinators who have accidentally jabbed themselves have developed painful swollen fingers or even lost thumbs, doctors said. Effectiveness may also be limited. Chicken vaccines are often only vaguely similar to circulating flu strains – some contain an H5N2 strain isolated in Mexico years ago. 'With a chicken, if you use a vaccine that's only 85 percent related, you'll get protection,' Dr. Cardona said. 'In humans, you can get a single point mutation, and a vaccine that's 99.99 percent related won't protect you.' And they are weaker [than human vaccines]. 'Chickens are smaller and you only need to protect them for six weeks, because that's how long they live till you eat them,' said Dr. John J. Treanor, a vaccine expert at the University of Rochester. Human seasonal flu vaccines contain about 45 micrograms of antigen, while an experimental A( H5N1 ) vaccine contains 180. Chicken vaccines may contain less than one microgram. 'You have to be careful about extrapolating data from poultry to humans,' warned Dr. David E. Swayne, director of the agriculture department's Southeast Poultry Research Laboratory. 'Birds are more closely related to dinosaurs .'" Researchers, led by Nicholas Savill of the University of Edinburgh in Scotland, used mathematical models to simulate the spread of H5N1 and concluded that "at least 95 percent of birds need to be protected to prevent the virus spreading silently. In practice, it is difficult to protect more than 90 percent of a flock; protection levels achieved by a vaccine are usually much lower than this." The Food and Agriculture Organization of the United Nations has issued recommendations on the prevention and control of avian influenza in poultry, including the use of vaccination. A filtered and purified Influenza A vaccine for humans is being developed [ when? ] and many countries have recommended it be stockpiled so if an Avian influenza pandemic starts jumping to humans, the vaccine can quickly be administered to avoid loss of life. Avian influenza is sometimes called avian flu, and commonly bird flu. Swine influenza vaccines are extensively used in pig farming in Europe and North America. Most swine flu vaccines include an H1N1 and an H3N2 strain. Swine influenza has been recognized as a major problem since the outbreak in 1976 . Evolution of the virus has resulted in inconsistent responses to traditional vaccines. Standard commercial swine flu vaccines are effective in controlling the problem when the virus strains match enough to have significant cross-protection. Customised (autogenous) vaccines made from the specific viruses isolated, are made and used in the more difficult cases. The vaccine manufacturer Novartis claims that the H3N2 strain (first identified in 1998) has brought major losses to pig farmers. Abortion storms are a common sign and sows stop eating for a few days and run a high fever. The mortality rate can be as high as fifteen percent. In 2004, influenza A virus subtype H3N8 was discovered to cause canine influenza . Because of the lack of previous exposure to this virus, dogs have no natural immunity to this virus. However, a vaccine was found in 2004. Horses with horse flu can run a fever, have a dry hacking cough, have a runny nose, and become depressed and reluctant to eat or drink for several days but usually recover in two to three weeks. "Vaccination schedules generally require a primary course of two doses, 3–6 weeks apart, followed by boosters at 6–12 month intervals. It is generally recognized that in many cases such schedules may not maintain protective levels of antibody and more frequent administration is advised in high-risk situations." It is a common requirement at shows in the United Kingdom that horses be vaccinated against equine flu and a vaccination card must be produced; the International Federation for Equestrian Sports (FEI) requires vaccination every six months. Poultry vaccines for bird flu are made inexpensively and are not filtered and purified like human vaccines to remove bits of bacteria or other viruses. They usually contain whole virus, not just hemagglutinin as in most human flu vaccines. Another difference between human and poultry vaccines is that poultry vaccines are adjuvated with mineral oil, which induces a strong immune reaction but can cause inflammation and abscesses. "Chicken vaccinators who have accidentally jabbed themselves have developed painful swollen fingers or even lost thumbs, doctors said. Effectiveness may also be limited. Chicken vaccines are often only vaguely similar to circulating flu strains – some contain an H5N2 strain isolated in Mexico years ago. 'With a chicken, if you use a vaccine that's only 85 percent related, you'll get protection,' Dr. Cardona said. 'In humans, you can get a single point mutation, and a vaccine that's 99.99 percent related won't protect you.' And they are weaker [than human vaccines]. 'Chickens are smaller and you only need to protect them for six weeks, because that's how long they live till you eat them,' said Dr. John J. Treanor, a vaccine expert at the University of Rochester. Human seasonal flu vaccines contain about 45 micrograms of antigen, while an experimental A( H5N1 ) vaccine contains 180. Chicken vaccines may contain less than one microgram. 'You have to be careful about extrapolating data from poultry to humans,' warned Dr. David E. Swayne, director of the agriculture department's Southeast Poultry Research Laboratory. 'Birds are more closely related to dinosaurs .'" Researchers, led by Nicholas Savill of the University of Edinburgh in Scotland, used mathematical models to simulate the spread of H5N1 and concluded that "at least 95 percent of birds need to be protected to prevent the virus spreading silently. In practice, it is difficult to protect more than 90 percent of a flock; protection levels achieved by a vaccine are usually much lower than this." The Food and Agriculture Organization of the United Nations has issued recommendations on the prevention and control of avian influenza in poultry, including the use of vaccination. A filtered and purified Influenza A vaccine for humans is being developed [ when? ] and many countries have recommended it be stockpiled so if an Avian influenza pandemic starts jumping to humans, the vaccine can quickly be administered to avoid loss of life. Avian influenza is sometimes called avian flu, and commonly bird flu. Swine influenza vaccines are extensively used in pig farming in Europe and North America. Most swine flu vaccines include an H1N1 and an H3N2 strain. Swine influenza has been recognized as a major problem since the outbreak in 1976 . Evolution of the virus has resulted in inconsistent responses to traditional vaccines. Standard commercial swine flu vaccines are effective in controlling the problem when the virus strains match enough to have significant cross-protection. Customised (autogenous) vaccines made from the specific viruses isolated, are made and used in the more difficult cases. The vaccine manufacturer Novartis claims that the H3N2 strain (first identified in 1998) has brought major losses to pig farmers. Abortion storms are a common sign and sows stop eating for a few days and run a high fever. The mortality rate can be as high as fifteen percent. In 2004, influenza A virus subtype H3N8 was discovered to cause canine influenza . Because of the lack of previous exposure to this virus, dogs have no natural immunity to this virus. However, a vaccine was found in 2004. Each year, three strains are chosen for selection in that year's flu vaccination by the WHO Global Influenza Surveillance and Response System . The chosen strains are the H1N1, H3N2, and Type-B strains thought most likely to cause significant human suffering in the coming season. Starting with the 2012–2013 Northern Hemisphere influenza season (coincident with the approval of quadrivalent influenza vaccines), the WHO has also recommended a 2nd B-strain for use in quadrivalent vaccines. The World Health Organization (WHO) coordinates the contents of the vaccine each year to contain the most likely strains of the virus to attack the next year. The Global Influenza Surveillance and Response System's selection of viruses for the vaccine manufacturing process is based on its best estimate of which strains will predominate the next year, amounting in the end to well-informed but fallible guesswork. Formal WHO recommendations were first issued in 1973. Beginning in 1999 there have been two recommendations per year: one for the northern hemisphere and the other for the southern hemisphere. For the 2024–2025 Northern Hemisphere influenza season, the FDA recommends removing B/Yamagata from all influenza vaccines.

Wiki

Avian influenza

https://api.wikimedia.org/core/v1/wikipedia/en/page/Global_spread_of_H5N1/html

Global spread of H5N1

The global spread of H5N1 influenza in birds is considered a significant pandemic threat. While other H5N1 influenza strains are known, they are significantly different on a genetic level from a recent, highly pathogenic, emergent strain of H5N1, which was able to achieve hitherto unprecedented global spread in 2008. The H5N1 strain is a fast-mutating , highly pathogenic avian influenza virus (HPAI) found in multiple bird species. It is both epizootic (an epidemic in non-humans) and panzootic (a disease affecting animals of many species especially over a wide area). Unless otherwise indicated, "H5N1" in this timeline refers to the recent highly pathogenic strain of H5N1. Notes: Tens of millions of birds have died of H5N1 influenza and hundreds of millions of birds have been slaughtered and disposed of, to limit the spread of H5N1. Countries that have reported one or more major highly pathogenic H5N1 outbreaks in birds (causing at least thousands but in some cases millions of dead birds) are (in order of first outbreak occurrence): South Korea , Vietnam , Japan , Thailand , Cambodia , Laos , Indonesia , China , Malaysia , Russia , Kazakhstan , Mongolia , Turkey , Romania , Croatia , Ukraine , Cyprus , Iraq , Nigeria , Egypt , India , France , Niger , Bosnia , Azerbaijan , Albania , Cameroon , Myanmar , Afghanistan , Israel , Pakistan , Jordan , Burkina Faso , Germany , Sudan , Ivory Coast , Djibouti , Hungary , United Kingdom , Kuwait , Bangladesh , Saudi Arabia , Ghana , Czech Republic , Togo , Nepal , Bhutan , the Philippines , and Chile . Highly pathogenic H5N1 has been found in birds in the wild in numerous other countries: Austria , Bulgaria , Denmark , Greece , Iran , Italy , Poland , Serbia and Montenegro , Slovakia , Slovenia , Spain , Sweden , Switzerland , and Uruguay . Surveillance of H5N1 in humans, poultry, wild birds, cats and other animals remains very weak in many parts of Asia and Africa. Much remains unknown about the exact extent of its spread. H5N1 has low pathogenic varieties endemic in birds in North America. H5N1 has a highly pathogenic variety that is endemic in dozens of species of birds throughout south Asia and parts of Africa . So far, it is very difficult for humans to become infected with H5N1. The presence of highly pathogenic (deadly) H5N1 around the world in both birds in the wild ( swans , magpies , ducks , geese , pigeons , eagles , etc.) and in chickens and turkeys on farms has been demonstrated in millions of cases with the virus isolate actually sequenced in hundreds of cases yielding definitive proof of the evolution of this strain of this subtype of the species Influenzavirus A (bird flu virus). According to Robert G. Webster : The epicenters of both the Asian influenza pandemic of 1957 and the Hong Kong influenza pandemic of 1968 were in Southeast Asia, and it is in this region that multiple clades of H5N1 influenza virus have already emerged. The Asian H5N1 virus was first detected in Guangdong Province , China, in 1996, when it killed some geese, but it received little attention until it spread through live-poultry markets in Hong Kong to humans in May 1997, killing 6 of 18 infected people. [...] From 1997 to May 2005, H5N1 viruses were largely confined to Southeast Asia, but after they had infected wild birds in Qinghai Lake, China, they rapidly spread westward. [...] The intermittent spread to humans will continue, and the virus will continue to evolve. Map On July 25, 2008, the Food and Agriculture Organization (FAO) released an Avian Influenza Disease Emergency Situation Update, reporting that H5N1 pathogenicity was continuing to gradually rise in endemic areas but the avian influenza disease situation in farmed birds was being held in check by vaccination. Eleven outbreaks of H5N1 were reported worldwide in June 2008 in five countries (China, Egypt, Indonesia, Pakistan and Vietnam) compared to 65 outbreaks in June 2006 and 55 in June 2007. In January 2004 a major new outbreak of H5N1 surfaced in Vietnam and Thailand 's poultry industry, and within weeks spread to ten countries and regions in Asia , including Indonesia , South Korea , Japan and China . In October 2004 researchers discovered H5N1 is far more dangerous than previously believed because waterfowl , especially ducks , were directly spreading the highly pathogenic strain of H5N1 to chickens , crows , pigeons , and other birds and that it was increasing its ability to infect mammals as well. From this point on, avian influenza experts increasingly refer to containment as a strategy that can delay but not prevent a future avian flu pandemic. In January 2005 an outbreak of avian influenza affected thirty three out of sixty four cities and provinces in Vietnam , leading to the forced killing of nearly 1.2 million poultry. Up to 140 million birds are believed to have died or been killed because of the outbreak. In April 2005 there begins an unprecedented die-off of over 6,000 migratory birds at Qinghai Lake in central China over three months. This strain of H5N1 is the same strain as is spread west by migratory birds over at least the next ten months. In August 2005 H5N1 spread to Kazakhstan , Mongolia and Russia . On September 29, 2005, David Nabarro , the newly appointed Senior United Nations System Coordinator for Avian and Human Influenza, warned the world that an outbreak of avian influenza could kill 5 to 150 million people. David Nabarro later stated that as the virus had spread to migratory birds, an outbreak could start in Africa or the Middle East . Later in 2005 H5N1 spread to Turkey , Romania , Croatia and Kuwait . In January, Japan , Hungary , Russia , and the United Kingdom joined the list of nations seeing a resurgence of bird deaths due to H5N1. In February, Pakistan , Turkey , Afghanistan , and Myanmar joined the list and Kuwait saw its first major outbreak of H5N1 avian influenza . In March Bangladesh and Saudi Arabia each saw their first major outbreak of H5N1 avian influenza and Ghana in May. As H5N1 continued killing many birds and a few people throughout the spring in countries where it is now endemic, in June Malaysia and Germany saw a resurgence of bird deaths due to H5N1, while the Czech Republic and Togo experienced their first major outbreak of H5N1 avian influenza . In July France and India also saw a resurgence of bird deaths due to H5N1. As of the July 25, 2008 FAO Avian Influenza Disease Emergency Situation Update, H5N1 pathogenicity is continuing to gradually rise in wild birds in endemic areas but the avian influenza disease situation in farmed birds is being held in check by vaccination. Eleven outbreaks of H5N1 were reported worldwide in June 2008 in five countries (China, Egypt, Indonesia, Pakistan and Vietnam) compared to 65 outbreaks in June 2006 and 55 in June 2007. The "global HPAI situation can be said to have improved markedly in the first half of 2008 [but] cases of HPAI are still underestimated and underreported in many countries because of limitations in country disease surveillance systems". In January 2004 a major new outbreak of H5N1 surfaced in Vietnam and Thailand 's poultry industry, and within weeks spread to ten countries and regions in Asia , including Indonesia , South Korea , Japan and China . In October 2004 researchers discovered H5N1 is far more dangerous than previously believed because waterfowl , especially ducks , were directly spreading the highly pathogenic strain of H5N1 to chickens , crows , pigeons , and other birds and that it was increasing its ability to infect mammals as well. From this point on, avian influenza experts increasingly refer to containment as a strategy that can delay but not prevent a future avian flu pandemic.In January 2005 an outbreak of avian influenza affected thirty three out of sixty four cities and provinces in Vietnam , leading to the forced killing of nearly 1.2 million poultry. Up to 140 million birds are believed to have died or been killed because of the outbreak. In April 2005 there begins an unprecedented die-off of over 6,000 migratory birds at Qinghai Lake in central China over three months. This strain of H5N1 is the same strain as is spread west by migratory birds over at least the next ten months. In August 2005 H5N1 spread to Kazakhstan , Mongolia and Russia . On September 29, 2005, David Nabarro , the newly appointed Senior United Nations System Coordinator for Avian and Human Influenza, warned the world that an outbreak of avian influenza could kill 5 to 150 million people. David Nabarro later stated that as the virus had spread to migratory birds, an outbreak could start in Africa or the Middle East . Later in 2005 H5N1 spread to Turkey , Romania , Croatia and Kuwait .In January, Japan , Hungary , Russia , and the United Kingdom joined the list of nations seeing a resurgence of bird deaths due to H5N1. In February, Pakistan , Turkey , Afghanistan , and Myanmar joined the list and Kuwait saw its first major outbreak of H5N1 avian influenza . In March Bangladesh and Saudi Arabia each saw their first major outbreak of H5N1 avian influenza and Ghana in May. As H5N1 continued killing many birds and a few people throughout the spring in countries where it is now endemic, in June Malaysia and Germany saw a resurgence of bird deaths due to H5N1, while the Czech Republic and Togo experienced their first major outbreak of H5N1 avian influenza . In July France and India also saw a resurgence of bird deaths due to H5N1.As of the July 25, 2008 FAO Avian Influenza Disease Emergency Situation Update, H5N1 pathogenicity is continuing to gradually rise in wild birds in endemic areas but the avian influenza disease situation in farmed birds is being held in check by vaccination. Eleven outbreaks of H5N1 were reported worldwide in June 2008 in five countries (China, Egypt, Indonesia, Pakistan and Vietnam) compared to 65 outbreaks in June 2006 and 55 in June 2007. The "global HPAI situation can be said to have improved markedly in the first half of 2008 [but] cases of HPAI are still underestimated and underreported in many countries because of limitations in country disease surveillance systems". As of the July 25, 2008 FAO Avian Influenza Disease Emergency Situation Update, H5N1 pathogenicity is continuing to gradually rise in wild birds in endemic areas but the avian influenza disease situation in farmed birds is being held in check by vaccination. Eleven outbreaks of H5N1 were reported worldwide in June 2008 in five countries (China, Egypt, Indonesia, Pakistan and Vietnam) compared to 65 outbreaks in June 2006 and 55 in June 2007. The "global HPAI situation can be said to have improved markedly in the first half of 2008 [but] cases of HPAI are still underestimated and underreported in many countries because of limitations in country disease surveillance systems". Avian influenza virus H3N2 is endemic in pigs (" swine flu ") in China and has been detected in pigs in Vietnam, increasing fears of the emergence of new variant strains. Health experts say pigs can carry human influenza viruses, which can combine (i.e. exchange homologous genome sub-units by genetic reassortment ) with H5N1 , passing genes and mutating into a form which can pass easily among humans. H3N2 evolved from H2N2 by antigenic shift and caused the Hong Kong Flu pandemic of 1968 and 1969 that killed up to 750,000 humans. The dominant strain of annual flu in humans in January 2006 is H3N2 . Measured resistance to the standard antiviral drugs amantadine and rimantadine in H3N2 in humans has increased to 91% in 2005. A combination of these two subtypes of the species known as the avian influenza virus in a country like China is a worst-case scenario. In August 2004, researchers in China found H5N1 in pigs. In 2005, it was discovered that H5N1 "could be infecting up to half of the pig population in some areas of Indonesia , but without causing symptoms [...] Chairul Nidom, a virologist at Airlangga University 's tropical disease center in Surabaya , Java, was conducting independent research earlier this year. He tested the blood of 10 apparently healthy pigs housed near poultry farms in western Java where avian flu had broken out, Nature reported. Five of the pig samples contained the H5N1 virus. The Indonesian government has since found similar results in the same region, Nature reported. Additional tests of 150 pigs outside the area were negative." In Bangkok, Thailand , all the cats in one household are known to have died of H5N1 in 2004. Tigers and leopards in Thai zoos also died, while in 2007 two cats near an outbreak in poultry and people in Iraq were confirmed to have died of H5N1, as were three German cats that ate wild birds. In Austria , cats were infected but remained healthy. Cats in Indonesia were also found to have been infected with H5N1. The spread to species and populations of birds, and the ability of felids (cats) to catch H5N1 from eating this natural prey, means the creation of a reservoir for H5N1 in cats where the virus can adapt to mammals is one of the many possible pathways to a pandemic . Variants have been found in a number of domestic cats, leopards , and tigers in Thailand , with high lethality. "The Thailand Zoo tiger outbreak killed more than 140 tigers, causing health officials to make the decision to cull all the sick tigers in an effort to stop the zoo from becoming a reservoir for H5N1 influenza. A study of domestic cats showed H5N1 virus infection by ingestion of infected poultry and also by contact with other infected cats (Kuiken et al., 2004)." The initial OIE report reads: "the clinical manifestations began on 11 October 2004 with weakness, lethargy, respiratory distress, and high fever (about 41-42 degrees Celsius). There was no response to any antibiotic treatment. Death occurred within three days following the onset of clinical signs with severe pulmonary lesions." A dead cat infected with the H5N1 bird flu virus was found in Germany . Hans Seitinger, the top agriculture official in the southern state of Styria , Austria announced that several still living cats in Styria have tested positive for H5N1: It was announced in the August 2006 CDC EID journal that while literature describing HPAI H5N1 infection in cats had been limited to a subset of clade I viruses; a Qinghai-like virus (they are genetically distinct from other clade II viruses) killed up to five cats and 51 chickens from February 3 to 5, 2006 in Grd Jotyar (~10 km north of Erbil City , Iraq). Two of the cats were available for examination. "Chairul Anwar Nidom of Airlangga University in Surabaya, Indonesia , told journalists last week that he had taken blood samples from 500 stray cats near poultry markets in four areas of Java , including the capital, Jakarta , and one area in Sumatra , all of which have recently had outbreaks of H5N1 in poultry and people. Of these cats, 20% carried antibodies to H5N1. This does not mean that they were still carrying the virus, only that they had been infected - probably through eating birds that had H5N1. Many other cats that were infected are likely to have died from the resulting illness, so many more than 20% of the original cat populations may have acquired H5N1." On 20 and 21 June in Poland multiple reports of cats dying from unknown causes with neurological and respiratory symptoms that matched H5N1 to some degree. Some viral alerts have risen, mostly posted on Facebook by veterinary clinics alerting their clients. At that time most of the data was anecdotal. On 26 June it was confirmed by Polands Chief Veterinary Officer Paweł Niemczuk, who stated that in 9 of 11 tested cases it is indeed H5N1: "The results of subsequently tested samples taken from cats from Lublin and Poznań are available. Until June 26 at 11:00 11 samples were tested at the National Veterinary Institute in Puławy, of which 9 gave a positive result for H5N1 influenza. Positive samples come from Poznań, Tri-City, and Lublin. Further detailed studies of the genetic material of viruses are underway. Preliminary research excludes the origin of the influenza virus that has been causing gulls to become ill in recent weeks. Today, a sanitary and epizootic meeting was held, where a plan for further action was discussed." Variants have been found in a number of domestic cats, leopards , and tigers in Thailand , with high lethality. "The Thailand Zoo tiger outbreak killed more than 140 tigers, causing health officials to make the decision to cull all the sick tigers in an effort to stop the zoo from becoming a reservoir for H5N1 influenza. A study of domestic cats showed H5N1 virus infection by ingestion of infected poultry and also by contact with other infected cats (Kuiken et al., 2004)." The initial OIE report reads: "the clinical manifestations began on 11 October 2004 with weakness, lethargy, respiratory distress, and high fever (about 41-42 degrees Celsius). There was no response to any antibiotic treatment. Death occurred within three days following the onset of clinical signs with severe pulmonary lesions." A dead cat infected with the H5N1 bird flu virus was found in Germany . Hans Seitinger, the top agriculture official in the southern state of Styria , Austria announced that several still living cats in Styria have tested positive for H5N1: It was announced in the August 2006 CDC EID journal that while literature describing HPAI H5N1 infection in cats had been limited to a subset of clade I viruses; a Qinghai-like virus (they are genetically distinct from other clade II viruses) killed up to five cats and 51 chickens from February 3 to 5, 2006 in Grd Jotyar (~10 km north of Erbil City , Iraq). Two of the cats were available for examination."Chairul Anwar Nidom of Airlangga University in Surabaya, Indonesia , told journalists last week that he had taken blood samples from 500 stray cats near poultry markets in four areas of Java , including the capital, Jakarta , and one area in Sumatra , all of which have recently had outbreaks of H5N1 in poultry and people. Of these cats, 20% carried antibodies to H5N1. This does not mean that they were still carrying the virus, only that they had been infected - probably through eating birds that had H5N1. Many other cats that were infected are likely to have died from the resulting illness, so many more than 20% of the original cat populations may have acquired H5N1." On 20 and 21 June in Poland multiple reports of cats dying from unknown causes with neurological and respiratory symptoms that matched H5N1 to some degree. Some viral alerts have risen, mostly posted on Facebook by veterinary clinics alerting their clients. At that time most of the data was anecdotal. On 26 June it was confirmed by Polands Chief Veterinary Officer Paweł Niemczuk, who stated that in 9 of 11 tested cases it is indeed H5N1: "The results of subsequently tested samples taken from cats from Lublin and Poznań are available. Until June 26 at 11:00 11 samples were tested at the National Veterinary Institute in Puławy, of which 9 gave a positive result for H5N1 influenza. Positive samples come from Poznań, Tri-City, and Lublin. Further detailed studies of the genetic material of viruses are underway. Preliminary research excludes the origin of the influenza virus that has been causing gulls to become ill in recent weeks. Today, a sanitary and epizootic meeting was held, where a plan for further action was discussed." H5N1 has been transmitted in laboratories to many species including mice and ferrets to study its effects. A purposely mutated strain in ferrets has engendered a notable international policy debate regarding the openness of scientific research, the mandates of public health, and the potential for bioterrorism. H5N1 was transmitted in the wild to three civet cats in Vietnam in August 2005 and a stone marten in Germany in March 2006. The BBC reported that a stray dog in Azerbaijan died from the disease on March 15, 2006. People living in areas where the A(H5N1) virus has infected birds are advised to keep their cats indoors. "Cats can be infected through the respiratory tract. Cats can also be infected when they ingest the virus, which is a novel route for influenza transmission in mammals. But cats excrete only one-thousandth the amount of virus that chickens do [...] The concern is that if large numbers of felines and other carnivores become infected, the virus might mutate in a series of events that could lead to an epidemic among humans. Dogs, foxes, seals, and other carnivores may be vulnerable to A(H5N1) virus infection, Dr. Osterhaus said. Tests in Thailand have shown that the virus has infected dogs without causing apparent symptoms." H5N1 has the potential to infect cattle . Asymptomatic shedding of H5N1 by infected calves and subsequent seroconversion is possible. Bird-to-calf transmission resulting in seroconversion is probable. While the incidence of clinical infections of cattle with H5N1 in H5N1 endemic regions should be low, "serum from bovine species would be a valuable source of additional information about transmission events, especially in regions like Asia and Egypt, where HPAIV (H5N1) is endemic and probability of contact between poultry and cattle is high."

