FAQ | Plague | CDC Plague Is a vaccine available to prevent plague? What is plague? Plague is an infectious disease that affects rodents, certain other animals, and humans. It is caused by the Yersinia pestis bacteria. These bacteria are found in many areas of the world, including the United States. How do people become infected with plague? People most commonly acquire plague when they are bitten by a flea that is infected with the plague bacteria. People can also become infected from direct contact with infected tissues or fluids while handling an animal that is sick with or that has died from plague. Finally, people can become infected from inhaling respiratory droplets after close contact with cats and humans with pneumonic plague. What are the different forms of plague? There are three forms of plague: Bubonic plague: Patients develop sudden onset of fever, headache, chills, and weakness and one or more swollen, tender and painful lymph nodes (called buboes). This form is usually the result of an infected flea bite. The bacteria multiply in the lymph node closest to where the bacteria entered the human body. If the patient is not treated with appropriate antibiotics, the bacteria can spread to other parts of the body.

Septicemic plague: Patients develop fever, chills, extreme weakness, abdominal pain, shock, and possibly bleeding into the skin and other organs. Skin and other tissues may turn black and die, especially on fingers, toes, and the nose. Septicemic plague can occur as the first symptoms of plague, or may develop from untreated bubonic plague. This form results from bites of infected fleas or from handling an infected animal. Pneumonic plague: Patients develop fever, headache, weakness, and a rapidly developing pneumonia with shortness of breath, chest pain, cough, and sometimes bloody or watery mucous. Pneumonic plague may develop from inhaling infectious droplets or from untreated bubonic or septicemic plague that spreads to the lungs. The pneumonia may cause respiratory failure and shock. Pneumonic plague is the most serious form of the disease and is the only form of plague that can be spread from person to person (by infectious droplets). Forms of plague. Top of Page What is the basic transmission cycle of plague?

Fleas become infected by feeding on rodents, such as chipmunks, prairie dogs, ground squirrels, mice, and other mammals that are infected with the bacterium Yersinia pestis. Fleas transmit the plague bacteria to humans and other mammals during a subsequent feeding. The plague bacteria survive briefly (a few days) in the blood of rodents and for longer periods in the fleas. An illustration of plague ecology in the United States is available. Top of Page Could one person get plague from another person? Yes, when a person has plague pneumonia they may cough droplets containing the plague bacteria into air. If these bacteria-containing droplets are breathed in by another person they can cause pneumonic plague. Human-to-human transmission is rare and typically requires direct and close contact with the person with pneumonic plague. Top of Page What is the incubation period for plague? A person usually becomes ill with bubonic plague 2 to 6 days after being infected. Someone exposed to Yersinia pestis through the air would become ill within 1 to 3 days. When bubonic plague is left untreated, plague bacteria can invade the bloodstream.

When plague bacteria multiply in the bloodstream, they spread rapidly throughout the body and cause a severe and often fatal condition called septicemic plague. Untreated bubonic plague can also progress into an infection of the lungs, causing pneumonic plague. If plague patients are not given specific antibiotic therapy, all forms of plague can progress rapidly to death. Top of Page How is plague diagnosed? The first step in plague diagnosis is evaluation by a health worker. If the health worker suspects plague, samples of the patient’s blood, sputum, or lymph node aspirate are sent to a laboratory for testing. Once the laboratory receives the sample, preliminary results can be ready in less than two hours. Laboratory confirmation will take longer, usually 24 to 48 hours. Often, presumptive treatment with antibiotics will start as soon as samples are taken, if plague is suspected. Top of Page How many cases of plague occur in the United States? Globally? Plague was first introduced into the United States in 1900. Between 1900 and 2012, 1006 confirmed or probable human plague cases occurred in the United States.

Over 80% of United States plague cases have been the bubonic form. In recent decades, an average of 7 human plague cases are reported each year (range: 1-17 cases per year). Plague has occurred in people of all ages (infants up to age 96), though 50% of cases occur in people ages 12–45. Worldwide, between 1,000 and 2,000 cases each year are reported to the World Health Organization (WHO), though the true number is likely much higher. Top of Page What is the death rate of plague? In the pre-antibiotic era (1900 through 1941), mortality among those infected with plague in the United States was 66%. Antibiotics greatly reduced mortality, and by 1990-2010 overall mortality had decreased to 11%. Plague can still be fatal despite effective antibiotics, though it is lower for bubonic plague cases than for septicemic or pneumonic plague cases. It is hard to assess the mortality rate of plague in developing countries, as relatively few cases are reliably diagnosed and reported to health authorities.

WHO cites mortality rates of 8–10%, however some studies (WHO, 2004) suggest that mortality may be much higher in some plague endemic areas. Top of Page How is plague treated? Plague can be successfully treated with antibiotics. Once a patient is diagnosed with suspected plague they should be hospitalized and, in the case of pneumonic plague, medically isolated. Laboratory tests should be done, including blood cultures for plague bacteria and microscopic examination of lymph node, blood, and sputum samples. Antibiotic treatment should begin as soon as possible after laboratory specimens are taken. To prevent a high risk of death in patients with pneumonic plague, antibiotics should be given as soon as possible, preferably within 24 hours of the first symptoms. Top of Page Is the disease seasonal in its occurrence? Yes. Although cases can occur any time of the year, most cases in the United States are acquired from late spring to early fall. Top of Page Where is plague most common in the United States? Plague occurs in rural and semi-rural areas of the western United States. Plague is most common in the southwestern states, particularly New Mexico, Arizona, and Colorado.

Top of Page Who is at risk for getting plague in the United States? Human plague occurs in areas where the bacteria are present in wild rodent populations. The risks are generally highest in rural and semi-rural areas, including homes that provide food and shelter for various ground squirrels, chipmunks and wood rats, or other areas where you may encounter rodents. Top of Page Is a vaccine available to prevent plague? A plague vaccine is not available. New plague vaccines are in development but are not expected to be commercially available in the immediate future. Plague facts Plague facts Causative agent Plague is an infectious disease of animals and humans caused by Yersinia pestis (alternatively, Yersinia pseudotuberculosis ssp. pestis), a bacterium. Natural distribution Plague exists in nature as a disease of wild rodents, including rats, ground squirrels, and prairie dogs. Carnivores (e.g., dogs, coyotes, raccoons, and skunks) may become infected, but with the exception of cats, they rarely develop clinical signs. Domestic cats appear to be at increased susceptibility and about 50% of those affected will eventually succumb to the disease.

Wild felids are believed to be at similar risk. Natural infection of goats, sheep, and camels has also been reported. Humans may develop bubonic, primary septicemic, or pneumonic plague from the bite of infected fleas; by handling tissues of infected animals, especially rodents and rabbits; by contact with airborne droplets from human patients or household pets (especially cats) with plague pharyngitis or pneumonia; or through careless manipulation of laboratory cultures. Geographically, enzootic plague is associated with semiarid environments. Foci exist on all continents, with the exception of Australia. In North America, plague is found in animals and their associated fleas from the Pacific Coast to the Great Plains, and from southwestern Canada to Mexico. Human cases have developed in New Mexico, Arizona, Colorado, Nevada, and California. Common characteristics of endemic areas include the availability of rodent hosts with a short natural life expectancy and high reproductive potential and vector flea activity throughout the year. Transmission Plague is transmitted primarily by fleas as part of an etiologic agent (Y. pestis)-arthropod vector-vertebrate host cycle with enzootic and epizootic components.

Enzootic (maintenance) rodent hosts (e.g., wood rats) tend to be relatively resistant to the disease, whereas epizootic (amplifying) hosts include those species with low to moderate resistance (e.g., rock squirrels). The most resistant individuals act as hosts for fleas, which in turn infect more susceptible animals. Susceptible animals usually die, but increase the population of infected fleas through their bacteremia. Raptors may assist in the dissemination of plague through transport of infected fleas or prey. Carnivores are effective transporters of infective fleas to other rodent populations and to humans and are most often the direct source of human infection. Infection of carnivores is most likely due to ingestion of plague-infected animals rather than fleabites. Similarly, ingestion appears to be the source of the disease in goats, sheep, and camels. Human-to-human spread from individuals with plague pneumonia has not occurred in the United States since 1924; however, six cases of respiratory tract infection have resulted from exposure to domestic pets with plague pneumonia. Direct contact with infected human or animal blood and tissues is another route of transmission.