Wiki

Avian influenza

https://api.wikimedia.org/core/v1/wikipedia/en/page/Fujian_flu/html

Fujian flu

All other subtypes and strains of Influenza A virus Fujian flu refers to flu caused by either a Fujian human flu strain of the H3N2 subtype of the Influenza A virus or a Fujian bird flu strain of the H5N1 subtype of the Influenza A virus . These strains are named after Fujian , a coastal province in Southeast China . [note 1] A/Fujian (H3N2) human flu (from A/Fujian/411/2002(H3N2) -like flu virus strains) caused an unusually severe 2003–2004 flu season. This was due to a reassortment event that caused a minor clade to provide a haemagglutinin gene that later became part of the dominant strain in the 2002–2003 flu season. A/Fujian (H3N2) was made part of the trivalent influenza vaccine for the 2004-2005 flu season and its descendants are still the most common human H3N2 strain. A/Fujian (H5N1) bird flu is notable for its resistance to standard medical countermeasures and its rapid spread. This variant of the H5N1 virus also illustrates the continuing evolution of the H5N1 virus, and its emergence has caused political controversy.A variety of names were used before being standardized. Phrases used to identify the flu or the causative agent include "Fujian-like" and "Fujian virus" for the H5N1 version and "Fujian-like" for the H3N2 version. Both are also sometimes specified as "Type A Fujian flu" or "A/Fujian flu" referring to the species Influenza A virus . Both are also sometimes specified according to their species subtype: "Fujian Flu (H3N2)" or "Fujian Flu (H5N1)". Or both, example: "A-Fujian-H3N2". "A/Fujian/411/2002-like (H3N2)" and "Influenza A/Fujian/411/02(H3N2)-lineage viruses" are examples of using the full name of the virus strains. [ citation needed ]In the 2003-2004 flu season the influenza vaccine was produced to protect against A/Panama ( H3N2 ), A/New Caledonia ( H1N1 ), and B /Hong Kong. A new strain, A/Fujian (H3N2), was discovered after production of the vaccine started and vaccination gave only partial protection against this strain. Nature magazine reported that the Influenza Genome Sequencing Project , using phylogenetic analysis of 156 H3N2 genomes, "explains the appearance, during the 2003–2004 season, of the 'Fujian/411/2002'-like strain, for which the existing vaccine had limited effectiveness" as due to an epidemiologically significant reassortment. "Through a reassortment event, a minor clade provided the haemagglutinin gene that later became part of the dominant strain after the 2002–2003 season. Two of our samples, A/New York/269/2003 ( H3N2 ) and A/New York/32/2003 ( H3N2 ), show that this minor clade continued to circulate in the 2003–2004 season, when most other isolates were reassortants." In January 2004, the predominant flu virus circulating in humans in Europe was influenza A/Fujian/411/2002 (H3N2)-like. As of 15 June 2004, CDC had antigenically characterized 1,024 influenza viruses collected by U.S. laboratories since 1 October 2003: 949 influenza A ( H3N2 ) viruses, three influenza A (H1) viruses, one influenza A ( H7N2 ) virus, and 71 influenza B viruses. Of the 949 influenza A (H3N2) isolates characterized, 106 (11.2%) were similar antigenically to the vaccine strain A/Panama/2007/1999 (H3N2), and 843 (88.8%) were similar to the drift variant, A/Fujian/411/2002 (H3N2). The 2004-2005 flu season trivalent influenza vaccine for the United States contained A/New Caledonia/20/1999-like (H1N1), A/Fujian/411/2002-like (H3N2), and B/Shanghai/361/2002-like viruses. Flu Watch reported for 13 to 19 February 2005 that:Specific H5N1 isolates labeled as Fujian include A/Fujian/1/2005 and A/DK/Fujian/1734/05 (or A/Ck/Fujian/1734/2005). A/Fujian (H5N1) bird flu is notable for its resistance to standard medical countermeasures, its rapid spread, what it tells us about the continuing evolution of the H5N1 virus, and the political controversy surrounding it. CIDRAP says "A new subtype of H5N1 avian influenza virus has become predominant in southern China over the past year, possibly through its resistance to vaccines used in poultry, and has been found in human H5N1 cases in China, according to researchers from Hong Kong and the United States. The rise of the Fujian-like strain seems to be the cause of increased poultry outbreaks and recent human cases in China, according to the team from the University of Hong Kong and St. Jude's Children's Research Hospital in Memphis. The researchers also found an overall increase of H5N1 infection in live-poultry markets in southern China." According to the New York Times: "[P]oultry vaccines, made on the cheap, are not filtered and purified [like human vaccines] to remove bits of bacteria or other viruses. They usually contain whole virus, not just the hemagglutinin spike that attaches to cells. Purification is far more expensive than the work in eggs, Dr. Stöhr said; a modest factory for human vaccine costs $100 million, and no veterinary manufacturer is ready to build one. Also, poultry vaccines are "adjuvated" – boosted – with mineral oil, which induces a strong immune reaction but can cause inflammation and abscesses. Chicken vaccinators who have accidentally jabbed themselves have developed painful swollen fingers or even lost thumbs, doctors said. Effectiveness may also be limited. Chicken vaccines are often only vaguely similar to circulating flu strains – some contain an H5N2 strain isolated in Mexico years ago. 'With a chicken, if you use a vaccine that's only 85 percent related, you'll get protection,' Dr. Cardona said. 'In humans, you can get a single point mutation, and a vaccine that's 99.99 percent related won't protect you.' And they are weaker [than human vaccines]. 'Chickens are smaller and you only need to protect them for six weeks, because that's how long they live till you eat them,' said Dr. John J. Treanor, a vaccine expert at the University of Rochester. Human seasonal flu vaccines contain about 45 micrograms of antigen, while an experimental A( H5N1 ) vaccine contains 180. Chicken vaccines may contain less than 1 microgram. 'You have to be careful about extrapolating data from poultry to humans,' warned Dr. David E. Swayne, director of the agriculture department's Southeast Poultry Research Laboratory. 'Birds are more closely related to dinosaurs .'" [ excessive quote ] Researchers, led by Nicholas Savill of the University of Edinburgh in Scotland, used mathematical models to simulate the spread of H5N1 and concluded that "at least 95 per cent of birds need to be protected to prevent the virus spreading silently. In practice, it is difficult to protect more than 90 per cent of a flock; protection levels achieved by a vaccine are usually much lower than this." Referring to the Fujian-like strain, an October 2006 National Academy of Sciences article reports: "The development of highly pathogenic avian H5N1 influenza viruses in poultry in Eurasia accompanied with the increase in human infection in 2006 suggests that the virus has not been effectively contained and that the pandemic threat persists. [...] Serological studies suggest that H5N1 seroconversion in market poultry is low and that vaccination may have facilitated the selection of the Fujian-like sublineage. The predominance of this virus over a large geographical region within a short period directly challenges current disease control measures." The research team tested more than 53,000 birds in southern China from July 2005 through June 2006. 2.4% of the birds had H5N1, more than double the previous 0.9% rate. 68% them were in the new Fujian-like lineage. First detected in March 2005, it constituted 103 of 108 bird hosted isolates tested from April through June 2006, five Chinese human hosted isolates, 16 from Hong Kong birds, and two from Laos and Malaysia birds. Chickens in southern China were found to be poorly immunized against Fujian-like viruses in comparison with other sublineages. "All the analyzed Fujian-like viruses had molecular characteristics that indicated sensitivity to oseltamivir, the first-choice antiviral drug for H5N1 infection. In addition, only six of the viruses had a mutation that confers resistance to amantadine, an older antiviral drug used to treat flu." "China's official Xinhua news agency says a new bird flu outbreak has killed more than 3,000 chickens in the northwest. The Ministry of Agriculture told Xinhua that the July 14 outbreak in Xinjiang region's Aksu city is under control. No human infections have been reported. Saturday's report says the deadly H5N1 virus killed 3,045 chickens, and nearly 357,000 more were destroyed in an emergency response. Xinhua says the local agriculture department has quarantined the infected area. The government's last reported outbreak was in the northwestern region of Ningxia earlier this month." The October 2006 National Academy of Sciences article also says: "Updated virological and epidemiological findings from our market surveillance in southern China demonstrate that H5N1 influenza viruses continued to be panzootic in different types of poultry. Genetic and antigenic analyses revealed the emergence and predominance of a previously uncharacterized H5N1 virus sublineage (Fujian-like) in poultry since late 2005. Viruses from this sublineage gradually replaced those multiple regional distinct sublineages and caused recent human infection in China. These viruses have already transmitted to Hong Kong, Laos, Malaysia, and Thailand, resulting in a new transmission and outbreak wave in Southeast Asia." The first known strain of HPAI A(H5N1) (called A/chicken/Scotland/59) killed two flocks of chickens in Scotland in 1959; but that strain was very different from the current highly pathogenic strain of H5N1. The dominant strain of HPAI A(H5N1) in 2004 evolved from 1999 to 2002 creating the Z genotype. It has also been called "Asian lineage HPAI A(H5N1)". H5N1 is an Influenza A virus subtype. Experts believe it might mutate into a form that transmits easily from person to person. If such a mutation occurs, it might remain an H5N1 subtype or could shift subtypes as did H2N2 when it evolved into the Hong Kong Flu strain of H3N2 . [ citation needed ] H5N1 has mutated through antigenic drift into dozens of highly pathogenic varieties, but all currently belonging to genotype Z of avian influenza virus H5N1. Genotype Z emerged through reassortment in 2002 from earlier highly pathogenic genotypes of H5N1 that first appeared in China in 1996 in birds and in Hong Kong in 1997 in humans . The "H5N1 viruses from human infections and the closely related avian viruses isolated in 2004 and 2005 belong to a single genotype, often referred to as genotype Z." In July 2004, researchers led by H. Deng of the Harbin Veterinary Research Institute , Harbin , China and Professor Robert G. Webster of the St. Jude Children's Research Hospital , Memphis, Tennessee , reported results of experiments in which mice had been exposed to 21 isolates of confirmed H5N1 strains obtained from ducks in China between 1999 and 2002. They found "a clear temporal pattern of progressively increasing pathogenicity". Results reported by Dr. Webster in July 2005 reveal further progression toward pathogenicity in mice and longer virus shedding by ducks. Asian lineage HPAI A(H5N1) is divided into two antigenic clades. "Clade 1 includes human and bird isolates from Vietnam , Thailand , and Cambodia and bird isolates from Laos and Malaysia . Clade 2 viruses were first identified in bird isolates from China, Indonesia , Japan , and South Korea before spreading westward to the Middle East , Europe , and Africa . The clade 2 viruses have been primarily responsible for human H5N1 infections that have occurred during late 2005 and 2006, according to WHO. Genetic analysis has identified six subclades of clade 2, three of which have a distinct geographic distribution and have been implicated in human infections: On 18 August 2006, the World Health Organization (WHO) changed the H5N1 avian influenza strains recommended for candidate vaccines for the first time since 2004. "Many experts who follow the ongoing analysis of the H5N1 virus sequences are alarmed at how fast the virus is evolving into an increasingly more complex network of clades and subclades, Osterholm said. The evolving nature of the virus complicates vaccine planning. He said if an avian influenza pandemic emerges, a strain-specific vaccine will need to be developed to treat the disease. Recognition of the three new subclades means researchers face increasingly complex options about which path to take to stay ahead of the virus." "Human disease associated with influenza A subtype H5N1 re-emerged in January 2003, for the first time since an outbreak in Hong Kong in 1997." Three people in one family were infected after visiting Fujian province in mainland China and 2 died. By midyear of 2003 outbreaks of poultry disease caused by H5N1 occurred in Asia, but were not recognized as such. That December animals in a Thai zoo died after eating infected chicken carcasses. Later that month H5N1 infection was detected in 3 flocks in the Republic of Korea . H5N1 in China in this and later periods is less than fully reported. Blogs have described many discrepancies between official China government announcements concerning H5N1 and what people in China see with their own eyes. Many reports of total H5N1 cases exclude China due to widespread disbelief in China's official numbers. According to the CDC article H5N1 Outbreaks and Enzootic Influenza by Robert G. Webster et al.:"Transmission of highly pathogenic H5N1 from domestic poultry back to migratory waterfowl in western China has increased the geographic spread. The spread of H5N1 and its likely reintroduction to domestic poultry increase the need for good agricultural vaccines. In fact, the root cause of the continuing H5N1 pandemic threat may be the way the pathogenicity of H5N1 viruses is masked by cocirculating influenza viruses or bad agricultural vaccines." Dr. Robert Webster explains: "If you use a good vaccine you can prevent the transmission within poultry and to humans. But if they have been using vaccines now [in China] for several years, why is there so much bird flu? There is bad vaccine that stops the disease in the bird but the bird goes on pooping out virus and maintaining it and changing it. And I think this is what is going on in China. It has to be. Either there is not enough vaccine being used or there is substandard vaccine being used. Probably both. It's not just China. We can't blame China for substandard vaccines. I think there are substandard vaccines for influenza in poultry all over the world." In response to the same concerns, Reuters reports Hong Kong infectious disease expert Lo Wing-lok saying, "The issue of vaccines has to take top priority," and Julie Hall, in charge of the WHO's outbreak response in China, saying "China's vaccinations might be masking the virus." The BBC reported that Dr Wendy Barclay, a virologist at the University of Reading, UK said: "The Chinese have made a vaccine based on reverse genetics made with H5N1 antigens, and they have been using it. There has been a lot of criticism of what they have done, because they have protected their chickens against death from this virus but the chickens still get infected; and then you get drift - the virus mutates in response to the antibodies - and now we have a situation where we have five or six 'flavours' of H5N1 out there." In October 2006, China and WHO traded accusations over the Fujian-like strain. Chinese authorities rejected the Fujian-like strain interpretation altogether saying "Gene sequence analysis shows that all the variants of the virus found in southern China share high uniformity, meaning they all belong to the same gene type. No distinctive change was found in their biological characteristics." While a World Health Organization official in China renewed previous complaints that the Chinese have been stingy with information about H5N1 in poultry saying "There's a stark contrast between what we're hearing from the researchers and what the Ministry of Agriculture says. Unless the ministry tells us what's going on and shares viruses on a regular basis, we will be doing diagnostics on strains that are old." In November 2006, China and WHO traded favors over their H5N1 disagreements with a face-saving WHO apology and China promising to share more avian influenza virus samples. Also in November, Margaret Chan , a former top government health official for Hong Kong, was made Director-General elect of the WHO. The Chinese government said they "would fully support her work in the WHO so that she could wholeheartedly carry out her responsibility and serve the health cause of the world." In December 2006, Chinese authorities agreed that Fujian flu exists; but said that " Anhui " should replace the word " Fujian " in its name. Other names it has been called include "waterfowl clade" and "clade 2.3". (Or more specifically, "Clade 2.3.4" ) China provided 20 H5N1 samples from birds in late 2006 gleaned from birds a year earlier and in 2006 shared a significant amount of H5N1 information generated by its labs. On 31 May 2007, for the first time in almost a year, China shared H5N1 avian flu virus samples taken from humans with WHO . The samples were taken from two people and arrived at a World Health Organization (WHO) laboratory in the United States that is part of CDC. A WHO official said that these are two of the three samples promised to WHO and have been sent by China's health ministry. The specimens are from a 2006 case from Xinjiang province in far western China and a 2007 case from Fujian province in the south. The third promised but not yet delivered sample is from a 24-year-old soldier who died in 2003. China previously sent six human H5N1 virus samples to WHO laboratories: two in December 2005 and four in May 2006. According to the New York Times: "[P]oultry vaccines, made on the cheap, are not filtered and purified [like human vaccines] to remove bits of bacteria or other viruses. They usually contain whole virus, not just the hemagglutinin spike that attaches to cells. Purification is far more expensive than the work in eggs, Dr. Stöhr said; a modest factory for human vaccine costs $100 million, and no veterinary manufacturer is ready to build one. Also, poultry vaccines are "adjuvated" – boosted – with mineral oil, which induces a strong immune reaction but can cause inflammation and abscesses. Chicken vaccinators who have accidentally jabbed themselves have developed painful swollen fingers or even lost thumbs, doctors said. Effectiveness may also be limited. Chicken vaccines are often only vaguely similar to circulating flu strains – some contain an H5N2 strain isolated in Mexico years ago. 'With a chicken, if you use a vaccine that's only 85 percent related, you'll get protection,' Dr. Cardona said. 'In humans, you can get a single point mutation, and a vaccine that's 99.99 percent related won't protect you.' And they are weaker [than human vaccines]. 'Chickens are smaller and you only need to protect them for six weeks, because that's how long they live till you eat them,' said Dr. John J. Treanor, a vaccine expert at the University of Rochester. Human seasonal flu vaccines contain about 45 micrograms of antigen, while an experimental A( H5N1 ) vaccine contains 180. Chicken vaccines may contain less than 1 microgram. 'You have to be careful about extrapolating data from poultry to humans,' warned Dr. David E. Swayne, director of the agriculture department's Southeast Poultry Research Laboratory. 'Birds are more closely related to dinosaurs .'" [ excessive quote ] Researchers, led by Nicholas Savill of the University of Edinburgh in Scotland, used mathematical models to simulate the spread of H5N1 and concluded that "at least 95 per cent of birds need to be protected to prevent the virus spreading silently. In practice, it is difficult to protect more than 90 per cent of a flock; protection levels achieved by a vaccine are usually much lower than this." Referring to the Fujian-like strain, an October 2006 National Academy of Sciences article reports: "The development of highly pathogenic avian H5N1 influenza viruses in poultry in Eurasia accompanied with the increase in human infection in 2006 suggests that the virus has not been effectively contained and that the pandemic threat persists. [...] Serological studies suggest that H5N1 seroconversion in market poultry is low and that vaccination may have facilitated the selection of the Fujian-like sublineage. The predominance of this virus over a large geographical region within a short period directly challenges current disease control measures." The research team tested more than 53,000 birds in southern China from July 2005 through June 2006. 2.4% of the birds had H5N1, more than double the previous 0.9% rate. 68% them were in the new Fujian-like lineage. First detected in March 2005, it constituted 103 of 108 bird hosted isolates tested from April through June 2006, five Chinese human hosted isolates, 16 from Hong Kong birds, and two from Laos and Malaysia birds. Chickens in southern China were found to be poorly immunized against Fujian-like viruses in comparison with other sublineages. "All the analyzed Fujian-like viruses had molecular characteristics that indicated sensitivity to oseltamivir, the first-choice antiviral drug for H5N1 infection. In addition, only six of the viruses had a mutation that confers resistance to amantadine, an older antiviral drug used to treat flu." "China's official Xinhua news agency says a new bird flu outbreak has killed more than 3,000 chickens in the northwest. The Ministry of Agriculture told Xinhua that the July 14 outbreak in Xinjiang region's Aksu city is under control. No human infections have been reported. Saturday's report says the deadly H5N1 virus killed 3,045 chickens, and nearly 357,000 more were destroyed in an emergency response. Xinhua says the local agriculture department has quarantined the infected area. The government's last reported outbreak was in the northwestern region of Ningxia earlier this month." The October 2006 National Academy of Sciences article also says: "Updated virological and epidemiological findings from our market surveillance in southern China demonstrate that H5N1 influenza viruses continued to be panzootic in different types of poultry. Genetic and antigenic analyses revealed the emergence and predominance of a previously uncharacterized H5N1 virus sublineage (Fujian-like) in poultry since late 2005. Viruses from this sublineage gradually replaced those multiple regional distinct sublineages and caused recent human infection in China. These viruses have already transmitted to Hong Kong, Laos, Malaysia, and Thailand, resulting in a new transmission and outbreak wave in Southeast Asia." The first known strain of HPAI A(H5N1) (called A/chicken/Scotland/59) killed two flocks of chickens in Scotland in 1959; but that strain was very different from the current highly pathogenic strain of H5N1. The dominant strain of HPAI A(H5N1) in 2004 evolved from 1999 to 2002 creating the Z genotype. It has also been called "Asian lineage HPAI A(H5N1)". H5N1 is an Influenza A virus subtype. Experts believe it might mutate into a form that transmits easily from person to person. If such a mutation occurs, it might remain an H5N1 subtype or could shift subtypes as did H2N2 when it evolved into the Hong Kong Flu strain of H3N2 . [ citation needed ] H5N1 has mutated through antigenic drift into dozens of highly pathogenic varieties, but all currently belonging to genotype Z of avian influenza virus H5N1. Genotype Z emerged through reassortment in 2002 from earlier highly pathogenic genotypes of H5N1 that first appeared in China in 1996 in birds and in Hong Kong in 1997 in humans . The "H5N1 viruses from human infections and the closely related avian viruses isolated in 2004 and 2005 belong to a single genotype, often referred to as genotype Z." In July 2004, researchers led by H. Deng of the Harbin Veterinary Research Institute , Harbin , China and Professor Robert G. Webster of the St. Jude Children's Research Hospital , Memphis, Tennessee , reported results of experiments in which mice had been exposed to 21 isolates of confirmed H5N1 strains obtained from ducks in China between 1999 and 2002. They found "a clear temporal pattern of progressively increasing pathogenicity". Results reported by Dr. Webster in July 2005 reveal further progression toward pathogenicity in mice and longer virus shedding by ducks. Asian lineage HPAI A(H5N1) is divided into two antigenic clades. "Clade 1 includes human and bird isolates from Vietnam , Thailand , and Cambodia and bird isolates from Laos and Malaysia . Clade 2 viruses were first identified in bird isolates from China, Indonesia , Japan , and South Korea before spreading westward to the Middle East , Europe , and Africa . The clade 2 viruses have been primarily responsible for human H5N1 infections that have occurred during late 2005 and 2006, according to WHO. Genetic analysis has identified six subclades of clade 2, three of which have a distinct geographic distribution and have been implicated in human infections: On 18 August 2006, the World Health Organization (WHO) changed the H5N1 avian influenza strains recommended for candidate vaccines for the first time since 2004. "Many experts who follow the ongoing analysis of the H5N1 virus sequences are alarmed at how fast the virus is evolving into an increasingly more complex network of clades and subclades, Osterholm said. The evolving nature of the virus complicates vaccine planning. He said if an avian influenza pandemic emerges, a strain-specific vaccine will need to be developed to treat the disease. Recognition of the three new subclades means researchers face increasingly complex options about which path to take to stay ahead of the virus." "Human disease associated with influenza A subtype H5N1 re-emerged in January 2003, for the first time since an outbreak in Hong Kong in 1997." Three people in one family were infected after visiting Fujian province in mainland China and 2 died. By midyear of 2003 outbreaks of poultry disease caused by H5N1 occurred in Asia, but were not recognized as such. That December animals in a Thai zoo died after eating infected chicken carcasses. Later that month H5N1 infection was detected in 3 flocks in the Republic of Korea . H5N1 in China in this and later periods is less than fully reported. Blogs have described many discrepancies between official China government announcements concerning H5N1 and what people in China see with their own eyes. Many reports of total H5N1 cases exclude China due to widespread disbelief in China's official numbers. According to the CDC article H5N1 Outbreaks and Enzootic Influenza by Robert G. Webster et al.:"Transmission of highly pathogenic H5N1 from domestic poultry back to migratory waterfowl in western China has increased the geographic spread. The spread of H5N1 and its likely reintroduction to domestic poultry increase the need for good agricultural vaccines. In fact, the root cause of the continuing H5N1 pandemic threat may be the way the pathogenicity of H5N1 viruses is masked by cocirculating influenza viruses or bad agricultural vaccines." Dr. Robert Webster explains: "If you use a good vaccine you can prevent the transmission within poultry and to humans. But if they have been using vaccines now [in China] for several years, why is there so much bird flu? There is bad vaccine that stops the disease in the bird but the bird goes on pooping out virus and maintaining it and changing it. And I think this is what is going on in China. It has to be. Either there is not enough vaccine being used or there is substandard vaccine being used. Probably both. It's not just China. We can't blame China for substandard vaccines. I think there are substandard vaccines for influenza in poultry all over the world." In response to the same concerns, Reuters reports Hong Kong infectious disease expert Lo Wing-lok saying, "The issue of vaccines has to take top priority," and Julie Hall, in charge of the WHO's outbreak response in China, saying "China's vaccinations might be masking the virus." The BBC reported that Dr Wendy Barclay, a virologist at the University of Reading, UK said: "The Chinese have made a vaccine based on reverse genetics made with H5N1 antigens, and they have been using it. There has been a lot of criticism of what they have done, because they have protected their chickens against death from this virus but the chickens still get infected; and then you get drift - the virus mutates in response to the antibodies - and now we have a situation where we have five or six 'flavours' of H5N1 out there." In October 2006, China and WHO traded accusations over the Fujian-like strain. Chinese authorities rejected the Fujian-like strain interpretation altogether saying "Gene sequence analysis shows that all the variants of the virus found in southern China share high uniformity, meaning they all belong to the same gene type. No distinctive change was found in their biological characteristics." While a World Health Organization official in China renewed previous complaints that the Chinese have been stingy with information about H5N1 in poultry saying "There's a stark contrast between what we're hearing from the researchers and what the Ministry of Agriculture says. Unless the ministry tells us what's going on and shares viruses on a regular basis, we will be doing diagnostics on strains that are old." In November 2006, China and WHO traded favors over their H5N1 disagreements with a face-saving WHO apology and China promising to share more avian influenza virus samples. Also in November, Margaret Chan , a former top government health official for Hong Kong, was made Director-General elect of the WHO. The Chinese government said they "would fully support her work in the WHO so that she could wholeheartedly carry out her responsibility and serve the health cause of the world." In December 2006, Chinese authorities agreed that Fujian flu exists; but said that " Anhui " should replace the word " Fujian " in its name. Other names it has been called include "waterfowl clade" and "clade 2.3". (Or more specifically, "Clade 2.3.4" ) China provided 20 H5N1 samples from birds in late 2006 gleaned from birds a year earlier and in 2006 shared a significant amount of H5N1 information generated by its labs. On 31 May 2007, for the first time in almost a year, China shared H5N1 avian flu virus samples taken from humans with WHO . The samples were taken from two people and arrived at a World Health Organization (WHO) laboratory in the United States that is part of CDC. A WHO official said that these are two of the three samples promised to WHO and have been sent by China's health ministry. The specimens are from a 2006 case from Xinjiang province in far western China and a 2007 case from Fujian province in the south. The third promised but not yet delivered sample is from a 24-year-old soldier who died in 2003. China previously sent six human H5N1 virus samples to WHO laboratories: two in December 2005 and four in May 2006.