Interhuman transmission via human ectoparasites is rare and has been observed only in heavily infested environments. Use of Y. pestis as a biological weapon would most likely involve aerosolization of the bacterial agent. Types and clinical signs of plague in animals and humans Plague primarily affects wild and domestic rodents. Rabbits and hares are sometimes affected. Cats are also very susceptible. Rare cases have developed in goats, sheep, and camels. The source of infection for carnivores, goats, sheep, and camels is most likely contact with or ingestion of infected animals, rather than fleabites. Rodents—In rodents, the disease may take acute, subacute, or resolving forms. In the acute form, rodents develop hemorrhagic buboes (swollen lymph nodes) and splenomegaly, without evidence of other internal lesions, and succumb within 3 to 5 days of infection. Rodents affected by subacute plague develop necrotic buboes and necrotic nodules in the liver, spleen, and lungs, with death 6 or more days after infection. Clinical signs in the acute and subacute forms include nasal bleeding, petechia, abscess formation, and pneumonitis.

The resolving form of plague is characterized by lymphadenopathy with focal purulent necrosis. Cats—Abscesses, lymphadenopathy (especially of the submandibular and cervical lymph nodes), lethargy, and fever are typical signs in cats infected with Y. pestis. Secondary pneumonia may also be present. Pathologic lesions include necrotic nodules in the spleen and liver and evidence of suppurative pneumonia. Mortality is approximately 50% among experimentally infected cats. Dogs—Dogs inoculated orally with Y. pestis react only with fever. All orally infected dogs have developed antibodies and recovered. Most naturally occurring cases of plague in humans result from the bite of a plague-infected flea. Clinical signs usually develop within 2 to 8 days of the insect bite and include sudden onset of headache, fever, chills, and weakness. A bubo (an acutely swollen and painful lymph node) may develop in any regional lymph node site, but most often appears in the axillary, cervical, or inguinal regions, approximately 24 hours after the start of clinical signs. The skin overlying the bubo is frequently reddened, warm, and edematous (bubonic plague).

Some individuals may develop septicemia without a bubo (primary septicemic plague) or septicemia may occur secondary to bubonic plague. Gangrene (hence the name "black death"), coagulopathies, and multiple organ failure may result from advanced plague septicemia. Secondary pneumonic plague develops in about 10 to 15% of patients with bubonic or primary septicemic plague by hematogenous spread of Y. pestis to the lungs. Clinical signs in patients with pneumonic plague include cough, chest pain, bronchopneumonia, and hemoptysis. Primary pneumonic plague caused by inhalation of Y. pestis is rare, but has been reported after handling of cats with pneumonic plague. In addition to respiratory disease, patients with pneumonic plague often show gastrointestinal signs such as nausea, abdominal pain, vomiting, and diarrhea. Other types of plague in humans include plague meningitis and plague pharyngitis. The case fatality rate for untreated bubonic plague in humans is about 50%. Untreated primary septicemic plague and pneumonic plague are invariably fatal. Modern therapy has markedly reduced fatalities from bubonic plague.

Pneumonic and septicemic plague also respond if recognized and treated early. Diagnosis Y. pestis may be identified microscopically by examination of Gram, Wright, Giemsa, or Wayson's stained smears of peripheral blood, sputum, and bubo or cerebrospinal fluids. Finding bipolar-staining, ovoid, Gram-negative organisms permits a rapid presumptive diagnosis of plague. Organisms may also be identified through bacteriologic culture of these same fluids in appropriate media and use of specific phagocytolysis, immunofluorescence, agglutination, phage typing, or PCR tests. A four-fold rise in antibody titer in patient serum is also diagnostic. Prevention Prevention of plague is based on control of rodents and vectors. In areas where natural foci exist, continued surveillance for plague cases and epizootic plague activity is important. Resistant species, such as dogs and coyotes, may be used as sentinels by checking antibody titers. Insecticides should be used to control insect populations, and these should be applied prior to or simultaneously with methods to eradicate rodent reservoir populations. Preventing contact between domestic hosts and wild rodent sources of infection is also important.