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Avian influenza

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Influenza A virus subtype H7N3

Influenza A virus subtype H7N3 (A/H7N3) is a subtype of the species Influenza A virus (sometimes called bird flu virus). In North America , the presence of H7N3 was confirmed at several poultry farms in British Columbia in February 2004; flocks were culled to halt the spread of the virus. Two humans, both poultry workers, were infected and had symptoms including conjunctivitis and mild influenza -like illness. Both fully recovered and were treated with oseltamivir . In 1963, H7N3 was first found in Britain, in turkeys. For the first time since 1979, H7N3 was found in the UK in April 2006. It infected birds and one poultry worker (whose only symptom was conjunctivitis) in a Norfolk, England Witford Lodge Farm. Oseltamivir was used for prevention and 35,000 chickens were culled. In 2005, H7N3 was detected in migratory bird droppings in Taiwan. On September 27, 2007, another outbreak of H7N3 was detected in a poultry operation in Saskatchewan, Canada. The Canadian Food Inspection Agency has announced the euthanization of the flock and the disinfection of all building, materials, and equipment in contact with the birds or their droppings. In June, 2012, an outbreak was found on about 10 farms in Jalisco , Mexico. Of the over 6 million birds checked, 1.7 million were found to be sick. The area primarily produces layers and supplies eggs. The virus is not transmitted from hens to their eggs.

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Avian influenza

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2020–2023 H5N8 outbreak

In the early 2020s , an ongoing outbreak of avian influenza subtype H5N8 has been occurring at poultry farms and among wild bird populations in several countries and continents, leading to the subsequent cullings of millions of birds to prevent a pandemic similar to that of the H5N1 outbreak in 2008 . The first case of human transmission of avian flu, also known as bird flu, was reported by Russian authorities in February 2021, as several poultry farm workers tested positive for the virus.On 4 February 2020, the Saudi Arabian government reported an outbreak of the highly pathogenic H5N8 virus on a poultry farm. The outbreak, which occurred in the central Sudair region, killed more than 22,000 birds in a few weeks. In the summer months, H5N8 was detected in wild birds in western Russia and Kazakhstan. Because this included waterbirds that migrate into northern and western Europe, it was considered likely that the virus would be detected there later in the year (as would be confirmed in October–November). On October 22, the agriculture minister Carola Schouten of the Netherlands confirmed that H5N8 had been found in samples from wild birds in the country. As a countermeasure, it was required that birds in poultry farms were kept indoors and isolated. From late October to mid-November, it had spread to three chicken farms and a duck farm in the country, and the 320,000 birds in the farms had been eradicated to stop the spread. Shortly after the first detection in the Netherlands, it was confirmed in the United Kingdom (October: poultry; November: wild birds and poultry), Germany (October: wild birds; November: wild birds and poultry), Republic of Ireland (October and November: wild birds), Belgium (November: wild birds), Denmark (November: wild birds and poultry), France (November: poultry) and Sweden (November: poultry). These outbreaks resulted in countermeasures that were similar to those already taken in the Netherlands. According to official confirmed reports from the Ministry of Agriculture Forestry and Fisheries of Japan, multiple dead chickens were found in 49 poultry farms: 16 on Shikoku Island , 15 on Kyushu Island , ten in Kanto region , five in western Honshu , one each on Awaji Island , Gifu Prefecture and Toyama Prefecture , Japan from November 5, 2020, to February 25, 2021. According to a local official confirmed the report, these cases were the highly pathogenic H5N8 type flu. [ citation needed ] On November 10, South Korea's agriculture ministry said it had confirmed the highly pathogenic H5N8 strain of bird flu in samples from wild birds in the central west of the country and issued its bird flu warning. On November 27, China's agriculture ministry reported that H5N8 had been found in wild swans in Shanxi province , while Norway detected its first case of the highly pathogenic H5N8 strain of bird flu in wild geese in Sandnes municipality, prompting the Norwegian Food Safety Authority to introduce a regional ban on outdoor poultry. On November 30, South Korea reported an outbreak of pathogenic H5N8 avian influenza at a farm in Jeongeup , North Jeolla Province , killing over 19,000 ducks . The H5N8 avian influenza was reported in two districts of Indian state of Kerala in early January 2021 which killed hundreds of birds in late December 2020. Thousands of birds were culled. Avian influenza outbreaks of unknown subtypes were later also reported in five other states of India. 160,000 birds in two poultry farms in Barwala, Panchkula and Raipur Rani are to be culled. 437,000 birds died in this poultry belt between mid-December and 8 January 2021. By 9 January 2021, seven states confirmed the outbreak. On January 15, authorities in Namibia suspended the importation and transit of poultry from European countries where an outbreak of the Avian influenza subtype H5N8 has been reported. On January 20, Iraq reported an outbreak of highly pathogenic H5N8 bird flu on a farm in the city of Samarra , which killed 63,700 birds out of the 68,800-strong flock, according to the Paris-based World Organisation for Animal Health (OIE). The remaining birds were subsequently culled. On February 1, the Ministry of Agriculture and Rural Affairs of China reported an outbreak of highly pathogenic H5N8 in wild Swans at the Winter Palace, Beijing . On February 2, authorities in Brandenburg , Germany, culled 14,000 turkeys on a farm due to a confirmed outbreak of H5N8 in the Uckermark area. On February 9, Algeria reported an outbreak of H5N8 on a poultry farm in the town of Aïn Fakroun . The outbreak killed 50,000 birds, with the remaining 1,200 birds in the flock being culled, according to a report from the Agriculture Ministry. Afghanistan reported an outbreak of H5N8 bird flu on a poultry farm in Herat Province on February 25. The outbreak killed 794 birds, while the remaining 22,000-strong flock were subsequently culled, according to the World Organisation for Animal Health. Warwickshire, UK reported an outbreak on November 8, 2021. A 3 km protection zone and a 10 km surveillance zone have been established. Avian flu was detected at a poultry farm in Akita Prefecture in northeastern Japan, prompting the culling of roughly 143,000 chickens, according to the prefectural government on November 10, 2021. From February to April 2022, avian flu outbreaks in United States have resulted in the culling of more than 22.8 million birds in 24 states. Avian flu has affected England. In Norfolk , Suffolk and parts of Essex , poultry has been mandated to be kept indoors after the affected areas were placed in an Avian Influenza Prevention Zone. In October 2022, wildlife experts patrolling the Norfolk Broads were looking for swans that showed signs of being ill and had to euthanatize them on the spot. In the beginning of the year, an outbreak of H5N8 began in Argentina . In February 2023, Argentina confirmed its first poultry case in Río Negro Province and decided to suspend poultry exports due to the case. By that date, other 25 cases had been detected in wild birds across the country. Currently experts are predicting large outbreaks in penguin populations on Antarctica later this year. [ citation needed ] On 20 February 2021, Russian authorities reported the first known human cases of H5N8 as seven farm workers tested positive. There is no evidence of human-to-human transmission and the cases were described as "mild" or asymptomatic. The World Health Organization was notified. On 4 February 2020, the Saudi Arabian government reported an outbreak of the highly pathogenic H5N8 virus on a poultry farm. The outbreak, which occurred in the central Sudair region, killed more than 22,000 birds in a few weeks. In the summer months, H5N8 was detected in wild birds in western Russia and Kazakhstan. Because this included waterbirds that migrate into northern and western Europe, it was considered likely that the virus would be detected there later in the year (as would be confirmed in October–November). On October 22, the agriculture minister Carola Schouten of the Netherlands confirmed that H5N8 had been found in samples from wild birds in the country. As a countermeasure, it was required that birds in poultry farms were kept indoors and isolated. From late October to mid-November, it had spread to three chicken farms and a duck farm in the country, and the 320,000 birds in the farms had been eradicated to stop the spread. Shortly after the first detection in the Netherlands, it was confirmed in the United Kingdom (October: poultry; November: wild birds and poultry), Germany (October: wild birds; November: wild birds and poultry), Republic of Ireland (October and November: wild birds), Belgium (November: wild birds), Denmark (November: wild birds and poultry), France (November: poultry) and Sweden (November: poultry). These outbreaks resulted in countermeasures that were similar to those already taken in the Netherlands. According to official confirmed reports from the Ministry of Agriculture Forestry and Fisheries of Japan, multiple dead chickens were found in 49 poultry farms: 16 on Shikoku Island , 15 on Kyushu Island , ten in Kanto region , five in western Honshu , one each on Awaji Island , Gifu Prefecture and Toyama Prefecture , Japan from November 5, 2020, to February 25, 2021. According to a local official confirmed the report, these cases were the highly pathogenic H5N8 type flu. [ citation needed ] On November 10, South Korea's agriculture ministry said it had confirmed the highly pathogenic H5N8 strain of bird flu in samples from wild birds in the central west of the country and issued its bird flu warning. On November 27, China's agriculture ministry reported that H5N8 had been found in wild swans in Shanxi province , while Norway detected its first case of the highly pathogenic H5N8 strain of bird flu in wild geese in Sandnes municipality, prompting the Norwegian Food Safety Authority to introduce a regional ban on outdoor poultry. On November 30, South Korea reported an outbreak of pathogenic H5N8 avian influenza at a farm in Jeongeup , North Jeolla Province , killing over 19,000 ducks . The H5N8 avian influenza was reported in two districts of Indian state of Kerala in early January 2021 which killed hundreds of birds in late December 2020. Thousands of birds were culled. Avian influenza outbreaks of unknown subtypes were later also reported in five other states of India. 160,000 birds in two poultry farms in Barwala, Panchkula and Raipur Rani are to be culled. 437,000 birds died in this poultry belt between mid-December and 8 January 2021. By 9 January 2021, seven states confirmed the outbreak. On January 15, authorities in Namibia suspended the importation and transit of poultry from European countries where an outbreak of the Avian influenza subtype H5N8 has been reported. On January 20, Iraq reported an outbreak of highly pathogenic H5N8 bird flu on a farm in the city of Samarra , which killed 63,700 birds out of the 68,800-strong flock, according to the Paris-based World Organisation for Animal Health (OIE). The remaining birds were subsequently culled. On February 1, the Ministry of Agriculture and Rural Affairs of China reported an outbreak of highly pathogenic H5N8 in wild Swans at the Winter Palace, Beijing . On February 2, authorities in Brandenburg , Germany, culled 14,000 turkeys on a farm due to a confirmed outbreak of H5N8 in the Uckermark area. On February 9, Algeria reported an outbreak of H5N8 on a poultry farm in the town of Aïn Fakroun . The outbreak killed 50,000 birds, with the remaining 1,200 birds in the flock being culled, according to a report from the Agriculture Ministry. Afghanistan reported an outbreak of H5N8 bird flu on a poultry farm in Herat Province on February 25. The outbreak killed 794 birds, while the remaining 22,000-strong flock were subsequently culled, according to the World Organisation for Animal Health. Warwickshire, UK reported an outbreak on November 8, 2021. A 3 km protection zone and a 10 km surveillance zone have been established. Avian flu was detected at a poultry farm in Akita Prefecture in northeastern Japan, prompting the culling of roughly 143,000 chickens, according to the prefectural government on November 10, 2021. From February to April 2022, avian flu outbreaks in United States have resulted in the culling of more than 22.8 million birds in 24 states. Avian flu has affected England. In Norfolk , Suffolk and parts of Essex , poultry has been mandated to be kept indoors after the affected areas were placed in an Avian Influenza Prevention Zone. In October 2022, wildlife experts patrolling the Norfolk Broads were looking for swans that showed signs of being ill and had to euthanatize them on the spot. In the beginning of the year, an outbreak of H5N8 began in Argentina . In February 2023, Argentina confirmed its first poultry case in Río Negro Province and decided to suspend poultry exports due to the case. By that date, other 25 cases had been detected in wild birds across the country. Currently experts are predicting large outbreaks in penguin populations on Antarctica later this year. [ citation needed ]The H5N8 avian influenza was reported in two districts of Indian state of Kerala in early January 2021 which killed hundreds of birds in late December 2020. Thousands of birds were culled. Avian influenza outbreaks of unknown subtypes were later also reported in five other states of India. 160,000 birds in two poultry farms in Barwala, Panchkula and Raipur Rani are to be culled. 437,000 birds died in this poultry belt between mid-December and 8 January 2021. By 9 January 2021, seven states confirmed the outbreak. On January 15, authorities in Namibia suspended the importation and transit of poultry from European countries where an outbreak of the Avian influenza subtype H5N8 has been reported. On January 20, Iraq reported an outbreak of highly pathogenic H5N8 bird flu on a farm in the city of Samarra , which killed 63,700 birds out of the 68,800-strong flock, according to the Paris-based World Organisation for Animal Health (OIE). The remaining birds were subsequently culled. On February 1, the Ministry of Agriculture and Rural Affairs of China reported an outbreak of highly pathogenic H5N8 in wild Swans at the Winter Palace, Beijing . On February 2, authorities in Brandenburg , Germany, culled 14,000 turkeys on a farm due to a confirmed outbreak of H5N8 in the Uckermark area. On February 9, Algeria reported an outbreak of H5N8 on a poultry farm in the town of Aïn Fakroun . The outbreak killed 50,000 birds, with the remaining 1,200 birds in the flock being culled, according to a report from the Agriculture Ministry. Afghanistan reported an outbreak of H5N8 bird flu on a poultry farm in Herat Province on February 25. The outbreak killed 794 birds, while the remaining 22,000-strong flock were subsequently culled, according to the World Organisation for Animal Health. Warwickshire, UK reported an outbreak on November 8, 2021. A 3 km protection zone and a 10 km surveillance zone have been established. Avian flu was detected at a poultry farm in Akita Prefecture in northeastern Japan, prompting the culling of roughly 143,000 chickens, according to the prefectural government on November 10, 2021. From February to April 2022, avian flu outbreaks in United States have resulted in the culling of more than 22.8 million birds in 24 states. Avian flu has affected England. In Norfolk , Suffolk and parts of Essex , poultry has been mandated to be kept indoors after the affected areas were placed in an Avian Influenza Prevention Zone. In October 2022, wildlife experts patrolling the Norfolk Broads were looking for swans that showed signs of being ill and had to euthanatize them on the spot. In the beginning of the year, an outbreak of H5N8 began in Argentina . In February 2023, Argentina confirmed its first poultry case in Río Negro Province and decided to suspend poultry exports due to the case. By that date, other 25 cases had been detected in wild birds across the country. Currently experts are predicting large outbreaks in penguin populations on Antarctica later this year. [ citation needed ]On 20 February 2021, Russian authorities reported the first known human cases of H5N8 as seven farm workers tested positive. There is no evidence of human-to-human transmission and the cases were described as "mild" or asymptomatic. The World Health Organization was notified.