Cats and dogs should be kept indoors and food and shelter should be denied to rats or wild rodents around residences and recreational areas. Pets should be regularly defleaed. A US-licensed vaccine was discontinued in 1999 and is no longer available. In other parts of the world killed vaccines and live, attenuated plague vaccines are available. Seven days of postexposure prophylaxis (doxycycline, ciprofloxacin, or chloramphenicol) is recommended for asymptomatic individuals having close (less than 2 meters) contact with plague victims. Treatment Historically, the treatment of choice for bubonic, septicemic, and pneumonic plague has been streptomycin; however, this drug is no longer readily available. Alternatives include gentamicin, doxycycline, ciprofloxacin, and chloramphenicol. Infection control For animals and humans, plague is a reportable disease in the United States. Local and state health departments, federal animal health officials, and the CDC's National Center for Infectious Diseases, Meningitis and Special Pathogens Branch should immediately be notified of any suspected cases.

In addition, diagnostic laboratories should be informed that plague is a possible diagnosis when specimens are submitted, to ensure that safe processing protocols are followed. Patients should be isolated during the first 48 to 72 hours of antibiotic treatment and until clinical improvement occurs. Strict isolation precautions should be followed for patients with pneumonic plague, along with disinfection of clothing, and management of contacts. Available evidence suggests that human-to-human transmission of plague occurs via respiratory droplets; therefore, routine barrier precautions (surgical gowns, gloves, eye protection, and masks) should be followed. Bodies of animal and human patients that have died following infection with Y. pestis should also be handled with care. Contact with remains should be limited to trained personnel, and necropsy or autopsy procedures that are likely to generate aerosols (such as bone sawing) should not be performed. Decontamination Y. pestis is sensitive to sunlight and heat and does not survive for long periods outside a host. A household bleach solution, with a contact time of 30 minutes, may be used effectively for decontamination prior to normal cleaning. Organic material will quickly denature a bleach solution; therefore, if organic material is present, cleaning should precede decontamination.

Use of plague as a biological weapon Plague resulting from aerosolization of Y. pestis is of most concern when considering the use of plague as a biological weapon. The first indication of an attack would most likely be a sudden outbreak of severe pneumonia and sepsis. The presence of hemoptysis in previously healthy patients with fever, cough, shortness of breath, chest pain, and rapid death would suggest the possibility of plague. This information has been prepared as a service by the American Veterinary Medical Association. Redistribution is acceptable, but the document's original content and format must be maintained, and its source must be prominently identified. OTHER AVMA SITES Molecular Clues Hint at What Really Caused the Black Death Molecular Clues Hint at What Really Caused the Black Death By Wynne Parry | September 7, 2011 12:25pm ET MORE The Black Death arrived in London in the fall of 1348, and although the worst passed in less than a year, the disease took a catastrophic toll.

An emergency cemetery in East Smithfield received more than 200 bodies a day between the following February and April, in addition to bodies buried in other graveyards, according to a report from the time. The disease that killed Londoners buried in East Smithfield and at least one of three Europeans within a few years time is commonly believed to be bubonic plague , a bacterial infection marked by painful, feverish, swollen lymph nodes, called buboes. Plague is still with us in many parts of the world, although now antibiotics can halt its course. [ Pictures of A Killer: A Plague Gallery ] But did this disease really cause the Black Death? The story behind this near-apocalypse in 14th century Europe is not clear-cut, since what we know about modern plague in many ways does not match with what we know about the Black Death. And if plague isn't responsible for the Black Death, scientists wonder what could've caused the sweeping massacre and whether that killer is still lurking somewhere.

Now, a new study using bone and teeth taken from East Smithfield adds to mounting evidence exhumed from Black Death graves and tantalizes skeptics with hints at the true nature of the disease that wiped out more than a third of Europeans 650 years ago. This team of researchers approached the topic with open minds when they began looking for genetic evidence of the killer. "Essentially by looking at the literature on the Black Death there were several candidates for what could have been the cause," said Sharon DeWitte, one of the researchers who is now an assistant professor of anthropology at the University of South Carolina. Their first suspect: Yersinia pestis, the bacterium that causes modern plague, including bubonic plague. The speed of plague In 1894, Alexander Yersin and another scientist separately identified Y. pestis during an epidemic in Hong Kong. Years later the bacterium was given his name. Yersin also connected his discovery to the pestilence that swept Europe during the Black Death, an association that has stuck. One problem, however, is that compared to the wildfire-like spread of the Black Death, the modern plague moves more leisurely.

The modern plague pandemic began in the Yunnan Province of China in the mid-19th century, then spread to Hong Kong and then via ship, to India, where it exacted the heaviest toll, and to San Francisco in 1899, among many other places. The disease that caused the Black Death is believed to have traveled much quicker, arriving in Europe from Asia in 1347, after the Golden Horde, a Mongol Army, catapulted plague-infected bodies into a Genoese settlement near the Black Sea. The disease traveled with the Italian traders and later appeared in Sicily, according to Samuel Cohn, a professor of medieval history at the University of Glasglow and author of "The Black Death Transformed: Disease and Culture in the Early Renaissance Europe" (Bloomsbury USA, 2003). By about 1352, roughly five years after arriving in Europe, it had not only spread across the continent, the worst of the disease had already run its course. This wave of devastation becomes particularly surprising considering the complicated and time-consuming process by which plague has been thought to spread.

You can't catch bubonic plague from another person; instead, the process involves two classic villains: rats and fleas. Once a flea bites a rat infected with plague, the pathogen Y. pestis grows in its gut. After about two weeks, the bacteria block the valve that opens into the flea's stomach. The starving flea then bites its host, by now probably a new, healthy rat or a person, more aggressively in an attempt to feed. All the while, the flea tries to clear out the bacterial obstruction and so regurgitates the pathogen onto the bite wounds, according to Ken Gage, chief of flea-borne disease activity with the U.S. Centers for Disease Control and Prevention. The bulk of cases during the modern plague pandemic are believed to have been spread by rats and their fleas, according to Gage. The last rat-borne plague epidemic in the U.S. occurred in 1925; wild rodents have since become the primary source for infections. However, rat-associated outbreaks continue to occur in developing countries, according to the CDC. Fast, furious and unfamiliar Not only has the disease slowed down, it also seems to have become more restrained.

The Black Death wiped out at least 30 percent of Europe's population at the time. But the peak of the modern pandemic, in India, killed less than 2 percent of the population, DeWitte has calculated from census data. The list of discrepancies goes on: There is evidence the Black Death spread directly between humans — no rats and their fleas involved — and to areas where rats and their fleas didn't even live. In fact, archaeological and documentary evidence indicates rats were scarce during the mid-14th century. What's more, bubonic plague doubters point out, deaths during the Black Death appear to have followed a different seasonal cycle than plague deaths in modern times. Some also point to discrepancies in the symptoms. Alternative theories With the plague's role called into question, other theories have been offered to fill the gap. "There is a lot of evidence that suggests that Yersinia pestis may not have been the causative agent for the Black Death, and it was likely something else, and something else that is out there right now," said Brian Bossak, an environmental health scientist at Georgia Southern University.

He is among those who suspect a hemorrhagic virus — which causes bleeding and fever, like ebola — swept through 14th-century Europe. The high lethality, rapid transmission and periodic resurgences seen in the Black Death are characteristic of a virus, according to Bossak, who frames this as a question in urgent need of resolution. "Who knows if it won't happen again," he said. "It seems like every so often some disease comes out of nowhere." Two other proponents of the virus theory, Susan Scott and Christopher Duncan of the University of Liverpool in the United Kingdom, have pointed to a possible genetic legacy left by a viral Black Death: a mutation, known as CCR5-delta32, found among Europeans, particularly those in the north. This mutation confers resistance against HIV , another virus, but does not prevent plague. It's possible that by passing over those with this mutation, the Black Death selected for this change in the genetic code, making it more common among Europeans, they argue. To at least some degree, an alternative form of plague, pneumonic plague , offers a solution.