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Avian influenza

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Influenza A virus subtype H6N1

Influenza A virus subtype H6N1 (A/H6N1) , is a subtype of the influenza A virus . It has only infected one person, a woman in Taiwan, who recovered. Known to infect Eurasian teal , it is closely related to subtype H5N1 .

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Avian influenza

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Transmission and infection of H5N1

Transmission and infection of H5N1 from infected avian sources to humans has been a concern since the first documented case of human infection in 1997, due to the global spread of H5N1 that constitutes a pandemic threat. Infected birds pass on H5N1 through their saliva , nasal secretions , and feces . Other birds may pick up the virus through direct contact with these excretions or when they have contact with surfaces contaminated with this material. Because migratory birds are among the carriers of the H5N1 virus it may spread to all parts of the world. Past outbreaks of avian flu have often originated in crowded conditions in southeast and east Asia , where humans, pigs , and poultry live in close quarters. In these conditions a virus is more likely to mutate into a form that more easily infects humans. A few isolated cases of suspected human to human transmission exist, with the latest such case in June 2006 (among members of a family in Sumatra). No pandemic strain of H5N1 has yet been found. Notes: H5N1 vaccines for chickens exist and are sometimes used, although there are many difficulties, and it's difficult to decide whether it helps more or hurts more. H5N1 pre-pandemic vaccines exist in quantities sufficient to inoculate a few million people and might be useful for priming to "boost the immune response to a different H5N1 vaccine tailor-made years later to thwart an emerging pandemic". H5N1 pandemic vaccines and technologies to rapidly create them are in the H5N1 clinical trials stage but can not be verified as useful until after there exists a pandemic strain.Avian flu virus can last indefinitely at a temperature dozens of degrees below freezing, as is found in the northernmost areas that migratory birds frequent. [ citation needed ] Heat kills H5N1 (i.e. inactivates the virus). Influenza A viruses can survive: Over 30 days at 0 °C (32.0 °F) (over one month at freezing temperature) 6 days at 37 °C (98.6 °F) (one week at human body temperature) decades in permanently frozen lakes on hard non-porous surface such as plastic or stainless steel for 24–48 hours on clothes, paper and tissues for 8 – 12 hours While cooking poultry to 70 °C (158 °F) kills the H5N1 virus, it is recommended to cook meat to 74 °C (165 °F) to kill all foodborne pathogens. Inactivation of the virus also occurs under the following conditions: Ordinary levels of chlorine in tap water kill H5N1 in public water systems. To kill avian flu viruses, (the) World Health Organization recommends that environmental surfaces be cleaned by the following: Disinfectants such as sodium hypochlorite , 1% in-use dilution, 5% solution to be diluted 1:5 in clean water, for materials contaminated with blood and body fluids Bleaching powder seven grams per liter with 70% available chlorine for toilets and bathrooms 70% alcohol for smooth surfaces, tabletops, and other surfaces where bleach cannot be used H5N1 "can remain infectious in municipal landfills for almost 2 years. [...] The two factors that most reduced influenza survival times were elevated temperature and acidic or alkaline pH." According to Avian Influenza by Timm C. Harder and Ortrud Werner: The current method of prevention in animal populations is to destroy infected animals, as well as animals suspected of being infected. In southeast Asia , millions of domestic birds have been slaughtered to prevent the spread of the virus. There have been a number of farming practices that have changed in response to outbreaks of the H5N1 virus, including: For example, after nearly two years of using mainly culling to control the virus, the Vietnamese government in 2005 adopted a combination of mass poultry vaccination, disinfecting, culling, information campaigns and bans on live poultry in cities. The majority of H5N1 flu cases have been reported in southeast and east Asia. Once an outbreak is detected, local authorities often order a mass slaughter of birds or animals infected or suspected to be infected. [ citation needed ] Dr. Robert G. Webster et al. write Webster speculates that substandard vaccines may be preventing the expression of the disease in the birds but not stopping them from carrying or transmitting the virus through feces, or the virus from mutating. In order to protect their poultry from death from H5N1, China reportedly made a vaccine based on reverse genetics produced with H5N1 antigens, that Dr Wendy Barclay, a virologist at the University of Reading believes have generated up to six variations of H5N1. According to the United Nations FAO , wild water fowl likely plays a role in the avian influenza cycle and could be the initial source for AI viruses, which may be passed on through contact with resident water fowl or domestic poultry, particularly domestic ducks . A newly mutated virus could circulate within the domestic and possibly resident bird populations until highly pathogenic avian influenza (HPAI) arises. This new virus is pathogenic to poultry and possibly to the wild birds that it arose from. [ citation needed ] Wild birds found to have been infected with HPAI were either sick or dead. This could possibly affect the ability of these birds to carry HPAI for long distances. However, the findings in Qinghai Lake - China , suggest that H5N1 viruses could possibly be transmitted between migratory birds. Additionally, the new outbreaks of HPAI in poultry and wild birds in Russia, Kazakhstan, Western China and Mongolia may indicate that migratory birds probably act as carriers for the transport of HPAI over longer distances. Short-distance transmission between farms, villages or contaminated local water bodies is likewise a distinct possibility. [ citation needed ] The AI virus has adapted to the environment in ways such as using water for survival and to spread, and creating a reservoir (ducks) strictly tied to water. The water in turn influences movement, social behavior and migration patterns of water bird species. It is therefore of great importance to know the ecological strategy of influenza virus as well, in order to fully understand this disease and to control outbreaks when they occur. Most research is needed concerning HPAI viruses in wild birds. For example, small birds like sparrows and starlings can be infected with deadly H5N1 strains and they can carry the virus from chicken house to chicken house causing massive epidemics among the chickens. However, pigeons do not present a risk as they neither catch nor carry the virus. There have been a number of farming practices that have changed in response to outbreaks of the H5N1 virus, including: For example, after nearly two years of using mainly culling to control the virus, the Vietnamese government in 2005 adopted a combination of mass poultry vaccination, disinfecting, culling, information campaigns and bans on live poultry in cities. The majority of H5N1 flu cases have been reported in southeast and east Asia. Once an outbreak is detected, local authorities often order a mass slaughter of birds or animals infected or suspected to be infected. [ citation needed ]Dr. Robert G. Webster et al. write Webster speculates that substandard vaccines may be preventing the expression of the disease in the birds but not stopping them from carrying or transmitting the virus through feces, or the virus from mutating. In order to protect their poultry from death from H5N1, China reportedly made a vaccine based on reverse genetics produced with H5N1 antigens, that Dr Wendy Barclay, a virologist at the University of Reading believes have generated up to six variations of H5N1. According to the United Nations FAO , wild water fowl likely plays a role in the avian influenza cycle and could be the initial source for AI viruses, which may be passed on through contact with resident water fowl or domestic poultry, particularly domestic ducks . A newly mutated virus could circulate within the domestic and possibly resident bird populations until highly pathogenic avian influenza (HPAI) arises. This new virus is pathogenic to poultry and possibly to the wild birds that it arose from. [ citation needed ] Wild birds found to have been infected with HPAI were either sick or dead. This could possibly affect the ability of these birds to carry HPAI for long distances. However, the findings in Qinghai Lake - China , suggest that H5N1 viruses could possibly be transmitted between migratory birds. Additionally, the new outbreaks of HPAI in poultry and wild birds in Russia, Kazakhstan, Western China and Mongolia may indicate that migratory birds probably act as carriers for the transport of HPAI over longer distances. Short-distance transmission between farms, villages or contaminated local water bodies is likewise a distinct possibility. [ citation needed ] The AI virus has adapted to the environment in ways such as using water for survival and to spread, and creating a reservoir (ducks) strictly tied to water. The water in turn influences movement, social behavior and migration patterns of water bird species. It is therefore of great importance to know the ecological strategy of influenza virus as well, in order to fully understand this disease and to control outbreaks when they occur. Most research is needed concerning HPAI viruses in wild birds. For example, small birds like sparrows and starlings can be infected with deadly H5N1 strains and they can carry the virus from chicken house to chicken house causing massive epidemics among the chickens. However, pigeons do not present a risk as they neither catch nor carry the virus. The WHO believes that another influenza pandemic is as likely to occur at any time since 1968, when the last century's third of three pandemics took place. The WHO describes a series of six phases, starting with the inter-pandemic period, where there are no new influenza virus subtypes detected in humans, and progressing numerically to the pandemic period, where there is efficient and sustained human-to-human transmission of the virus in the general population. At the present moment, we are at phase 3 on the scale, meaning a new influenza virus subtype is causing disease in humans, but is not yet spreading efficiently and sustainably among humans. So far, H5N1 infections in humans are attributed to bird-to-human transmission of the virus in most cases. Until May 2006, the WHO estimate of the number of human to human transmission had been "two or three cases". On May 24, 2006, Dr. Julie L. Gerberding, director of the United States Centers for Disease Control and Prevention in Atlanta , estimated that there had been "at least three." On May 30, Maria Cheng, a WHO spokeswoman, said there were "probably about half a dozen," but that no one "has got a solid number." A few isolated cases of suspected human to human transmission exist. with the latest such case in June 2006 (among members of a family in Sumatra). No pandemic strain of H5N1 has yet been found. Notwithstanding possible mutation of the virus, the probability of a "humanized" form of H5N1 emerging through genetic recombination in the body of a human co-infected with H5N1 and another influenza virus type (a process called reassortment ) could be reduced by widespread seasonal influenza vaccination in the general population. It is not clear at this point whether vaccine production and immunization could be stepped up sufficiently to meet this demand. [ citation needed ] If an outbreak of pandemic flu does occur, its spread might be slowed by increasing hygiene in aircraft, and by examining airline cabin air filters for presence of H5N1 virus . [ citation needed ] The American Centers for Disease Control and Prevention advises travelers to areas of Asia where outbreaks of H5N1 have occurred to avoid poultry farms and animals in live food markets. Travelers should also avoid surfaces that appear to be contaminated by feces from any kind of animal, especially poultry. There are several H5N1 vaccines for several of the avian H5N1 varieties. H5N1 continually mutates rendering them, so far for humans, of little use. While there can be some cross-protection against related flu strains, the best protection would be from a vaccine specifically produced for any future pandemic flu virus strain. Daniel R. Lucey , co-director of the Biohazardous Threats and Emerging Diseases graduate program at Georgetown University has made this point, "There is no H5N1 pandemic so there can be no pandemic vaccine." However, "pre-pandemic vaccines" have been created; are being refined and tested; and do have some promise both in furthering research and preparedness for the next pandemic. Vaccine manufacturing companies are being encouraged to increase capacity so that if a pandemic vaccine is needed, facilities will be available for rapid production of large amounts of a vaccine specific to a new pandemic strain. It is not likely that use of antiviral drugs could prevent the evolution of a pandemic flu virus. The human incubation period of avian influenza A (H5N1) is 2 to 17 days. Once infected, the virus can spread by cell-to-cell contact, bypassing receptors. So even if a strain is very hard to initially catch, once infected, it spreads rapidly within a body. For highly pathogenic H5N1 avian influenza in a human, "the time from the onset to presentation (median, 4 days) or to death (median, 9 to 10 days) has remained unchanged from 2003 through 2006." Avian influenza HA bind alpha 2-3 sialic acid receptors while human influenza HA bind alpha 2-6 sialic acid receptors. Usually other differences also exist. There is as yet no human form of H5N1, so all humans who have caught it so far have caught avian H5N1. Human flu symptoms usually include fever , cough , sore throat , muscle aches , conjunctivitis and, in severe cases, severe breathing problems and pneumonia that may be fatal. The severity of the infection will depend to a large part on the state of the infected person's immune system and if the victim has been exposed to the strain before, and is therefore partially immune. No one knows if these or other symptoms will be the symptoms of a humanized H5N1 flu. Highly pathogenic H5N1 avian influenza in a human appears to be far worse, killing over 50% of humans reported infected with the virus, although it is unknown how many cases (with milder symptoms) go unreported. In one case, a boy with H5N1 experienced diarrhea followed rapidly by a coma without developing respiratory or flu-like symptoms. As of February 2008, the "median age of patients with influenza A (H5N1) virus infection is approximately 18 years [...] The overall case fatality proportion is 61% [...] Handling of sick or dead poultry during the week before the onset of illness is the most commonly recognized risk factor [...] The primary pathologic process that causes death is fulminant viral pneumonia." There have been studies of the levels of cytokines in humans infected by the H5N1 flu virus. Of particular concern is elevated levels of tumor necrosis factor-alpha (TNFα), a protein that is associated with tissue destruction at sites of infection and increased production of other cytokines. Flu virus-induced increases in the level of cytokines is also associated with flu symptoms including fever, chills, vomiting and headache. Tissue damage associated with pathogenic flu virus infection can ultimately result in death. The inflammatory cascade triggered by H5N1 has been called a ' cytokine storm ' by some, because of what seems to be a positive feedback process of damage to the body resulting from immune system stimulation. H5N1 type flu virus induces higher levels of cytokines than the more common flu virus types such as H1N1. Other important mechanisms also exist "in the acquisition of virulence in avian influenza viruses " according to the CDC. The NS1 protein of the highly pathogenic avian H5N1 viruses circulating in poultry and waterfowl in Southeast Asia is currently believed to be responsible for the enhanced proinflammatory cytokine response. H5N1 NS1 is characterized by a single amino acid change at position 92. By changing the amino acid from glutamic acid to aspartic acid , researchers were able to abrogate the effect of the H5N1 NS1. This single amino acid change in the NS1 gene greatly increased the pathogenicity of the H5N1 influenza virus. [ citation needed ] In short, this one amino acid difference in the NS1 protein produced by the NS RNA molecule of the H5N1 virus is believed to be largely responsible for an increased pathogenicity (on top of the already increased pathogenicity of its hemagglutinin type which allows it to grow in organs other than lungs) that can manifest itself by causing a cytokine storm in a patient's body, often causing pneumonia and death . [ citation needed ] Neuraminidase inhibitors are a class of drugs that includes zanamivir and oseltamivir , the latter being licensed for prophylaxis treatment in the United Kingdom . Oseltamivir inhibits the influenza virus from spreading inside the user's body. It is marketed by Roche as Tamiflu . This drug has become a focus for some governments and organizations trying to be seen as making preparations for a possible H5N1 pandemic. In August 2005, Roche agreed to donate three million courses of Tamiflu to be deployed by the WHO to contain a pandemic in its region of origin. Although Tamiflu is patented, international law gives governments wide freedom to issue compulsory licenses for life-saving drugs. A second class of drugs, which include amantadine and rimantadine , target the M2 protein, but have become ineffective against most strains of H5N1, due to their use in poultry in China in the 1990s, which created resistant strains. However, recent data suggest that some strains of H5N1 are susceptible to the older drugs, which are inexpensive and widely available. Research indicates that therapy to block one cytokine to lessen a cytokine storm in a patient may not be clinically beneficial. The thin line represents average mortality of recent cases. The thicker line represents mortality averaged over all cases. According to WHO: " Assessment of mortality rates and the time intervals between symptom onset and hospitalization and between symptom onset and death suggests that the illness pattern has not changed substantially during the three years. " From the first laboratory-confirmed case through November 21, 2016, the number of confirmed human cases of H5N1 reported to WHO stands at 856, with 452 fatalities, reflecting a 53% fatality rate. The global case fatality ratio looks only to the official tally of cases confirmed by the WHO. It takes no account of other cases, such as those appearing in press reports. Nor does it reflect any estimate of the global extent of mild, asymptomatic, or other cases which are undiagnosed, unreported by national governments to the WHO, or for any reason cannot be confirmed by the WHO. While the WHO's case count is clearly the most authoritative, these unavoidable limitations result in an unknown number of cases being omitted from it.The WHO believes that another influenza pandemic is as likely to occur at any time since 1968, when the last century's third of three pandemics took place. The WHO describes a series of six phases, starting with the inter-pandemic period, where there are no new influenza virus subtypes detected in humans, and progressing numerically to the pandemic period, where there is efficient and sustained human-to-human transmission of the virus in the general population. At the present moment, we are at phase 3 on the scale, meaning a new influenza virus subtype is causing disease in humans, but is not yet spreading efficiently and sustainably among humans. So far, H5N1 infections in humans are attributed to bird-to-human transmission of the virus in most cases. Until May 2006, the WHO estimate of the number of human to human transmission had been "two or three cases". On May 24, 2006, Dr. Julie L. Gerberding, director of the United States Centers for Disease Control and Prevention in Atlanta , estimated that there had been "at least three." On May 30, Maria Cheng, a WHO spokeswoman, said there were "probably about half a dozen," but that no one "has got a solid number." A few isolated cases of suspected human to human transmission exist. with the latest such case in June 2006 (among members of a family in Sumatra). No pandemic strain of H5N1 has yet been found. Notwithstanding possible mutation of the virus, the probability of a "humanized" form of H5N1 emerging through genetic recombination in the body of a human co-infected with H5N1 and another influenza virus type (a process called reassortment ) could be reduced by widespread seasonal influenza vaccination in the general population. It is not clear at this point whether vaccine production and immunization could be stepped up sufficiently to meet this demand. [ citation needed ] If an outbreak of pandemic flu does occur, its spread might be slowed by increasing hygiene in aircraft, and by examining airline cabin air filters for presence of H5N1 virus . [ citation needed ] The American Centers for Disease Control and Prevention advises travelers to areas of Asia where outbreaks of H5N1 have occurred to avoid poultry farms and animals in live food markets. Travelers should also avoid surfaces that appear to be contaminated by feces from any kind of animal, especially poultry. There are several H5N1 vaccines for several of the avian H5N1 varieties. H5N1 continually mutates rendering them, so far for humans, of little use. While there can be some cross-protection against related flu strains, the best protection would be from a vaccine specifically produced for any future pandemic flu virus strain. Daniel R. Lucey , co-director of the Biohazardous Threats and Emerging Diseases graduate program at Georgetown University has made this point, "There is no H5N1 pandemic so there can be no pandemic vaccine." However, "pre-pandemic vaccines" have been created; are being refined and tested; and do have some promise both in furthering research and preparedness for the next pandemic. Vaccine manufacturing companies are being encouraged to increase capacity so that if a pandemic vaccine is needed, facilities will be available for rapid production of large amounts of a vaccine specific to a new pandemic strain. It is not likely that use of antiviral drugs could prevent the evolution of a pandemic flu virus. The human incubation period of avian influenza A (H5N1) is 2 to 17 days. Once infected, the virus can spread by cell-to-cell contact, bypassing receptors. So even if a strain is very hard to initially catch, once infected, it spreads rapidly within a body. For highly pathogenic H5N1 avian influenza in a human, "the time from the onset to presentation (median, 4 days) or to death (median, 9 to 10 days) has remained unchanged from 2003 through 2006." Avian influenza HA bind alpha 2-3 sialic acid receptors while human influenza HA bind alpha 2-6 sialic acid receptors. Usually other differences also exist. There is as yet no human form of H5N1, so all humans who have caught it so far have caught avian H5N1. Human flu symptoms usually include fever , cough , sore throat , muscle aches , conjunctivitis and, in severe cases, severe breathing problems and pneumonia that may be fatal. The severity of the infection will depend to a large part on the state of the infected person's immune system and if the victim has been exposed to the strain before, and is therefore partially immune. No one knows if these or other symptoms will be the symptoms of a humanized H5N1 flu. Highly pathogenic H5N1 avian influenza in a human appears to be far worse, killing over 50% of humans reported infected with the virus, although it is unknown how many cases (with milder symptoms) go unreported. In one case, a boy with H5N1 experienced diarrhea followed rapidly by a coma without developing respiratory or flu-like symptoms. As of February 2008, the "median age of patients with influenza A (H5N1) virus infection is approximately 18 years [...] The overall case fatality proportion is 61% [...] Handling of sick or dead poultry during the week before the onset of illness is the most commonly recognized risk factor [...] The primary pathologic process that causes death is fulminant viral pneumonia." There have been studies of the levels of cytokines in humans infected by the H5N1 flu virus. Of particular concern is elevated levels of tumor necrosis factor-alpha (TNFα), a protein that is associated with tissue destruction at sites of infection and increased production of other cytokines. Flu virus-induced increases in the level of cytokines is also associated with flu symptoms including fever, chills, vomiting and headache. Tissue damage associated with pathogenic flu virus infection can ultimately result in death. The inflammatory cascade triggered by H5N1 has been called a ' cytokine storm ' by some, because of what seems to be a positive feedback process of damage to the body resulting from immune system stimulation. H5N1 type flu virus induces higher levels of cytokines than the more common flu virus types such as H1N1. Other important mechanisms also exist "in the acquisition of virulence in avian influenza viruses " according to the CDC. The NS1 protein of the highly pathogenic avian H5N1 viruses circulating in poultry and waterfowl in Southeast Asia is currently believed to be responsible for the enhanced proinflammatory cytokine response. H5N1 NS1 is characterized by a single amino acid change at position 92. By changing the amino acid from glutamic acid to aspartic acid , researchers were able to abrogate the effect of the H5N1 NS1. This single amino acid change in the NS1 gene greatly increased the pathogenicity of the H5N1 influenza virus. [ citation needed ] In short, this one amino acid difference in the NS1 protein produced by the NS RNA molecule of the H5N1 virus is believed to be largely responsible for an increased pathogenicity (on top of the already increased pathogenicity of its hemagglutinin type which allows it to grow in organs other than lungs) that can manifest itself by causing a cytokine storm in a patient's body, often causing pneumonia and death . [ citation needed ]Neuraminidase inhibitors are a class of drugs that includes zanamivir and oseltamivir , the latter being licensed for prophylaxis treatment in the United Kingdom . Oseltamivir inhibits the influenza virus from spreading inside the user's body. It is marketed by Roche as Tamiflu . This drug has become a focus for some governments and organizations trying to be seen as making preparations for a possible H5N1 pandemic. In August 2005, Roche agreed to donate three million courses of Tamiflu to be deployed by the WHO to contain a pandemic in its region of origin. Although Tamiflu is patented, international law gives governments wide freedom to issue compulsory licenses for life-saving drugs. A second class of drugs, which include amantadine and rimantadine , target the M2 protein, but have become ineffective against most strains of H5N1, due to their use in poultry in China in the 1990s, which created resistant strains. However, recent data suggest that some strains of H5N1 are susceptible to the older drugs, which are inexpensive and widely available. Research indicates that therapy to block one cytokine to lessen a cytokine storm in a patient may not be clinically beneficial. The thin line represents average mortality of recent cases. The thicker line represents mortality averaged over all cases. According to WHO: " Assessment of mortality rates and the time intervals between symptom onset and hospitalization and between symptom onset and death suggests that the illness pattern has not changed substantially during the three years. " From the first laboratory-confirmed case through November 21, 2016, the number of confirmed human cases of H5N1 reported to WHO stands at 856, with 452 fatalities, reflecting a 53% fatality rate. The global case fatality ratio looks only to the official tally of cases confirmed by the WHO. It takes no account of other cases, such as those appearing in press reports. Nor does it reflect any estimate of the global extent of mild, asymptomatic, or other cases which are undiagnosed, unreported by national governments to the WHO, or for any reason cannot be confirmed by the WHO. While the WHO's case count is clearly the most authoritative, these unavoidable limitations result in an unknown number of cases being omitted from it.

Wiki

Avian influenza

https://api.wikimedia.org/core/v1/wikipedia/en/page/H5N1_vaccine/html

H5N1 vaccine

A H5N1 vaccine is an influenza vaccine intended to provide immunization to influenza A virus subtype H5N1 . Vaccines have been formulated against several of the avian H5N1 influenza varieties. Vaccination of poultry against the H5N1 epizootic is widespread in certain countries. Some vaccines also exist for use in humans, and others are in testing, but none have been made available to civilian populations, however production could be scaled up to quantities sufficient to protect much of the Earth's population in the event of an H5N1 pandemic . In January 2020, the U.S. Food and Drug Administration (FDA) approved Audenz , an adjuvanted influenza A (H5N1) monovalent vaccine. Audenz is a vaccine indicated for active immunization for the prevention of disease caused by the influenza A virus H5N1 subtype contained in the vaccine. Audenz is approved for use in persons six months of age and older at increased risk of exposure to the influenza A virus H5N1 subtype contained in the vaccine. Some older, egg-based H5N1 vaccines for humans that have been licensed are: Other licensed H5N1 vaccines include: In November 2013, the U.S. Food and Drug Administration (FDA) approved an experimental H5N1 bird flu vaccine to be held in stockpiles. In a clinical trial including 3,400 adults, 91% of people age 18-64 and 74% of people age 65 or older formed an immune response sufficient to provide protection. Reported adverse effects were generally mild, with pain at the injection site being the most common adverse effect. H5N1 continually mutates, meaning vaccines based on current samples of avian H5N1 cannot be depended upon to work in the case of a future pandemic of H5N1. While there can be some cross-protection against related flu strains, the best protection would be from a vaccine specifically produced for any future pandemic flu virus strain. Daniel R. Lucey , co-director of the Biohazardous Threats and Emerging Diseases graduate program at Georgetown University, has made this point, "There is no H5N1 pandemic so there can be no pandemic vaccine ." However, "pre-pandemic vaccines" have been created; are being refined and tested; and do have some promise both in furthering research and preparedness for the next pandemic. Vaccine manufacturing companies are being encouraged to increase capacity so that if a pandemic vaccine is needed, facilities will be available for rapid production of large amounts of a vaccine specific to a new pandemic strain. [ medical citation needed ] Problems with H5N1 vaccine production include: [ medical citation needed ] lack of overall production capacity lack of surge production capacity (it is impractical to develop a system that depends on hundreds of millions of 11-day-old specialized eggs on a standby basis) the pandemic H5N1 might be lethal to chickens Cell culture (cell-based) manufacturing technology can be applied to influenza vaccines as they are with most viral vaccines and thereby solve the problems associated with creating flu vaccines using chicken eggs. According to the United States Department of Health and Human Services : Current U.S.-licensed vaccines stimulate an immune response based on the quantity of HA ( hemagglutinin ) antigen included in the dose. Methods to stimulate a strong immune response using less HA antigen are being studied in H5N1 and H9N2 vaccine trials. These include changing the mode of delivery from intramuscular to intradermal and the addition of immune-enhancing adjuvant to the vaccine formulation. Additionally, HHS is soliciting contract proposals from manufacturers of vaccines , adjuvants , and medical devices for the development and licensure of influenza vaccines that will provide dose-sparing alternative strategies. Chiron Corporation is now [ when? ] recertified and under contract with the National Institutes of Health to produce 8,000–10,000 investigational doses of Avian Flu (H5N1) vaccine . MedImmune and Aventis Pasteur are under similar contracts. The United States government hopes to obtain enough vaccine in 2006 to treat 4 million people. However, it is unclear whether this vaccine would be effective against a hypothetical mutated strain that would be easily transmitted through human populations, and the shelf life of stockpiled doses has yet to be determined. The New England Journal of Medicine reported on March 30, 2006, on one of dozens of vaccine studies being conducted. The Treanor et al. study was on vaccine produced from the human isolate (A/Vietnam/1203/2004 H5N1 ) of a virulent clade 1 influenza A (H5N1) virus with the use of a plasmid rescue system, with only the hemagglutinin and neuraminidase genes expressed and administered without adjuvant. "The rest of the genes were derived from an avirulent egg-adapted influenza A/PR/8/34 strain. The hemagglutinin gene was further modified to replace six basic amino acids associated with high pathogenicity in birds at the cleavage site between hemagglutinin 1 and hemagglutinin 2. Immunogenicity was assessed by microneutralization and hemagglutination-inhibition assays with the use of the vaccine virus, although a subgroup of samples were tested with the use of the wild-type influenza A/Vietnam/1203/2004 (H5N1) virus." The results of this study combined with others scheduled to be completed by spring 2007 is hoped will provide a highly immunogenic vaccine that is cross-protective against heterologous influenza strains. On August 18, 2006. the World Health Organization (WHO) changed the H5N1 strains recommended for candidate vaccines for the first time since 2004. "The WHO's new prototype strains, prepared by reverse genetics, include three new H5N1 subclades. The hemagglutinin sequences of most of the H5N1 avian influenza viruses circulating in the past few years fall into two genetic groups, or clades. Clade 1 includes human and bird isolates from Vietnam , Thailand , and Cambodia and bird isolates from Laos and Malaysia . Clade 2 viruses were first identified in bird isolates from China , Indonesia , Japan , and South Korea before spreading westward to the Middle East , Europe , and Africa . The clade 2 viruses have been primarily responsible for human H5N1 infections that have occurred during late 2005 and 2006, according to WHO. Genetic analysis has identified six subclades of clade 2, three of which have a distinct geographic distribution and have been implicated in human infections: Subclade 1, Indonesia Subclade 2, Middle East, Europe, and Africa Subclade 3, China On the basis of the three subclades, the WHO is offering companies and other groups that are interested in pandemic vaccine development these three new prototype strains: An A/Indonesia/2/2005-like virus An A/Bar headed goose/Quinghai/1A/2005-like virus An A/Anhui/1/2005-like virus [...] Until now, [ when? ] researchers have been working on prepandemic vaccines for H5N1 viruses in clade 1. In March, [ when? ] the first clinical trial of a U.S. vaccine for H5N1 showed modest results. In May, [ when? ] French researchers showed somewhat better results in a clinical trial of an H5N1 vaccine that included an adjuvant. Vaccine experts aren't sure if a vaccine effective against known H5N1 viral strains would be effective against future strains. Although the new viruses will now be available for vaccine research, WHO said clinical trials using the clade 1 viruses should continue as an essential step in pandemic preparedness, because the trials yield useful information on priming, cross-reactivity, and cross-protection by vaccine viruses from different clades and subclades." As of November 2006 [ update ] , the United States Department of Health and Human Services (HHS) had enough H5N1 pre-pandemic vaccine to treat about 3 million people (5.9 million full-potency doses) in spite of 0.2 million doses used for research and 1.4 million doses that have begun to lose potency (from the original 7.5 million full-potency doses purchased from Sanofi Pasteur and Chiron Corp. ). The expected shelf life of seasonal flu vaccine is about a year so the fact that most of the H5N1 pre-pandemic stockpile is still good after about two years is considered encouraging. Current U.S.-licensed vaccines stimulate an immune response based on the quantity of HA ( hemagglutinin ) antigen included in the dose. Methods to stimulate a strong immune response using less HA antigen are being studied in H5N1 and H9N2 vaccine trials. These include changing the mode of delivery from intramuscular to intradermal and the addition of immune-enhancing adjuvant to the vaccine formulation. Additionally, HHS is soliciting contract proposals from manufacturers of vaccines , adjuvants , and medical devices for the development and licensure of influenza vaccines that will provide dose-sparing alternative strategies. Chiron Corporation is now [ when? ] recertified and under contract with the National Institutes of Health to produce 8,000–10,000 investigational doses of Avian Flu (H5N1) vaccine . MedImmune and Aventis Pasteur are under similar contracts. The United States government hopes to obtain enough vaccine in 2006 to treat 4 million people. However, it is unclear whether this vaccine would be effective against a hypothetical mutated strain that would be easily transmitted through human populations, and the shelf life of stockpiled doses has yet to be determined. The New England Journal of Medicine reported on March 30, 2006, on one of dozens of vaccine studies being conducted. The Treanor et al. study was on vaccine produced from the human isolate (A/Vietnam/1203/2004 H5N1 ) of a virulent clade 1 influenza A (H5N1) virus with the use of a plasmid rescue system, with only the hemagglutinin and neuraminidase genes expressed and administered without adjuvant. "The rest of the genes were derived from an avirulent egg-adapted influenza A/PR/8/34 strain. The hemagglutinin gene was further modified to replace six basic amino acids associated with high pathogenicity in birds at the cleavage site between hemagglutinin 1 and hemagglutinin 2. Immunogenicity was assessed by microneutralization and hemagglutination-inhibition assays with the use of the vaccine virus, although a subgroup of samples were tested with the use of the wild-type influenza A/Vietnam/1203/2004 (H5N1) virus." The results of this study combined with others scheduled to be completed by spring 2007 is hoped will provide a highly immunogenic vaccine that is cross-protective against heterologous influenza strains. On August 18, 2006. the World Health Organization (WHO) changed the H5N1 strains recommended for candidate vaccines for the first time since 2004. "The WHO's new prototype strains, prepared by reverse genetics, include three new H5N1 subclades. The hemagglutinin sequences of most of the H5N1 avian influenza viruses circulating in the past few years fall into two genetic groups, or clades. Clade 1 includes human and bird isolates from Vietnam , Thailand , and Cambodia and bird isolates from Laos and Malaysia . Clade 2 viruses were first identified in bird isolates from China , Indonesia , Japan , and South Korea before spreading westward to the Middle East , Europe , and Africa . The clade 2 viruses have been primarily responsible for human H5N1 infections that have occurred during late 2005 and 2006, according to WHO. Genetic analysis has identified six subclades of clade 2, three of which have a distinct geographic distribution and have been implicated in human infections: Subclade 1, Indonesia Subclade 2, Middle East, Europe, and Africa Subclade 3, China On the basis of the three subclades, the WHO is offering companies and other groups that are interested in pandemic vaccine development these three new prototype strains: An A/Indonesia/2/2005-like virus An A/Bar headed goose/Quinghai/1A/2005-like virus An A/Anhui/1/2005-like virus [...] Until now, [ when? ] researchers have been working on prepandemic vaccines for H5N1 viruses in clade 1. In March, [ when? ] the first clinical trial of a U.S. vaccine for H5N1 showed modest results. In May, [ when? ] French researchers showed somewhat better results in a clinical trial of an H5N1 vaccine that included an adjuvant. Vaccine experts aren't sure if a vaccine effective against known H5N1 viral strains would be effective against future strains. Although the new viruses will now be available for vaccine research, WHO said clinical trials using the clade 1 viruses should continue as an essential step in pandemic preparedness, because the trials yield useful information on priming, cross-reactivity, and cross-protection by vaccine viruses from different clades and subclades." As of November 2006 [ update ] , the United States Department of Health and Human Services (HHS) had enough H5N1 pre-pandemic vaccine to treat about 3 million people (5.9 million full-potency doses) in spite of 0.2 million doses used for research and 1.4 million doses that have begun to lose potency (from the original 7.5 million full-potency doses purchased from Sanofi Pasteur and Chiron Corp. ). The expected shelf life of seasonal flu vaccine is about a year so the fact that most of the H5N1 pre-pandemic stockpile is still good after about two years is considered encouraging. H5N1 clinical trials are clinical trials concerning H5N1 vaccines. They are intended to discover pharmacological effects and identify any adverse reactions the vaccines may achieve in humans.