While bubonic is the most common form of plague, plague can also infect the lungs, causing high fever, cough, bloody sputum and chills. This infection can spread person-to-person, and without antibiotic treatment it is nearly 100 percent fatal. Outbreaks have occurred in modern times, and it can develop as a result of a bubonic infection. But, it is unclear how much of a role it played in the Black Death — some evidence suggests it is not as contagious as commonly thought. Rats and fleas The Black Death just doesn't appear to have behaved the way the typical, modern rat-associated plague does, according to Gage, the flea expert. Even so, he says he is convinced that bubonic plague was responsible. A group of French researchers found another possible insect carrier for the Black Death: lice. They were able to transmit fatal plague infections from sick rabbits to healthy ones via human body lice that fed on the rabbits. Substitute humans for bunnies, and this scenario offers a simpler, more cold-climate-friendly explanation than the conventional rat-flea model. But fleas aren't out of the picture yet.

Gage and his colleagues have found that many species of flea — including the Oriental rat flea, a widespread and important spreader of plague — can begin transmitting the infection much sooner than thought, before the bacterium blocks off its stomach. This supports the idea that a species of human-inhabiting fleas, whose guts the bacterium can't block well, could have spread the infection from person to person in areas without rats, Gage said. [ 10 Deadly Diseases That Hopped Across Species ] Plague isn't picky about its warm-blooded victims; it can infect almost any mammal, although some, like humans, cats and rats, become severely ill when infected, according to Gage. The lack of records of massive rat die-offs during the Black Death also calls into question the role rats may have played then. CSI: Black Death Plague kills quickly and does not leave marks on the remains that archeologists are digging up centuries later. But in recent years scientists have begun searching for the molecular clues in the remains of the dead, including DNA left by the killer bacterium. While a number of studies have turned up positive results from graves believed to hold European plague victims, the results haven't always been clear-cut.

For instance, a 2004 study of remains in five burial sites, including East Smithfield, was unable to find any evidence of the bacteria. Looking for evidence of the genetic traces of a pathogen within 650-year-old bones is a challenging proposition, according to Hendrik Poinar, an evolutionary geneticist at McMaster University who worked with DeWitte, then at the University of Albany, on the most recent study. After so many years in the ground, the DNA is damaged and present only in tiny fragments, and, what's more, each sample contains only a miniscule amount of the pathogen — the rest belongs to the person and interlopers like soil bacteria, fungi, insects, even animals. "You have to come up with a way to pull out the things of interest," Poinar said. So, after screening to detect the presence of Yersinia pestis in the 109 samples from the cemetery in East Smithfield, his lab employed a sort of sensitive fishing technique, using tiny segments of DNA that matched up with segments from a ring of DNA, called a plasmid, found in the bacterium.

Once they had retrieved this DNA, they assembled the full plasmid and compared it with modern versions of the bug. They found this plasmid matched many of the modern versions. They also sequenced a short section of DNA from the bacterium's nucleus and revealed three small changes unseen in the modern strains. The results prove that a variant of Yersinia pestis infected the victims of the Black Death , the authors write in a recent issue of the journal Proceedings of the National Academy of Sciences. Same bug, different disease? This finding comes about a year after another genetic study, led by Stephanie Haensch of Johannes Gutenberg University in Germany, found evidence of two previously unknown strains of Yersinia pestis in the remains of European victims, and hints at a solution that could allow both sides to be right. "People have always assumed the two diseases were the same," said Cohn, the medieval historian, referring to modern plague and the Black Death. "Even if it is the same pathogen, the diseases are very different." Bossak, who has questioned the role of plague in the Black Death, agrees. "This new (study) seems to support these earlier claims, and reinforces the notion that what we know of the epidemiology in modern Y.

pestis plague may not fit the Black Death, perhaps because these ancient strains of Y. pestis are no longer present (assuming Y. pestis was indeed the causative agent)," he wrote in an email. However, Poinar is more cautious. Although they had hoped to find changes that explained why the pathogen might have become less aggressive over the centuries, none have turned up so far. In fact, it's too early to say the changes detected represent any significant difference between the modern and ancient versions of the bacterium, according to him. "We need the entire genome to say anything about this," Poinar wrote in an email, "and that is for future work." You can follow LiveScience writer Wynne Parry on Twitter @Wynne_Parry . Follow LiveScience for the latest in science news and discoveries on Twitter @livescience and on Facebook . Editor's Recommendations Transmission | Plague | CDC Plague ecology in the United States. A downloadable version [PDF - 1 page] is also available. The bacteria that cause plague, Yersinia pestis, maintain their existence in a cycle involving rodents and their fleas.