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Avian influenza

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Chicken

Gallus domesticus L. The chicken ( Gallus gallus domesticus ) is a large and round short-winged bird , domesticated from the red junglefowl of Southeast Asia around 8,000 years ago. Most chickens are raised for food, providing meat and eggs ; others are kept as pets or for cockfighting . Chickens are common and widespread domestic animals, with a total population of 23.7 billion as of 2018 [ update ] , and an annual production of more than 50 billion birds. A hen bred for laying can produce over 300 eggs per year. There are numerous cultural references to chickens in folklore, religion, and literature.Terms for chickens include: Chicken may mean a chick (as in Hen and Chicken Islands ). In older sources, and still often in trade and scientific contexts, chickens as a species are described as common fowl or domestic fowl . Chickens are relatively large birds , active by day . The body is round, the legs are unfeathered in most breeds, and the wings are short. Wild junglefowl can fly ; chickens and their flight muscles are too heavy to allow them to fly more than a short distance. Size and coloration vary widely between breeds. Adult chickens of both sexes have a fleshy crest on their heads called a comb or cockscomb, and hanging flaps of skin on either side under their beaks called wattles ; combs and wattles are more prominent in males . Some breeds have a mutation that causes extra feathering under the face, giving the appearance of a beard. Chickens are omnivores . In the wild, they scratch at the soil to search for seeds, insects, and animals as large as lizards , small snakes, and young mice . A chicken may live for 5–10 years, depending on the breed . The world's oldest known chicken lived for 16 years. Chickens are gregarious , living in flocks , and incubate eggs and raise young communally. Individual chickens dominate others, establishing a pecking order ; dominant individuals take priority for access to food and nest sites. The concept of dominance, involving pecking, was described in female chickens by Thorleif Schjelderup-Ebbe in 1921 as the "pecking order". Male chickens tend to leap and use their claws in conflicts. Chickens are capable of mobbing and killing a weak or inexperienced predator, such as a young fox. A male's crowing is a loud and sometimes shrill call, serving as a territorial signal to other males, and in response to sudden disturbances within their surroundings. Hens cluck loudly after laying an egg and to call their chicks. Chickens give different warning calls to indicate that a predator is approaching from the air or on the ground. To initiate courting, some roosters may dance in a circle around or near a hen (a circle dance), often lowering the wing which is closest to the hen. The dance triggers a response in the hen and when she responds to his call, the rooster may mount the hen and proceed with the mating. Mating typically involves a sequence in which the male approaches the female and performs a waltzing display. If the female is unreceptive, she runs off; otherwise, she crouches, and the male mounts, treading with both feet on her back. After copulation the male does a tail-bending display. Sperm transfer occurs by cloacal contact between the male and female, in an action called the 'cloacal kiss'. As with all birds, reproduction is controlled by a neuroendocrine system, the Gonadotropin-Releasing Hormone-I neurons in the hypothalamus . Reproductive hormones including estrogen , progesterone , and gonadotropins ( luteinizing hormone and follicle-stimulating hormone ) initiate and maintain sexual maturation changes. Reproduction declines with age, thought to be due to a decline in GnRH-I-N. Hens often try to lay in nests that already contain eggs and sometimes move eggs from neighbouring nests into their own. A flock thus uses only a few preferred locations, rather than having a different nest for every bird. Under natural conditions, most birds lay only until a clutch is complete; they then incubate all the eggs. This is called "going broody ". The hen sits on the nest, fluffing up or pecking defensively if disturbed. She rarely leaves the nest until the eggs have hatched. Eggs of chickens from the high-altitude region of Tibet have special physiological adaptations that result in a higher hatching rate in low oxygen environments. When eggs are placed in a hypoxic environment, chicken embryos from these populations express much more hemoglobin than embryos from other chicken populations. This hemoglobin has a greater affinity for oxygen, binding oxygen more readily. Fertile chicken eggs hatch at the end of the incubation period, about 21 days; the chick uses its egg tooth to break out of the shell. Hens remain on the nest for about two days after the first chick hatches; during this time the newly hatched chicks feed by absorbing the internal yolk sac . The hen guards her chicks and brood them to keep them warm. She leads them to food and water and calls them towards food. The chicks imprint on the hen and subsequently follow her continually. She continues to care for them until they are several weeks old. Water or ground-dwelling fowl similar to modern partridges , in the Galliformes , the order of bird that chickens belong to, survived the Cretaceous–Paleogene extinction event that killed all tree-dwelling birds and their dinosaur relatives. Chickens are descended primarily from the red junglefowl ( Gallus gallus ) and are scientifically classified as the same species. Domesticated chickens freely interbreed with populations of red junglefowl. The domestic chicken has subsequently hybridised with grey junglefowl , Sri Lankan junglefowl and green junglefowl ; a gene for yellow skin, for instance, was incorporated into domestic birds from the grey junglefowl ( G. sonneratii ). It is estimated that chickens share between 71 and 79% of their genome with red junglefowl. According to one early study, a single domestication event of the red junglefowl in present-day Thailand gave rise to the modern chicken with minor transitions separating the modern breeds. The red junglefowl is well adapted to take advantage of the vast quantities of seed produced during the end of the multi-decade bamboo seeding cycle , to boost its own reproduction. In domesticating the chicken, humans took advantage of the red junglefowl's ability to reproduce prolifically when exposed to a surge in its food supply. Exactly when and where the chicken was domesticated remains controversial. Genomic studies estimate that the chicken was domesticated 8,000 years ago in Southeast Asia and spread to China and India 2,000 to 3,000 years later. Archaeological evidence supports domestic chickens in Southeast Asia well before 6000 BC, China by 6000 BC and India by 2000 BC. A landmark 2020 Nature study that fully sequenced 863 chickens across the world suggests that all domestic chickens originate from a single domestication event of red junglefowl whose present-day distribution is predominantly in southwestern China, northern Thailand and Myanmar. These domesticated chickens spread across Southeast and South Asia where they interbred with local wild species of junglefowl, forming genetically and geographically distinct groups. Analysis of the most popular commercial breed shows that the White Leghorn breed possesses a mosaic of divergent ancestries inherited from subspecies of red junglefowl. According to one early study, a single domestication event of the red junglefowl in present-day Thailand gave rise to the modern chicken with minor transitions separating the modern breeds. The red junglefowl is well adapted to take advantage of the vast quantities of seed produced during the end of the multi-decade bamboo seeding cycle , to boost its own reproduction. In domesticating the chicken, humans took advantage of the red junglefowl's ability to reproduce prolifically when exposed to a surge in its food supply. Exactly when and where the chicken was domesticated remains controversial. Genomic studies estimate that the chicken was domesticated 8,000 years ago in Southeast Asia and spread to China and India 2,000 to 3,000 years later. Archaeological evidence supports domestic chickens in Southeast Asia well before 6000 BC, China by 6000 BC and India by 2000 BC. A landmark 2020 Nature study that fully sequenced 863 chickens across the world suggests that all domestic chickens originate from a single domestication event of red junglefowl whose present-day distribution is predominantly in southwestern China, northern Thailand and Myanmar. These domesticated chickens spread across Southeast and South Asia where they interbred with local wild species of junglefowl, forming genetically and geographically distinct groups. Analysis of the most popular commercial breed shows that the White Leghorn breed possesses a mosaic of divergent ancestries inherited from subspecies of red junglefowl. A word for the domestic chicken ( *manuk ) is part of the reconstructed Proto-Austronesian language , indicating they were domesticated by the Austronesian peoples since ancient times. Chickens, together with dogs and pigs, were carried throughout the entire range of the prehistoric Austronesian maritime migrations to Island Southeast Asia , Micronesia , Island Melanesia , Polynesia , and Madagascar , starting from at least 3000 BC from Taiwan . These chickens might have been introduced during pre-Columbian times to South America via Polynesian seafarers, but evidence for this is still putative. The possibility that domestic chickens were in the Americas before Western contact is debated by researchers, but blue-egged chickens, found only in the Americas and Asia, suggest an Asian origin for early American chickens. A lack of data from Thailand, Russia, the Indian subcontinent, Southeast Asia and Sub-Saharan Africa makes it difficult to lay out a clear map of the spread of chickens in these areas; better description and genetic analysis of local breeds threatened by extinction may also help with research into this area. Chicken bones from the Arauco Peninsula in south-central Chile were radiocarbon dated as pre-Columbian, and DNA analysis suggested they were related to prehistoric populations in Polynesia. However, further study of the same bones cast doubt on the findings. Chicken remains have been difficult to date, given the small and fragile bird bones; this may account for discrepancies in dates given by different sources. Archaeological evidence is supplemented by mentions in historical texts from the last few centuries BC, and by depictions in prehistoric artworks, such as across Central Asia. Chickens were widespread throughout southern Central Asia by the 4th century BC. Middle Eastern chicken remains go back to a little earlier than 2000 BC in Syria . Phoenicians spread chickens along the Mediterranean coasts as far as Iberia. During the Hellenistic period (4th–2nd centuries BC), in the southern Levant , chickens began to be widely domesticated for food. The first pictures of chickens in Europe are found on Corinthian pottery of the 7th century BC. Breeding increased under the Roman Empire and reduced in the Middle Ages . Genetic sequencing of chicken bones from archaeological sites in Europe revealed that in the High Middle Ages chickens became less aggressive and began to lay eggs earlier in the breeding season. Chickens reached Egypt via the Middle East for purposes of cockfighting about 1400 BC and became widely bred in Egypt around 300 BC. Three possible routes of introduction into Africa around the early first millennium AD could have been through the Egyptian Nile Valley, the East Africa Roman-Greek or Indian trade, or from Carthage and the Berbers, across the Sahara . The earliest known remains are from Mali , Nubia , East Coast, and South Africa and date back to the middle of the first millennium AD. A word for the domestic chicken ( *manuk ) is part of the reconstructed Proto-Austronesian language , indicating they were domesticated by the Austronesian peoples since ancient times. Chickens, together with dogs and pigs, were carried throughout the entire range of the prehistoric Austronesian maritime migrations to Island Southeast Asia , Micronesia , Island Melanesia , Polynesia , and Madagascar , starting from at least 3000 BC from Taiwan . These chickens might have been introduced during pre-Columbian times to South America via Polynesian seafarers, but evidence for this is still putative. The possibility that domestic chickens were in the Americas before Western contact is debated by researchers, but blue-egged chickens, found only in the Americas and Asia, suggest an Asian origin for early American chickens. A lack of data from Thailand, Russia, the Indian subcontinent, Southeast Asia and Sub-Saharan Africa makes it difficult to lay out a clear map of the spread of chickens in these areas; better description and genetic analysis of local breeds threatened by extinction may also help with research into this area. Chicken bones from the Arauco Peninsula in south-central Chile were radiocarbon dated as pre-Columbian, and DNA analysis suggested they were related to prehistoric populations in Polynesia. However, further study of the same bones cast doubt on the findings. Chicken remains have been difficult to date, given the small and fragile bird bones; this may account for discrepancies in dates given by different sources. Archaeological evidence is supplemented by mentions in historical texts from the last few centuries BC, and by depictions in prehistoric artworks, such as across Central Asia. Chickens were widespread throughout southern Central Asia by the 4th century BC. Middle Eastern chicken remains go back to a little earlier than 2000 BC in Syria . Phoenicians spread chickens along the Mediterranean coasts as far as Iberia. During the Hellenistic period (4th–2nd centuries BC), in the southern Levant , chickens began to be widely domesticated for food. The first pictures of chickens in Europe are found on Corinthian pottery of the 7th century BC. Breeding increased under the Roman Empire and reduced in the Middle Ages . Genetic sequencing of chicken bones from archaeological sites in Europe revealed that in the High Middle Ages chickens became less aggressive and began to lay eggs earlier in the breeding season. Chickens reached Egypt via the Middle East for purposes of cockfighting about 1400 BC and became widely bred in Egypt around 300 BC. Three possible routes of introduction into Africa around the early first millennium AD could have been through the Egyptian Nile Valley, the East Africa Roman-Greek or Indian trade, or from Carthage and the Berbers, across the Sahara . The earliest known remains are from Mali , Nubia , East Coast, and South Africa and date back to the middle of the first millennium AD. Chickens are susceptible both to parasites such as mites , and to diseases caused by pathogens such as bacteria and viruses . The parasite Dermanyssus gallinae feeds on blood, causing irritation and reducing egg production, and acts as a vector for bacterial diseases such as salmonellosis and spirochaetosis . Viral diseases include avian influenza . Chickens are common and widespread domestic animals, with a total population of 23.7 billion as of 2018 [ update ] . More than 50 billion chickens are reared annually as a source of meat and eggs. In the United States alone, more than 8 billion chickens are slaughtered each year for meat, and more than 300 million chickens are reared for egg production. The vast majority of poultry is raised in factory farms . According to the Worldwatch Institute , 74% of the world's poultry meat and 68% of eggs are produced this way. An alternative to intensive poultry farming is free-range farming. Friction between these two main methods has led to long-term issues of ethical consumerism . Opponents of intensive farming argue that it harms the environment, creates human health risks and is inhumane. Advocates of intensive farming say that their efficient systems save land and food resources owing to increased productivity, and that the animals are looked after in a controlled environment. Chickens farmed for meat are called broilers . Broiler breeds typically take less than six weeks to reach slaughter size, some weeks longer for free range and organic broilers. Chickens farmed primarily for eggs are called layer hens. The UK alone consumes more than 34 million eggs per day. Hens of some breeds can produce over 300 eggs per year; the highest authenticated rate of egg laying is 371 eggs in 364 days. After 12 months of laying, the commercial hen's egg-laying ability declines to the point where the flock is commercially unviable. Hens, particularly from battery cage systems, are sometimes infirm or have lost a significant amount of their feathers, and their life expectancy has been reduced from around seven years to less than two years. In the UK and Europe, laying hens are then slaughtered and used in processed foods, or sold as 'soup hens'. In some other countries, flocks are sometimes force moulted rather than being slaughtered to re-invigorate egg-laying. This involves complete withdrawal of food (and sometimes water) for 7–14 days or sufficiently long to cause a body weight loss of 25 to 35%, or up to 28 days under experimental conditions. This stimulates the hen to lose her feathers but also re-invigorates egg-production. Some flocks may be force-moulted several times. In 2003, more than 75% of all flocks were moulted in the US. Keeping chickens as pets became increasingly popular in the 2000s among urban and suburban residents. Many people obtain chickens for their egg production but often name them and treat them as any other pet like cats or dogs. Chickens provide companionship and have individual personalities. While many do not cuddle much, they will eat from one's hand, jump onto one's lap, respond to and follow their handlers, as well as show affection. Chickens are social, inquisitive, intelligent birds, and many people find their behaviour entertaining. Certain breeds, such as silkies and many bantam varieties, are generally docile and are often recommended as good pets around children with disabilities. A cockfight is a contest held in a ring called a cockpit between two cocks. Cockfighting is outlawed in many countries as involving cruelty to animals . The activity seems to have been practised in the Indus Valley civilisation from 2500 to 2100 BC. In the process of domestication, chickens were apparently kept initially for cockfighting, and only later used for food. Chickens have long been used as model organisms to study developing embryos. Large numbers of embryos can be provided commercially; fertilized eggs can easily be opened and used to observe the developing embryo. Equally important, embryologists can carry out experiments on such embryos, close the egg again and study the effects later in development. For instance, many important discoveries in limb development have been made using chicken embryos, such as the discovery of the apical ectodermal ridge and the zone of polarizing activity . The chicken was the first bird species to have its genome sequenced. At 1.21 Gb, the chicken genome is similarly sized compared to other birds, but smaller than nearly all mammals: the human genome is 3.2 Gb. The final gene set contained 26,640 genes (including noncoding genes and pseudogenes ), with a total of 19,119 protein-coding genes, a similar number to the human genome. In 2006, scientists researching the ancestry of birds switched on a chicken recessive gene , talpid2 , and found that the embryo jaws initiated formation of teeth, like those found in ancient bird fossils. Chickens feature widely in folklore , religion , literature , and popular culture. The chicken is a sacred animal in many cultures and deeply embedded in belief systems and religious practices. Roosters are sometimes used for divination , a practice called alectryomancy. This involves the sacrifice of a sacred rooster, often during a ritual cockfight , used as a form of communication with the gods. In Gabriel García Márquez 's Nobel-Prize-winning 1967 novel One Hundred Years Of Solitude , cockfighting is outlawed in the town of Macondo after the patriarch of the Buendia family murders his cockfighting rival and is haunted by the man's ghost. Chicken jokes have been made at least since The Knickerbocker published one in 1847. Chickens have featured in art in farmyard scenes such as Adriaen van Utrecht 's 1646 Turkeys and Chickens and Walter Osborne 's 1885 Feeding the Chickens . The nursery rhyme " Cock a doodle doo ", its chorus line imitating the cockerel's call, was published in Mother Goose's Melody in 1765. The 2000 animated adventure comedy film Chicken Run , directed by Peter Lord and Nick Park , featured anthropomorphic chickens with many chicken jokes. Chickens are common and widespread domestic animals, with a total population of 23.7 billion as of 2018 [ update ] . More than 50 billion chickens are reared annually as a source of meat and eggs. In the United States alone, more than 8 billion chickens are slaughtered each year for meat, and more than 300 million chickens are reared for egg production. The vast majority of poultry is raised in factory farms . According to the Worldwatch Institute , 74% of the world's poultry meat and 68% of eggs are produced this way. An alternative to intensive poultry farming is free-range farming. Friction between these two main methods has led to long-term issues of ethical consumerism . Opponents of intensive farming argue that it harms the environment, creates human health risks and is inhumane. Advocates of intensive farming say that their efficient systems save land and food resources owing to increased productivity, and that the animals are looked after in a controlled environment. Chickens farmed for meat are called broilers . Broiler breeds typically take less than six weeks to reach slaughter size, some weeks longer for free range and organic broilers. Chickens farmed primarily for eggs are called layer hens. The UK alone consumes more than 34 million eggs per day. Hens of some breeds can produce over 300 eggs per year; the highest authenticated rate of egg laying is 371 eggs in 364 days. After 12 months of laying, the commercial hen's egg-laying ability declines to the point where the flock is commercially unviable. Hens, particularly from battery cage systems, are sometimes infirm or have lost a significant amount of their feathers, and their life expectancy has been reduced from around seven years to less than two years. In the UK and Europe, laying hens are then slaughtered and used in processed foods, or sold as 'soup hens'. In some other countries, flocks are sometimes force moulted rather than being slaughtered to re-invigorate egg-laying. This involves complete withdrawal of food (and sometimes water) for 7–14 days or sufficiently long to cause a body weight loss of 25 to 35%, or up to 28 days under experimental conditions. This stimulates the hen to lose her feathers but also re-invigorates egg-production. Some flocks may be force-moulted several times. In 2003, more than 75% of all flocks were moulted in the US. Keeping chickens as pets became increasingly popular in the 2000s among urban and suburban residents. Many people obtain chickens for their egg production but often name them and treat them as any other pet like cats or dogs. Chickens provide companionship and have individual personalities. While many do not cuddle much, they will eat from one's hand, jump onto one's lap, respond to and follow their handlers, as well as show affection. Chickens are social, inquisitive, intelligent birds, and many people find their behaviour entertaining. Certain breeds, such as silkies and many bantam varieties, are generally docile and are often recommended as good pets around children with disabilities. A cockfight is a contest held in a ring called a cockpit between two cocks. Cockfighting is outlawed in many countries as involving cruelty to animals . The activity seems to have been practised in the Indus Valley civilisation from 2500 to 2100 BC. In the process of domestication, chickens were apparently kept initially for cockfighting, and only later used for food. Chickens have long been used as model organisms to study developing embryos. Large numbers of embryos can be provided commercially; fertilized eggs can easily be opened and used to observe the developing embryo. Equally important, embryologists can carry out experiments on such embryos, close the egg again and study the effects later in development. For instance, many important discoveries in limb development have been made using chicken embryos, such as the discovery of the apical ectodermal ridge and the zone of polarizing activity . The chicken was the first bird species to have its genome sequenced. At 1.21 Gb, the chicken genome is similarly sized compared to other birds, but smaller than nearly all mammals: the human genome is 3.2 Gb. The final gene set contained 26,640 genes (including noncoding genes and pseudogenes ), with a total of 19,119 protein-coding genes, a similar number to the human genome. In 2006, scientists researching the ancestry of birds switched on a chicken recessive gene , talpid2 , and found that the embryo jaws initiated formation of teeth, like those found in ancient bird fossils. Chickens feature widely in folklore , religion , literature , and popular culture. The chicken is a sacred animal in many cultures and deeply embedded in belief systems and religious practices. Roosters are sometimes used for divination , a practice called alectryomancy. This involves the sacrifice of a sacred rooster, often during a ritual cockfight , used as a form of communication with the gods. In Gabriel García Márquez 's Nobel-Prize-winning 1967 novel One Hundred Years Of Solitude , cockfighting is outlawed in the town of Macondo after the patriarch of the Buendia family murders his cockfighting rival and is haunted by the man's ghost. Chicken jokes have been made at least since The Knickerbocker published one in 1847. Chickens have featured in art in farmyard scenes such as Adriaen van Utrecht 's 1646 Turkeys and Chickens and Walter Osborne 's 1885 Feeding the Chickens . The nursery rhyme " Cock a doodle doo ", its chorus line imitating the cockerel's call, was published in Mother Goose's Melody in 1765. The 2000 animated adventure comedy film Chicken Run , directed by Peter Lord and Nick Park , featured anthropomorphic chickens with many chicken jokes.

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Avian influenza

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Poultry farming

Poultry farming is the form of animal husbandry which raises domesticated birds such as chickens , ducks , turkeys and geese to produce meat or eggs for food . Poultry – mostly chickens – are farmed in great numbers. More than 60 billion chickens are killed for consumption annually. Chickens raised for eggs are known as layers, while chickens raised for meat are called broilers . In the United States, the national organization overseeing poultry production is the Food and Drug Administration (FDA). In the UK, the national organisation is the Department for Environment, Food and Rural Affairs (DEFRA).Biomass of birds on Earth According to the World Watch Institute, 74 percent of the world's poultry meat, and 68 percent of eggs are produced intensively. One alternative to intensive poultry farming is free-range farming using lower stocking densities. Poultry producers routinely use nationally approved medications, such as antibiotics, in feed or drinking water, to treat disease or to prevent disease outbreaks. Some FDA-approved medications are also approved for improved feed utilization. A chicken coop or hen house is a structure where chickens or other fowl are kept safe and secure. There may be nest boxes and perches in the house. There is a long-standing controversy over the basic need for a chicken coop. One philosophy, known as the "fresh air school" is that chickens are mostly hardy but can be brought low by confinement, poor air quality and darkness, hence the need for a highly ventilated or open-sided coop with conditions more like the outdoors, even in winter. However, others who keep chickens believe they are prone to illness in outdoor weather and need a controlled-environment coop. This has led to two housing designs for chickens: fresh-air houses with wide openings and nothing more than wire mesh between chickens and the weather (even in Northern winters), or closed houses with doors, windows and hatches which can shut off most ventilation. Commercial hens usually begin laying eggs at 16–21 weeks of age, although production gradually declines soon after from approximately 25 weeks of age. This means that in many countries, by approximately 72 weeks of age, flocks are considered economically unviable and are slaughtered after approximately 12 months of egg production, although chickens will naturally live for 6 or more years. In some countries, hens are force moulted to re-invigorate egg-laying. Environmental conditions are often automatically controlled in egg-laying systems. For example, the duration of the light phase is initially increased to prompt the beginning of egg-laying at 16–20 weeks of age and then mimics summer day length which stimulates the hens to continue laying eggs all year round; normally, egg production occurs only in the warmer months. Some commercial breeds of hen can produce over 300 eggs a year. Free-range poultry farming allows chickens to roam freely for a period of the day, although they are usually confined in sheds at night to protect them from predators or kept indoors if the weather is particularly bad. In the UK, the Department for Environment, Food and Rural Affairs (DEFRA) states that a free-range chicken must have day-time access to open-air runs during at least half of its life. Unlike in the United States, this definition also applies to free-range egg-laying hens. The European Union regulates marketing standards for egg farming which specifies a minimum condition for free-range eggs that "hens have continuous daytime access to open air runs, except in the case of temporary restrictions imposed by veterinary authorities". The RSPCA "Welfare standards for laying hens and pullets" indicates that the stocking rate must not exceed 1,000 birds per hectare (10 m 2 per hen) of range available and a minimum area of overhead shade/shelter of 8 m 2 per 1,000 hens must be provided. Free-range farming of egg-laying hens is increasing its share of the market. DEFRA figures indicate that 45% of eggs produced in the UK throughout 2010 were free range, 5% were produced in barn systems and 50% from cages. This compares with 41% being free range in 2009. Suitable land requires adequate drainage to minimise worms and coccidial oocysts, suitable protection from prevailing winds, good ventilation, access and protection from predators. Excess heat, cold or damp can have a harmful effect on the animals and their productivity. Free range farmers have less control than farmers using cages in what food their chickens eat, which can lead to unreliable productivity, though supplementary feeding reduces this uncertainty. In some farms, the manure from free range poultry can be used to benefit crops. The benefits of free range poultry farming for laying hens include opportunities for natural behaviours such as pecking, scratching, foraging and exercise outdoors. Both intensive and free-range farming have animal welfare concerns. Cannibalism , feather pecking and vent pecking can be common, prompting some farmers to use beak trimming as a preventative measure, although reducing stocking rates would eliminate these problems. Diseases can be common and the animals are vulnerable to predators. Barn systems have been found to have the worst bird welfare. In South-East Asia, a lack of disease control in free range farming has been associated with outbreaks of Avian influenza . Instead of keeping them in cages, free-run laying hens roam freely within an enclosed barn. This type of housing also provides enrichment for the hens, including nesting boxes and perches that are often located along the floor of the barn. Many believe that this type of housing is better for the bird than any caging system, but it has its disadvantages, too. Due to the increase in activity of the birds, dust levels tend to elevate and the air quality decreases. When air quality drops, so does production as this compromises the health and welfare of both birds and their caretakers. In organic systems in the US, organic management starts with the selection of the livestock and should begin "no later than the second day of life". Organic poultry production requires organic management in nutrition, preventative health care, living conditions, handling/processing, and recordkeeping. The Soil Association standards used to certify organic flocks in the UK, indicate a maximum outdoors stocking density of 1,000 birds per hectare and a maximum of 2,000 hens in each poultry house. In the UK, organic laying hens are not routinely beak-trimmed. While often confused with free range farming, yarding is actually a separate method by which a hutch and fenced-off area outside are combined when farming poultry. The distinction is that free-range poultry are either totally unfenced, or the fence is so distant that it has little influence on their freedom of movement. Yarding is a common technique used by small farms in the Northeastern U.S. The birds are released daily from hutches or coops. The hens usually lay eggs either on the floor of the coop or in baskets if provided by the farmer. This husbandry technique can be complicated if used with roosters, mostly because of their aggressive behavior. The majority of hens in many countries are housed in battery cages , although the European Union Council Directive 1999/74/EC has banned the conventional battery cage in EU states from January 2012. As of April 1, 2017, no new battery cages are able to be installed in Canada. Farmers must move towards enriched housing or use a cage-free system. In 2016, the Egg Farmers of Canada announced that the country's egg farmers will be transitioning away from conventional hen housing systems (battery cages) and have no conventional caging left by 2036. These are small cages, usually made of metal in modern systems, housing 3 to 8 hens. The walls are made of either solid metal or mesh, and the floor is sloped wire mesh to allow the feces to drop through and eggs to roll onto an egg-collecting conveyor belt. Water is usually provided by overhead nipple systems, and food in a trough along the front of the cage replenished at regular intervals by a mechanical system. Battery cages are arranged in long rows as multiple tiers, often with cages back-to-back (hence the term). Within a single barn, there may be several floors containing battery cages meaning that a single shed may contain many tens of thousands of hens. Light intensity is often kept low (e.g. 10 lux) to reduce feather pecking and vent pecking. Benefits of battery cages include easier care for the birds, floor-laid eggs (which are expensive to collect) are eliminated, eggs are cleaner, capture at the end of lay is expedited, generally less feed is required to produce eggs, broodiness is eliminated, more hens may be housed in a given house floor space, internal parasites are more easily treated, and labor requirements are generally much reduced. In farms using cages for egg production, there are more birds per unit area; this allows for greater productivity and lower food costs. Floor space ranges upwards from 300 cm 2 per hen. EU standards in 2003 called for at least 550 cm 2 per hen. In the US, the current recommendation by the United Egg Producers is 67 to 86 in 2 (430 to 560 cm 2 ) per bird. The space available to battery hens has often been described as less than the size of a piece of A4 paper (623 cm 2 ). Animal welfare scientists have been critical of battery cages because they do not provide hens with sufficient space to stand, walk, flap their wings, perch, or make a nest, and it is widely considered that hens suffer through boredom and frustration through being unable to perform these behaviours. This can lead to a wide range of abnormal behaviours , some of which are injurious to the hens or their cagemates. In 1999, the European Union Council Directive 1999/74/EC banned conventional battery cages for laying hens throughout the European Union from January 1, 2012; they were banned previously in other countries including Switzerland . In response to these bans, development of prototype commercial furnished cage systems began in the 1980s. Furnished cages, sometimes called 'enriched' or 'modified' cages, are cages for egg-laying hens which have been designed to allow the hens to perform their "natural behaviors" whilst retaining their economic and husbandry advantages, and also provide some of the welfare advantages of non-cage systems. Many design features of furnished cages have been incorporated because research in animal welfare science has shown them to be of benefit to the hens. In the UK, the DEFRA "Code for the Welfare of Laying Hens" states furnished cages should provide at least 750 cm 2 of cage area per hen, 600 cm 2 of which should be usable; the height of the cage other than that above the usable area should be at least 20 cm at every point and no cage should have a total area that is less than 2000 cm 2 . In addition, furnished cages should provide a nest, litter such that pecking and scratching are possible, appropriate perches allowing at least 15 cm per hen, a claw-shortening device, and a feed trough which may be used without restriction providing 12 cm per hen. Furnished cages (Enriched) give the hens more space than the conventional battery cages, so that each bird may spread their wings without touching one another if desired. Enrichment such as nest boxes, perches, and dust baths are also provided so that the birds may carry out their natural behaviors such as nesting, roosting, and scratching as though they were outdoors. Enrichment of laying hen cages ultimately results in better bone quality. This is a result of the increased activity in the hens from the additional space and enrichment provided in the furnished housing system. Although the enriched housing system has its advantages such as reduced aggression towards one another and cleaner eggs, modern egg laying breeds often suffer from osteoporosis which results in the chicken's skeletal system being weakened. During egg production, large amounts of calcium are transferred from bones to create egg-shell. Although dietary calcium levels are adequate, absorption of dietary calcium is not always sufficient, given the intensity of production, to fully replenish bone calcium. This can lead to increases in bone breakages, particularly when the hens are being removed from cages at the end of laying. Osteoporosis may be prevented by free range and cage-free housing systems, as they have shown to have a beneficial impact on the skeletal system of the hens compared to those housed in caged systems. Countries such as Austria, Belgium or Germany are planning to ban furnished cages until 2025 additionally to the already banned conventional cages. Free-range poultry farming allows chickens to roam freely for a period of the day, although they are usually confined in sheds at night to protect them from predators or kept indoors if the weather is particularly bad. In the UK, the Department for Environment, Food and Rural Affairs (DEFRA) states that a free-range chicken must have day-time access to open-air runs during at least half of its life. Unlike in the United States, this definition also applies to free-range egg-laying hens. The European Union regulates marketing standards for egg farming which specifies a minimum condition for free-range eggs that "hens have continuous daytime access to open air runs, except in the case of temporary restrictions imposed by veterinary authorities". The RSPCA "Welfare standards for laying hens and pullets" indicates that the stocking rate must not exceed 1,000 birds per hectare (10 m 2 per hen) of range available and a minimum area of overhead shade/shelter of 8 m 2 per 1,000 hens must be provided. Free-range farming of egg-laying hens is increasing its share of the market. DEFRA figures indicate that 45% of eggs produced in the UK throughout 2010 were free range, 5% were produced in barn systems and 50% from cages. This compares with 41% being free range in 2009. Suitable land requires adequate drainage to minimise worms and coccidial oocysts, suitable protection from prevailing winds, good ventilation, access and protection from predators. Excess heat, cold or damp can have a harmful effect on the animals and their productivity. Free range farmers have less control than farmers using cages in what food their chickens eat, which can lead to unreliable productivity, though supplementary feeding reduces this uncertainty. In some farms, the manure from free range poultry can be used to benefit crops. The benefits of free range poultry farming for laying hens include opportunities for natural behaviours such as pecking, scratching, foraging and exercise outdoors. Both intensive and free-range farming have animal welfare concerns. Cannibalism , feather pecking and vent pecking can be common, prompting some farmers to use beak trimming as a preventative measure, although reducing stocking rates would eliminate these problems. Diseases can be common and the animals are vulnerable to predators. Barn systems have been found to have the worst bird welfare. In South-East Asia, a lack of disease control in free range farming has been associated with outbreaks of Avian influenza . Instead of keeping them in cages, free-run laying hens roam freely within an enclosed barn. This type of housing also provides enrichment for the hens, including nesting boxes and perches that are often located along the floor of the barn. Many believe that this type of housing is better for the bird than any caging system, but it has its disadvantages, too. Due to the increase in activity of the birds, dust levels tend to elevate and the air quality decreases. When air quality drops, so does production as this compromises the health and welfare of both birds and their caretakers. In organic systems in the US, organic management starts with the selection of the livestock and should begin "no later than the second day of life". Organic poultry production requires organic management in nutrition, preventative health care, living conditions, handling/processing, and recordkeeping. The Soil Association standards used to certify organic flocks in the UK, indicate a maximum outdoors stocking density of 1,000 birds per hectare and a maximum of 2,000 hens in each poultry house. In the UK, organic laying hens are not routinely beak-trimmed.Instead of keeping them in cages, free-run laying hens roam freely within an enclosed barn. This type of housing also provides enrichment for the hens, including nesting boxes and perches that are often located along the floor of the barn. Many believe that this type of housing is better for the bird than any caging system, but it has its disadvantages, too. Due to the increase in activity of the birds, dust levels tend to elevate and the air quality decreases. When air quality drops, so does production as this compromises the health and welfare of both birds and their caretakers. In organic systems in the US, organic management starts with the selection of the livestock and should begin "no later than the second day of life". Organic poultry production requires organic management in nutrition, preventative health care, living conditions, handling/processing, and recordkeeping. The Soil Association standards used to certify organic flocks in the UK, indicate a maximum outdoors stocking density of 1,000 birds per hectare and a maximum of 2,000 hens in each poultry house. In the UK, organic laying hens are not routinely beak-trimmed.While often confused with free range farming, yarding is actually a separate method by which a hutch and fenced-off area outside are combined when farming poultry. The distinction is that free-range poultry are either totally unfenced, or the fence is so distant that it has little influence on their freedom of movement. Yarding is a common technique used by small farms in the Northeastern U.S. The birds are released daily from hutches or coops. The hens usually lay eggs either on the floor of the coop or in baskets if provided by the farmer. This husbandry technique can be complicated if used with roosters, mostly because of their aggressive behavior.The majority of hens in many countries are housed in battery cages , although the European Union Council Directive 1999/74/EC has banned the conventional battery cage in EU states from January 2012. As of April 1, 2017, no new battery cages are able to be installed in Canada. Farmers must move towards enriched housing or use a cage-free system. In 2016, the Egg Farmers of Canada announced that the country's egg farmers will be transitioning away from conventional hen housing systems (battery cages) and have no conventional caging left by 2036. These are small cages, usually made of metal in modern systems, housing 3 to 8 hens. The walls are made of either solid metal or mesh, and the floor is sloped wire mesh to allow the feces to drop through and eggs to roll onto an egg-collecting conveyor belt. Water is usually provided by overhead nipple systems, and food in a trough along the front of the cage replenished at regular intervals by a mechanical system. Battery cages are arranged in long rows as multiple tiers, often with cages back-to-back (hence the term). Within a single barn, there may be several floors containing battery cages meaning that a single shed may contain many tens of thousands of hens. Light intensity is often kept low (e.g. 10 lux) to reduce feather pecking and vent pecking. Benefits of battery cages include easier care for the birds, floor-laid eggs (which are expensive to collect) are eliminated, eggs are cleaner, capture at the end of lay is expedited, generally less feed is required to produce eggs, broodiness is eliminated, more hens may be housed in a given house floor space, internal parasites are more easily treated, and labor requirements are generally much reduced. In farms using cages for egg production, there are more birds per unit area; this allows for greater productivity and lower food costs. Floor space ranges upwards from 300 cm 2 per hen. EU standards in 2003 called for at least 550 cm 2 per hen. In the US, the current recommendation by the United Egg Producers is 67 to 86 in 2 (430 to 560 cm 2 ) per bird. The space available to battery hens has often been described as less than the size of a piece of A4 paper (623 cm 2 ). Animal welfare scientists have been critical of battery cages because they do not provide hens with sufficient space to stand, walk, flap their wings, perch, or make a nest, and it is widely considered that hens suffer through boredom and frustration through being unable to perform these behaviours. This can lead to a wide range of abnormal behaviours , some of which are injurious to the hens or their cagemates.In 1999, the European Union Council Directive 1999/74/EC banned conventional battery cages for laying hens throughout the European Union from January 1, 2012; they were banned previously in other countries including Switzerland . In response to these bans, development of prototype commercial furnished cage systems began in the 1980s. Furnished cages, sometimes called 'enriched' or 'modified' cages, are cages for egg-laying hens which have been designed to allow the hens to perform their "natural behaviors" whilst retaining their economic and husbandry advantages, and also provide some of the welfare advantages of non-cage systems. Many design features of furnished cages have been incorporated because research in animal welfare science has shown them to be of benefit to the hens. In the UK, the DEFRA "Code for the Welfare of Laying Hens" states furnished cages should provide at least 750 cm 2 of cage area per hen, 600 cm 2 of which should be usable; the height of the cage other than that above the usable area should be at least 20 cm at every point and no cage should have a total area that is less than 2000 cm 2 . In addition, furnished cages should provide a nest, litter such that pecking and scratching are possible, appropriate perches allowing at least 15 cm per hen, a claw-shortening device, and a feed trough which may be used without restriction providing 12 cm per hen. Furnished cages (Enriched) give the hens more space than the conventional battery cages, so that each bird may spread their wings without touching one another if desired. Enrichment such as nest boxes, perches, and dust baths are also provided so that the birds may carry out their natural behaviors such as nesting, roosting, and scratching as though they were outdoors. Enrichment of laying hen cages ultimately results in better bone quality. This is a result of the increased activity in the hens from the additional space and enrichment provided in the furnished housing system. Although the enriched housing system has its advantages such as reduced aggression towards one another and cleaner eggs, modern egg laying breeds often suffer from osteoporosis which results in the chicken's skeletal system being weakened. During egg production, large amounts of calcium are transferred from bones to create egg-shell. Although dietary calcium levels are adequate, absorption of dietary calcium is not always sufficient, given the intensity of production, to fully replenish bone calcium. This can lead to increases in bone breakages, particularly when the hens are being removed from cages at the end of laying. Osteoporosis may be prevented by free range and cage-free housing systems, as they have shown to have a beneficial impact on the skeletal system of the hens compared to those housed in caged systems. Countries such as Austria, Belgium or Germany are planning to ban furnished cages until 2025 additionally to the already banned conventional cages. Meat chickens, commonly called broilers , are floor-raised on litter such as wood shavings, peanut shells, and rice hulls, indoors in climate-controlled housing. Under modern farming methods, meat chickens reared indoors reach slaughter weight at 5 to 9 weeks of age, as they have been selectively bred to do so. In the first week of a broiler's life, it can grow up to 300 percent of its body size. A nine-week-old broiler averages over 9 pounds (4 kg) in body weight. At nine weeks, a hen will average around 7 pounds (3.2 kg) and a rooster will weigh around 12 pounds (5.5 kg), having a nine-pound (4 kg) average. Broilers are not raised in cages. They are raised in large, open structures known as grow out houses. A farmer receives the birds from the hatchery at one day old. A grow out consists of 5 to 9 weeks according to how big the kill plant wants the chickens to be. These houses are equipped with mechanical systems to deliver feed and water to the birds. They have ventilation systems and heaters that function as needed. The floor of the house is covered with bedding material consisting of wood chips, rice hulls, or peanut shells. In some cases they can be grown over dry litter or compost. Because dry bedding helps maintain flock health, most growout houses have enclosed watering systems ("nipple drinkers") which reduce spillage. Keeping birds inside a house protects them from predators such as hawks and foxes. Some houses are equipped with curtain walls, which can be rolled up in good weather to admit natural light and fresh air. Most growout houses built in recent years feature "tunnel ventilation," in which a bank of fans draws fresh air through the house. Traditionally, a flock of broilers consist of about 20,000 birds in a growout house that measures 400/500 feet long and 40/50 feet wide, thus providing about eight-tenths of a square foot per bird. The Council for Agricultural Science and Technology (CAST) states that the minimum space is one-half square foot per bird. More modern houses are often larger and contain more birds, but the floor space allotment still meets the needs of the birds. The larger the bird is grown the fewer chickens are put in each house, to give the bigger bird more space per square foot. Because broilers are relatively young and have not reached sexual maturity, they exhibit very little aggressive conduct. Chicken feed consists primarily of corn and soybean meal with the addition of essential vitamins and minerals. No hormones or steroids are allowed in raising chickens. In intensive broiler sheds, the air can become highly polluted with ammonia from the droppings. In this case, a farmer must run more fans to bring in more clean fresh air. If not, this can damage the chickens' eyes and respiratory systems and can cause painful burns on their legs (called hock burns ) as well as blisters on their feet. Broilers bred for fast growth have a high rate of developing leg deformities because their large breast muscles cause distortions on their developing legs and pelvis, leading to them often being unable to support their body weight. In cases where the chickens become crippled and can no longer walk, farmers have to go in and pull them out. Because of their difficulty moving, the chickens cannot change their environment to avoid heat, cold, or dirt as they would in natural conditions. The added weight and overcrowding also puts a strain on their hearts and lungs, possibly leading to Ascites . In the UK, up to 19 million broilers die in their sheds from heart failure each year. In a heat wave, if a power failure shuts down the ventilation, 20,000 chickens could die in a short period of time. In a good grow out, a farmer should sell between 92% and 96% of their flock, with a 1.80 to a 2.0 feed conversion ratio . After marketing the birds, the farmer must clean out and prepare for another flock. A farmer should average 4 to 5 grow outs a year. In a "higher welfare" system, chickens are kept indoors but with more space (around 14 to 16 birds per square metre). They have a richer environment for example with natural light or straw bales that encourage foraging and perching. The chickens grow more slowly and live for up to two weeks longer than intensively farmed birds. The benefits of higher welfare indoor systems are the reduced growth rate, less crowding and more opportunities for natural behaviour. One example of indoor production with higher welfare production is the Better Chicken Commitment standard. Free-range broilers are reared under similar conditions to free-range egg-laying hens. The breeds grow more slowly than those used for indoor rearing and usually reach slaughter weight at approximately 8 weeks of age. In the EU, each chicken must have one square metre of outdoor space. The benefits of free-range poultry farming include opportunities for natural behaviours such as pecking, scratching, foraging and exercise outdoors. Because they grow slower and have opportunities for exercise, free-range broilers often have better leg and heart health. Organic broiler chickens are reared under similar conditions to free-range broilers but with restrictions on the routine use of in-feed or in-water medications, other food additives and synthetic amino acids. The breeds used are slower growing, more traditional breeds and typically reach slaughter weight at around 12 weeks of age. They have a larger space allowance outside (at least 2 square metres and sometimes up to 10 square metres per bird). The Soil Association standards indicate a maximum outdoors stocking density of 2,500 birds per hectare and a maximum of 1,000 broilers per poultry house.Meat chickens, commonly called broilers , are floor-raised on litter such as wood shavings, peanut shells, and rice hulls, indoors in climate-controlled housing. Under modern farming methods, meat chickens reared indoors reach slaughter weight at 5 to 9 weeks of age, as they have been selectively bred to do so. In the first week of a broiler's life, it can grow up to 300 percent of its body size. A nine-week-old broiler averages over 9 pounds (4 kg) in body weight. At nine weeks, a hen will average around 7 pounds (3.2 kg) and a rooster will weigh around 12 pounds (5.5 kg), having a nine-pound (4 kg) average. Broilers are not raised in cages. They are raised in large, open structures known as grow out houses. A farmer receives the birds from the hatchery at one day old. A grow out consists of 5 to 9 weeks according to how big the kill plant wants the chickens to be. These houses are equipped with mechanical systems to deliver feed and water to the birds. They have ventilation systems and heaters that function as needed. The floor of the house is covered with bedding material consisting of wood chips, rice hulls, or peanut shells. In some cases they can be grown over dry litter or compost. Because dry bedding helps maintain flock health, most growout houses have enclosed watering systems ("nipple drinkers") which reduce spillage. Keeping birds inside a house protects them from predators such as hawks and foxes. Some houses are equipped with curtain walls, which can be rolled up in good weather to admit natural light and fresh air. Most growout houses built in recent years feature "tunnel ventilation," in which a bank of fans draws fresh air through the house. Traditionally, a flock of broilers