In urban areas or places with dense rat infestations, the plague bacteria can cycle between rats and their fleas. The last urban outbreak of rat-associated plague in the United States occurred in Los Angeles in 1924-1925. Since that time, plague has occurred in rural and semi-rural areas of the western United States, primarily in semi-arid upland forests and grasslands where many types of rodent species can be involved. Many types of animals, such as rock squirrels, wood rats, ground squirrels, prairie dogs, chipmunks, mice, voles, and rabbits can be affected by plague. Wild carnivores can become infected by eating other infected animals. Scientists think that plague bacteria circulate at low rates within populations of certain rodents without causing excessive rodent die-off. These infected animals and their fleas serve as long-term reservoirs for the bacteria. This is called the enzootic cycle. Occasionally, other species become infected, causing an outbreak among animals, called an epizootic. Humans are usually more at risk during, or shortly after, a plague epizootic.

Scientific studies have suggested that epizootics in the southwestern United States are more likely during cooler summers that follow wet winters. Epizootics are most likely in areas with multiple types of rodents living in high densities and in diverse habitats. Transmission The plague bacteria can be transmitted to humans in the following ways: Flea bites. Plague bacteria are most often transmitted by the bite of an infected flea. During plague epizootics, many rodents die, causing hungry fleas to seek other sources of blood. People and animals that visit places where rodents have recently died from plague are at risk of being infected from flea bites. Dogs and cats may also bring plague-infected fleas into the home. Flea bite exposure may result in primary bubonic plague or septicemic plague. Contact with contaminated fluid or tissue. Humans can become infected when handling tissue or body fluids of a plague-infected animal. For example, a hunter skinning a rabbit or other infected animal without using proper precautions could become infected with plague bacteria. This form of exposure most commonly results in bubonic plague or septicemic plague . Infectious droplets. When a person has plague pneumonia, they may cough droplets containing the plague bacteria into air.

If these bacteria-containing droplets are breathed in by another person they can cause pneumonic plague . Typically this requires direct and close contact with the person with pneumonic plague. Transmission of these droplets is the only way that plague can spread between people. This type of spread has not been documented in the United States since 1924, but still occurs with some frequency in developing countries. Cats are particularly susceptible to plague, and can be infected by eating infected rodents. Sick cats pose a risk of transmitting infectious plague droplets to their owners or to veterinarians. Several cases of human plague have occurred in the United States in recent decades as a result of contact with infected cats. File Formats Help: Rats are exonerated as reservoir hosts for the Black Death - BugBitten BugBitten The black rat, Rattus rattus. Sourse: wiki commons Doctor Schnabel [Dr. Beak], a plague doctor in seventeenth-century Rome. Source: wiki commons The grim reaper, a symbol of the Black Death: wiki commons Most British school children are familiar with the story of the Black Death and subsequent plague epidemics that decimated the population of Europe in the Middle Ages.

It now seems that the villain of the plot, the black rat, may have been wrongly accused of acting as a European reservoir for the plague bacteria and initiating sporadic disease outbreaks for 400 years. Contrary to many people’s understanding, the plague is not a thing of the past. Although it disappeared from Europe in the early 1900s it still persists in many pockets around the world (see map), as witnessed by the current outbreak in Madagascar . Analysis of DNA and immunoprotein samples from the remains of medieval plague victims has confirmed that the Black Death and subsequent plague epidemics were caused by the same bacterium, Yersinia pestis , as modern day outbreaks. Shortly after Alexandre Yersin’s discovery, in the l890s, of the bacillus that caused the European plague pandemics, the accepted medical understanding was that plague was transmitted to humans from fleas infesting black rats; infected fleas thus acting as vectors. When rats began dying of the disease in large numbers infected fleas bit humans as an alternative host and thus infected them. However the role of the black rat has been challenged by several investigators.

For example, Anne Karin Hufthammer made a case against the involvement of black rats in plague epidemics in Scandinavia. She based her challenge on archeological information from bone assemblages that showed that black rats were very rare in medieval Norway, despite regular outbreaks of the plague. Indeed it is likely that the colder climatic conditions across Europe during this period would not have been conducive to the survival of populations of the black rat nor the Oriental rat flea, Xenopsylla cheopsis in most of Europe. The now common brown rat had not arrived in Europe at this time. One of the places where the plague bacterium persists is in the Central Asian Deserts, where the great gerbil, Rhombomys opimus, is the primary host. Gerbils are social animals, living in burrows infested with several parasitic arthropods, including the fleas that act as vectors for the bacterium. Gerbil populations fluctuate and the sylvatic plague bacterium will spread in the population when it exceeds an upper threshold level.

Work published in 2007 by Nils Christian Stenseth and colleagues, who were studying the gerbil populations in Kazakhstan, suggested a co-dependency exists between climatic conditions, vegetation cover, synchronised increase in gerbil densities and plague transmission. Warm, moist conditions promote vegetation growth in these arid areas, giving rise to large gerbil populations and large plague epizootics. As gerbil populations crash, flea populations rise, the plague bacteria spread and infected fleas spill-over onto domestic animals and humans. The latest study from this group has just been published . Here they asked whether climatic fluctuations were also responsible for the waves of plague pandemics that swept Europe after the initial Black Death of 1347-1353. There are, of course, no reliable climatic records from the 13th / 14th century and so Stenseth and his colleagues used tree-ring based data as a climate proxy when looking for a relationship between climate fluctuations and plague outbreaks in medieval Europe. They used historical records of 7,711 plague outbreaks that occurred after the Black Death and data from the analysis of 15 tree-ring based climate proxies taken across Europe and Asia.

Unlike modern Asian outbreaks, no association could be found between plague outbreaks and climatic conditions. Furthermore, there was little evidence that there was a local wildlife reservoir of Y. pestis that could have initiated new outbreaks. To determine this they selected outbreaks that occurred within 500 km of the location where one of the tree-ring samples had been taken and where, within a radius of 1000 km, there had been no previous plague outbreak in the past 2 years that could have been the source of the new outbreak. This analysis suggested that most outbreaks could be attributed to previous outbreaks nearby, as only 24 episodes remained that could only have been initiated by reservoirs of bacteria in the local rodent populations. In addition, 8 of these were historically documented to have been introduced with shipping from plague infested areas. These findings caused then to turn their attention to the possibility that each new wave of disease had a maritime origin. Using the same criteria to select locations, they were able to detect 61 potential maritime introductions that occurred between 1346 and 1856 in 17 harbours around the Mediterranean and the Black Sea coasts. These sea routes linked Europe with the overland routes to Asia.

Historical reports were used to identify 16 potential introductions from Asia. Periods of climatic fluctuations were identified from tree ring analysis at sites on these ancient trade routes to Central Asia. Here populations of long tailed ground squirrels and Altai marmots are the rodent reservoir of plague. Map of the spread of the Black Death: Source, #blackdeathanch They found that a period of approximately 15 years consistently occurred between a climatic fluctuation in the Karakorum mountain range in northern Pakistan and a plague reintroduction in Europe. This suggest a scenario whereby; 1-2 years after a climatic fluctuation, the rodent populations crashed and infected fleas sought alternative hosts. A period of 10-12 years followed when, they hypothesised, the disease travelled West via caravan routes to the sea (the ancient Silk Road). It took a further 2-3 years to spread into Europe via maritime trade routes. Evidence for the spread via the ancient caravan routes requires further investigation but camels are easily infected with plague from the bites of fleas and the bacillus could also have travelled in infected traders, other animals or fleas in their cargo.

It would appear that we may need to rewrite the history books and place the blame for these ancient scourges that changed the face of Europe upon the trade in exotic goods rather than the humble rat.

Question: What insect acts as the transmitting agent in the spread of the infectious disease "Bubonic Plague"?
Answer: FLEA