consist of about 20,000 birds in a growout house that measures 400/500 feet long and 40/50 feet wide, thus providing about eight-tenths of a square foot per bird. The Council for Agricultural Science and Technology (CAST) states that the minimum space is one-half square foot per bird. More modern houses are often larger and contain more birds, but the floor space allotment still meets the needs of the birds. The larger the bird is grown the fewer chickens are put in each house, to give the bigger bird more space per square foot. Because broilers are relatively young and have not reached sexual maturity, they exhibit very little aggressive conduct. Chicken feed consists primarily of corn and soybean meal with the addition of essential vitamins and minerals. No hormones or steroids are allowed in raising chickens. In intensive broiler sheds, the air can become highly polluted with ammonia from the droppings. In this case, a farmer must run more fans to bring in more clean fresh air. If not, this can damage the chickens' eyes and respiratory systems and can cause painful burns on their legs (called hock burns ) as well as blisters on their feet. Broilers bred for fast growth have a high rate of developing leg deformities because their large breast muscles cause distortions on their developing legs and pelvis, leading to them often being unable to support their body weight. In cases where the chickens become crippled and can no longer walk, farmers have to go in and pull them out. Because of their difficulty moving, the chickens cannot change their environment to avoid heat, cold, or dirt as they would in natural conditions. The added weight and overcrowding also puts a strain on their hearts and lungs, possibly leading to Ascites . In the UK, up to 19 million broilers die in their sheds from heart failure each year. In a heat wave, if a power failure shuts down the ventilation, 20,000 chickens could die in a short period of time. In a good grow out, a farmer should sell between 92% and 96% of their flock, with a 1.80 to a 2.0 feed conversion ratio . After marketing the birds, the farmer must clean out and prepare for another flock. A farmer should average 4 to 5 grow outs a year. In a "higher welfare" system, chickens are kept indoors but with more space (around 14 to 16 birds per square metre). They have a richer environment for example with natural light or straw bales that encourage foraging and perching. The chickens grow more slowly and live for up to two weeks longer than intensively farmed birds. The benefits of higher welfare indoor systems are the reduced growth rate, less crowding and more opportunities for natural behaviour. One example of indoor production with higher welfare production is the Better Chicken Commitment standard. In intensive broiler sheds, the air can become highly polluted with ammonia from the droppings. In this case, a farmer must run more fans to bring in more clean fresh air. If not, this can damage the chickens' eyes and respiratory systems and can cause painful burns on their legs (called hock burns ) as well as blisters on their feet. Broilers bred for fast growth have a high rate of developing leg deformities because their large breast muscles cause distortions on their developing legs and pelvis, leading to them often being unable to support their body weight. In cases where the chickens become crippled and can no longer walk, farmers have to go in and pull them out. Because of their difficulty moving, the chickens cannot change their environment to avoid heat, cold, or dirt as they would in natural conditions. The added weight and overcrowding also puts a strain on their hearts and lungs, possibly leading to Ascites . In the UK, up to 19 million broilers die in their sheds from heart failure each year. In a heat wave, if a power failure shuts down the ventilation, 20,000 chickens could die in a short period of time. In a good grow out, a farmer should sell between 92% and 96% of their flock, with a 1.80 to a 2.0 feed conversion ratio . After marketing the birds, the farmer must clean out and prepare for another flock. A farmer should average 4 to 5 grow outs a year. In a "higher welfare" system, chickens are kept indoors but with more space (around 14 to 16 birds per square metre). They have a richer environment for example with natural light or straw bales that encourage foraging and perching. The chickens grow more slowly and live for up to two weeks longer than intensively farmed birds. The benefits of higher welfare indoor systems are the reduced growth rate, less crowding and more opportunities for natural behaviour. One example of indoor production with higher welfare production is the Better Chicken Commitment standard. Free-range broilers are reared under similar conditions to free-range egg-laying hens. The breeds grow more slowly than those used for indoor rearing and usually reach slaughter weight at approximately 8 weeks of age. In the EU, each chicken must have one square metre of outdoor space. The benefits of free-range poultry farming include opportunities for natural behaviours such as pecking, scratching, foraging and exercise outdoors. Because they grow slower and have opportunities for exercise, free-range broilers often have better leg and heart health. Organic broiler chickens are reared under similar conditions to free-range broilers but with restrictions on the routine use of in-feed or in-water medications, other food additives and synthetic amino acids. The breeds used are slower growing, more traditional breeds and typically reach slaughter weight at around 12 weeks of age. They have a larger space allowance outside (at least 2 square metres and sometimes up to 10 square metres per bird). The Soil Association standards indicate a maximum outdoors stocking density of 2,500 birds per hectare and a maximum of 1,000 broilers per poultry house.Animal welfare groups have frequently criticized the poultry industry for engaging in practices which they assert to be inhumane. Many animal rights advocates object to killing chickens for food, the "factory farm conditions" under which they are raised, methods of transport, and slaughter. Animal Outlook (formerly Compassion Over Killing) and other groups have repeatedly conducted undercover investigations at chicken farms and slaughterhouses which they allege confirm their claims of cruelty. A common practice among hatcheries for egg-laying hens is the culling of newly hatched male chicks since they do not lay eggs and do not grow fast enough to be profitable for meat. There are plans to more ethically destroy the eggs before the chicks are hatched, using "in-ovo" sex determination. Chickens are often stunned before slaughter using carbon dioxide or electric shock in a water bath. More humane methods that could be used are low atmospheric pressure stunning and inert gas asphyxiation . Laying hens are routinely beak-trimmed at 1 day of age to reduce the damaging effects of aggression, feather pecking and cannibalism. Scientific studies have shown that beak trimming is likely to cause both acute and chronic pain. Severe beak trimming, or beak trimming birds at an older age, may cause chronic pain. Following beak trimming of older or adult hens, the nociceptors in the beak stump show abnormal patterns of neural discharge, indicating acute pain. Neuromas , tangled masses of swollen regenerating axon sprouts, are found in the healed stumps of birds beak trimmed at 5 weeks of age or older and in severely beak trimmed birds. Neuromas have been associated with phantom pain in human amputees and have therefore been linked to chronic pain in beak trimmed birds. If beak trimming is severe because of improper procedure or done in older birds, the neuromas will persist which suggests that beak trimmed older birds experience chronic pain , although this has been debated. Beak-trimmed chicks initially peck less than non-trimmed chickens, which animal behavioralist Temple Grandin attributes to guarding against pain. The animal rights activist, Peter Singer , claims this procedure is bad because beaks are sensitive, and the usual practice of trimming them without anaesthesia is considered inhumane by some. Some within the chicken industry claim that beak-trimming is not painful whereas others argue that the procedure causes chronic pain and discomfort, and decreases the ability to eat or drink. Antibiotics have been used in poultry farming in mass quantities since 1951, when the Food and Drug Administration (FDA) approved their use. Scientists had found that chickens fed an antibiotic residue grew 50 percent faster than controls. The chickens laid more eggs and experienced lower mortality and less illness. Upon this discovery, farmers transitioned from expensive animal proteins to comparatively inexpensive antibiotics and B12. Chickens were now reaching their market weight at a much faster rate and at a lower cost. With a growing population and greater demand on the farmers, antibiotics appeared to be an ideal and cost-effective way to increase the output of poultry. Since this discovery, antibiotics have been routinely used in poultry production, but more recently have been the topic of debate secondary to the fear of bacterial antibiotic resistance . Poultry feed can include roxarsone or nitarsone , arsenical antimicrobial drugs that also promote growth. Roxarsone was used as a broiler starter by about 70% of the broiler growers between 1995 and 2000. The drugs have generated controversy because it contains arsenic , which is highly toxic to humans. This arsenic could be transmitted through run-off from the poultry yards. A 2004 study by the U.S. magazine Consumer Reports reported "no detectable arsenic in our samples of muscle" but found "A few of our chicken-liver samples has an amount that according to EPA standards could cause neurological problems in a child who ate 2 ounces of cooked liver per week or in an adult who ate 5.5 ounces per week." The U.S. Food and Drug Administration (FDA), however, is the organization responsible for the regulation of foods in America, and all samples tested were "far less than the... amount allowed in a food product." Hormone use in poultry production is illegal in the United States. Similarly, no chicken meat for sale in Australia is fed hormones. Several scientific studies have documented the fact that chickens grow rapidly because they are bred to do so, not because of growth hormones. According to Consumer Reports , "1.1 million or more Americans [are] sickened each year by undercooked, tainted chicken." A USDA study discovered E. coli (Biotype I) in 99% of supermarket chicken, the result of chicken butchering not being a sterile process. However, the same study also shows that the strain of E. coli found was always a non-lethal form, and no chicken had any of the pathenogenic O157:H7 serotype. Many of these chickens, furthermore, had relatively low levels of contamination. Feces tend to leak from the carcass until the evisceration stage, and the evisceration stage itself gives an opportunity for the interior of the carcass to receive intestinal bacteria. (The skin of the carcass does as well, but the skin presents a better barrier to bacteria and reaches higher temperatures during cooking.) Before 1950, this was contained largely by not eviscerating the carcass at the time of butchering, deferring this until the time of retail sale or in the home. This gave the intestinal bacteria less opportunity to colonize the edible meat. The development of the "ready-to-cook broiler" in the 1950s added convenience while introducing risk, under the assumption that end-to-end refrigeration and thorough cooking would provide adequate protection. E. coli can be killed by proper cooking times, but there is still some risk associated with it, and its near-ubiquity in commercially farmed chicken is troubling to some. Irradiation has been proposed as a means of sterilizing chicken meat after butchering. The aerobic bacteria found in poultry housing can include not only E. coli , but Staphylococcus , Pseudomona , Micrococcus and others as well. These contaminants can contribute to dust that often causes issues with the respiratory systems of both the poultry and humans working in the environment. If bacterial levels in the poultry drinking water reach high levels, it can result in bacterial diarrhoea which can lead to blood poisoning should the bacteria spread from the damaged intestines. Salmonella too can be stressful on poultry production. How it causes disease has been investigated in some detail. There is also a risk that crowded conditions in chicken farms will allow avian influenza (bird flu) to spread quickly. A United Nations press release states: "Governments, local authorities and international agencies need to take a greatly increased role in combating the role of factory-farming, commerce in live poultry, and wildlife markets which provide ideal conditions for the virus to spread and mutate into a more dangerous form..." Several dermatitis conditions are significant in chickens especially gangrenous dermatitis . GD is caused by Clostridium septicum , Clostridium perfringens type A , Clostridium sordellii , Clostridium novyi , Staphylococcus aureus , Staphylococcus xylosus , Staphylococcus epidermidis , Escherichia coli , Pasteurella multocida , Pseudomonas aeruginosa , Enterococcus faecalis , Proteus spp., Bacillus spp., Erysipelothrix rhusiopathiae , and Gallibacterium anatis var. haemolytica . Beemer et al. 1970 finds Rhodotorula mucilaginosa to cause a dermatitis in chickens easily confused with GD. Farming of chickens on an industrial scale relies largely on high protein feeds derived from soybeans ; in the European Union the soybean dominates the protein supply for animal feed, and the poultry industry is the largest consumer of such feed. Two kilograms of grain must be fed to poultry to produce 1 kg of weight gain, much less than that required for pork or beef. However, for every gram of protein consumed, chickens yield only 0.33 g of edible protein. Changes in commodity prices for poultry feed have a direct effect on the cost of doing business in the poultry industry. For instance, a significant rise in the price of corn in the United States can put significant economic pressure on large industrial chicken farming operations. Poultry production requires regular control of excrement, and in many parts of the world, production operations, especially larger operations , need to comply with environmental regulations and protections. Different from mammalian excrement, in poultry (and all birds) urine and feces are excreted as a combined manure, and the result is both wetter and higher in concentrated nitrogen. Waste can be managed wet, dry or by some combination. Wet management is particularly used in battery egg laying operations, where the waste is sluiced out with constantly or occasionally flowing water. Water is also used to clean the floors around nesting sites that are separate from open runs. Dry management particularly refers to dry litter such as sawdust that is removed as needed. Dry can also include open pasture where manure is absorbed by the existing soil and vegetation, but needs to be monitored dillegently so as to not overwhelm the ground capacity and lead to runoff and other pollution problems. Both liquid sluicings and dry litter are used as organic fertilizers , but the wet bulk of liquids manure is harder to ship and is often limited to more local use, while the latter is easier to distribute in bulk and in commercial packaging. Mortality is a daily consideration for poultry farmers, and the carcasses must be disposed of in order to limit the spread of disease and the prevalence of pests. There are a variety of methods of disposal, the most common being burial, composting , incineration , and rendering . Environmental concerns surrounding each of these methods deal with nutrient pollution into the surrounding soil and groundwater – because of these concerns, in many countries and US states the practice of burial in pits is heavily regulated or disallowed. Farmers may construct their own facilities for composting, or purchase equipment to begin incineration or storage for rendering. Composting offers a safe and practical use for the organic material, while proper management of a composting site limits odor and presence of pests. Incineration offers a swifter disposal method, but uses fuel energy and thus brings varying costs. Rendering has the advantage of being handled off site, and the use of freezers can eliminate the spread of pathogens in storage awaiting pickup. Government organizations, like the USDA, may offer financial assistance to farmers looking to begin utilizing environmentally friendly mortality solutions. In North American production the most common predators are: Animal welfare groups have frequently criticized the poultry industry for engaging in practices which they assert to be inhumane. Many animal rights advocates object to killing chickens for food, the "factory farm conditions" under which they are raised, methods of transport, and slaughter. Animal Outlook (formerly Compassion Over Killing) and other groups have repeatedly conducted undercover investigations at chicken farms and slaughterhouses which they allege confirm their claims of cruelty. A common practice among hatcheries for egg-laying hens is the culling of newly hatched male chicks since they do not lay eggs and do not grow fast enough to be profitable for meat. There are plans to more ethically destroy the eggs before the chicks are hatched, using "in-ovo" sex determination. Chickens are often stunned before slaughter using carbon dioxide or electric shock in a water bath. More humane methods that could be used are low atmospheric pressure stunning and inert gas asphyxiation . Laying hens are routinely beak-trimmed at 1 day of age to reduce the damaging effects of aggression, feather pecking and cannibalism. Scientific studies have shown that beak trimming is likely to cause both acute and chronic pain. Severe beak trimming, or beak trimming birds at an older age, may cause chronic pain. Following beak trimming of older or adult hens, the nociceptors in the beak stump show abnormal patterns of neural discharge, indicating acute pain. Neuromas , tangled masses of swollen regenerating axon sprouts, are found in the healed stumps of birds beak trimmed at 5 weeks of age or older and in severely beak trimmed birds. Neuromas have been associated with phantom pain in human amputees and have therefore been linked to chronic pain in beak trimmed birds. If beak trimming is severe because of improper procedure or done in older birds, the neuromas will persist which suggests that beak trimmed older birds experience chronic pain , although this has been debated. Beak-trimmed chicks initially peck less than non-trimmed chickens, which animal behavioralist Temple Grandin attributes to guarding against pain. The animal rights activist, Peter Singer , claims this procedure is bad because beaks are sensitive, and the usual practice of trimming them without anaesthesia is considered inhumane by some. Some within the chicken industry claim that beak-trimming is not painful whereas others argue that the procedure causes chronic pain and discomfort, and decreases the ability to eat or drink. Antibiotics have been used in poultry farming in mass quantities since 1951, when the Food and Drug Administration (FDA) approved their use. Scientists had found that chickens fed an antibiotic residue grew 50 percent faster than controls. The chickens laid more eggs and experienced lower mortality and less illness. Upon this discovery, farmers transitioned from expensive animal proteins to comparatively inexpensive antibiotics and B12. Chickens were now reaching their market weight at a much faster rate and at a lower cost. With a growing population and greater demand on the farmers, antibiotics appeared to be an ideal and cost-effective way to increase the output of poultry. Since this discovery, antibiotics have been routinely used in poultry production, but more recently have been the topic of debate secondary to the fear of bacterial antibiotic resistance . Poultry feed can include roxarsone or nitarsone , arsenical antimicrobial drugs that also promote growth. Roxarsone was used as a broiler starter by about 70% of the broiler growers between 1995 and 2000. The drugs have generated controversy because it contains arsenic , which is highly toxic to humans. This arsenic could be transmitted through run-off from the poultry yards. A 2004 study by the U.S. magazine Consumer Reports reported "no detectable arsenic in our samples of muscle" but found "A few of our chicken-liver samples has an amount that according to EPA standards could cause neurological problems in a child who ate 2 ounces of cooked liver per week or in an adult who ate 5.5 ounces per week." The U.S. Food and Drug Administration (FDA), however, is the organization responsible for the regulation of foods in America, and all samples tested were "far less than the... amount allowed in a food product." Hormone use in poultry production is illegal in the United States. Similarly, no chicken meat for sale in Australia is fed hormones. Several scientific studies have documented the fact that chickens grow rapidly because they are bred to do so, not because of growth hormones. According to Consumer Reports , "1.1 million or more Americans [are] sickened each year by undercooked, tainted chicken." A USDA study discovered E. coli (Biotype I) in 99% of supermarket chicken, the result of chicken butchering not being a sterile process. However, the same study also shows that the strain of E. coli found was always a non-lethal form, and no chicken had any of the pathenogenic O157:H7 serotype. Many of these chickens, furthermore, had relatively low levels of contamination. Feces tend to leak from the carcass until the evisceration stage, and the evisceration stage itself gives an opportunity for the interior of the carcass to receive intestinal bacteria. (The skin of the carcass does as well, but the skin presents a better barrier to bacteria and reaches higher temperatures during cooking.) Before 1950, this was contained largely by not eviscerating the carcass at the time of butchering, deferring this until the time of retail sale or in the home. This gave the intestinal bacteria less opportunity to colonize the edible meat. The development of the "ready-to-cook broiler" in the 1950s added convenience while introducing risk, under the assumption that end-to-end refrigeration and thorough cooking would provide adequate protection. E. coli can be killed by proper cooking times, but there is still some risk associated with it, and its near-ubiquity in commercially farmed chicken is troubling to some. Irradiation has been proposed as a means of sterilizing chicken meat after butchering. The aerobic bacteria found in poultry housing can include not only E. coli , but Staphylococcus , Pseudomona , Micrococcus and others as well. These contaminants can contribute to dust that often causes issues with the respiratory systems of both the poultry and humans working in the environment. If bacterial levels in the poultry drinking water reach high levels, it can result in bacterial diarrhoea which can lead to blood poisoning should the bacteria spread from the damaged intestines. Salmonella too can be stressful on poultry production. How it causes disease has been investigated in some detail. There is also a risk that crowded conditions in chicken farms will allow avian influenza (bird flu) to spread quickly. A United Nations press release states: "Governments, local authorities and international agencies need to take a greatly increased role in combating the role of factory-farming, commerce in live poultry, and wildlife markets which provide ideal conditions for the virus to spread and mutate into a more dangerous form..." Several dermatitis conditions are significant in chickens especially gangrenous dermatitis . GD is caused by Clostridium septicum , Clostridium perfringens type A , Clostridium sordellii , Clostridium novyi , Staphylococcus aureus , Staphylococcus xylosus , Staphylococcus epidermidis , Escherichia coli , Pasteurella multocida , Pseudomonas aeruginosa , Enterococcus faecalis , Proteus spp., Bacillus spp., Erysipelothrix rhusiopathiae , and Gallibacterium anatis var. haemolytica . Beemer et al. 1970 finds Rhodotorula mucilaginosa to cause a dermatitis in chickens easily confused with GD. Farming of chickens on an industrial scale relies largely on high protein feeds derived from soybeans ; in the European Union the soybean dominates the protein supply for animal feed, and the poultry industry is the largest consumer of such feed. Two kilograms of grain must be fed to poultry to produce 1 kg of weight gain, much less than that required for pork or beef. However, for every gram of protein consumed, chickens yield only 0.33 g of edible protein. Changes in commodity prices for poultry feed have a direct effect on the cost of doing business in the poultry industry. For instance, a significant rise in the price of corn in the United States can put significant economic pressure on large industrial chicken farming operations. Poultry production requires regular control of excrement, and in many parts of the world, production operations, especially larger operations , need to comply with environmental regulations and protections. Different from mammalian excrement, in poultry (and all birds) urine and feces are excreted as a combined manure, and the result is both wetter and higher in concentrated nitrogen. Waste can be managed wet, dry or by some combination. Wet management is particularly used in battery egg laying operations, where the waste is sluiced out with constantly or occasionally flowing water. Water is also used to clean the floors around nesting sites that are separate from open runs. Dry management particularly refers to dry litter such as sawdust that is removed as needed. Dry can also include open pasture where manure is absorbed by the existing soil and vegetation, but needs to be monitored dillegently so as to not overwhelm the ground capacity and lead to runoff and other pollution problems. Both liquid sluicings and dry litter are used as organic fertilizers , but the wet bulk of liquids manure is harder to ship and is often limited to more local use, while the latter is easier to distribute in bulk and in commercial packaging.Mortality is a daily consideration for poultry farmers, and the carcasses must be disposed of in order to limit the spread of disease and the prevalence of pests. There are a variety of methods of disposal, the most common being burial, composting , incineration , and rendering . Environmental concerns surrounding each of these methods deal with nutrient pollution into the surrounding soil and groundwater – because of these concerns, in many countries and US states the practice of burial in pits is heavily regulated or disallowed. Farmers may construct their own facilities for composting, or purchase equipment to begin incineration or storage for rendering. Composting offers a safe and practical use for the organic material, while proper management of a composting site limits odor and presence of pests. Incineration offers a swifter disposal method, but uses fuel energy and thus brings varying costs. Rendering has the advantage of being handled off site, and the use of freezers can eliminate the spread of pathogens in storage awaiting pickup. Government organizations, like the USDA, may offer financial assistance to farmers looking to begin utilizing environmentally friendly mortality solutions. In North American production the most common predators are: Poultry workers experience substantially higher rates of illness and injury than manufacturing workers do on average. For 2013, there were an estimated 1.59 cases of occupation-related illness per 100 full-time U.S. meat and poultry workers, compared to 0.36 for manufacturing workers overall. Injuries are associated with repetitive movements, awkward postures, and cold temperatures. High rates of carpal tunnel syndrome and other muscular and skeletal disorders are reported. Disinfectant chemicals and infectious bacteria are causes of respiratory illnesses, allergic reactions, diarrhea , and skin infections. Poultry housing has been shown to have adverse effects on the respiratory health of workers, ranging from a cough to chronic bronchitis . Workers are exposed to concentrated airborne particulate matter (PM) and endotoxins (a harmful waste product of bacteria). In a conventional hen house a conveyor belt beneath the cages removes the manure. In a cage-free aviary system the manure coats the ground, resulting in the build-up of dust and bacteria over time. Eggs are often laid on the ground or under cages in the aviary housing, causing workers to come close to the floor and force dust and bacteria into the air, which they then inhale during egg collection. Oxfam America reports that huge industrialized poultry operations are under such pressure to maximize profits that workers are denied access to toilets . The Food and Agriculture Organization of the United Nations estimated that in 2002 there were nearly sixteen billion chickens in the world. In 2008, the top countries with the highest number of chickens in the world was led by China with the largest at approx 4.6 billion, followed by the US with approx over 2 billion and then followed by Indonesia, Brazil and Mexico. In 2019, China had over 5.14 billion chickens, a higher amount than any other country in the world, followed by Indonesia with approx 3.7 billion chickens. The countries with the next-highest amounts were the US, Brazil, Pakistan, Iran, India, Mexico, Russia and Myanmar respectively. In 1950, the average American consumed 20 pounds (9 kg) of chicken per year, but 92.2 pounds (41.9 kg) in 2017. Additionally, in 1980 most chickens were sold whole, but by 2000 almost 90 percent of chickens were sold after being butchered into parts.

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Avian influenza

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Influenza A virus subtype H7N4

H7N4 is a subtype of the species Influenza A virus (sometimes called bird flu virus). [ citation needed ] A highly pathogenic strain of it caused a minor flu outbreak in 1997 in New South Wales , Australia in chicken . On February 14, 2018, the Hong Kong Centre for Health Protection was notified by the National Health and Family Planning Commission of the People's Republic of China, that a 68-year-old female patient living in Changzhou of Jiangsu Province developed symptoms on Christmas day of 2017. According to the NHFPC, she was admitted to a hospital for medical treatment on the New Year's Day of 2018, and was discharged on January 22. She had had contact with live poultry before the onset of symptoms. No one who she had close contact with had any symptoms during the medical surveillance period.

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