Viral Hemorrhagic Fever Symptoms and Treatment *Viral hemorrhagic fever facts by Charles Patrick Davis, MD, PhD Viral hemorrhagic fevers are group of illnesses caused by viruses that cause vascular damage that result in symptomatic bleeding (hemorrhage). Hemorrhagic fever viruses are mainly zoonotic diseases caused by viruses that usually reside in an animal or arthropod hosts that may serve as vectors. Viral hemorrhagic fevers are usually seen associated with only one particular of species and consequently are usually contained in geographically restricted areas; however, if the virus is introduced accidentally to humans it becomes widespread (for example, the current Ebola outbreak). Hemorrhagic fever viruses are usually transmitted among animal or arthropod hosts; however, the viruses carried in these animal or arthropods can be transmitted to humans when humans come in contact with the urine, feces, saliva, or other bodily fluids of infected animals or arthropods, including if the animal is killed and eaten. In some instances, once the viruses infect humans, person-to-person transmission can occur when an uninfected person comes in contact with bodily fluids or (with some viruses) a bite by an arthropod vector.

Symptoms of viral hemorrhagic fever include fatigue , fever , weakness , dizziness , and muscle aches ; patients with more severe infections show bleeding under the skin, internal organs, or even from bodily orifices like the mouth, eyes, or ears. Some patients develop severe diarrhea that may also be bloody, and severely ill patients present with shock , delirium , seizures , kidney failure , and coma that often ends in death. Patients with viral hemorrhagic fevers usually receive only supportive therapy; there is no other established cure for viral hemorrhagic fevers. However, ribavirin ( Rebetol , Copegus ) has been effective in treating some individuals with Lassa fever , and treatment with convalescent-phase plasma has been used with success in a few patients -- other experimental antiviral agents have also been tried in a few patients. Prevention and control of hemorrhagic fevers is difficult; except for yellow fever and Argentine hemorrhagic fever, no vaccines have been made commercially available so that prevention efforts are concentrated on avoiding contacts with the host species, vectors, or humans infected with the viruses.

Scientists and researchers are addressing the threat of viral hemorrhagic fevers to humans by attempting to develop immunological, molecular, and containment methods to prevent these hemorrhagic fevers. What are viral hemorrhagic fevers? Share Your Story Viral hemorrhagic fevers (VHFs) refer to a group of illnesses that are caused by several distinct families of viruses. In general, the term "viral hemorrhagic fever" is used to describe a severe multisystem syndrome (multisystem in that multiple organ systems in the body are affected). Characteristically, the overall vascular system is damaged, and the body's ability to regulate itself is impaired. These symptoms are often accompanied by hemorrhage (bleeding); however, the bleeding is itself rarely life-threatening. While some types of hemorrhagic fever viruses can cause relatively mild illnesses, many of these viruses cause severe, life-threatening disease. The Special Pathogens Branch (SPB) primarily works with hemorrhagic fever viruses that are classified as biosafety level four (BSL-4) pathogens. A list of these viruses appears in the SPB disease information index .

The Division of Vector-Borne Infectious Diseases, also in the National Center for Infectious Diseases, works with the non-BSL-4 viruses that cause two other hemorrhagic fevers, dengue hemorrhagic fever and yellow fever. How are hemorrhagic fever viruses grouped? VHFs are caused by viruses of four distinct families: arenaviruses, filoviruses, bunyaviruses, and flaviviruses. Each of these families share a number of features: They are all RNA viruses, and all are covered, or enveloped, in a fatty ( lipid ) coating. Their survival is dependent on an animal or insect host, called the natural reservoir. The viruses are geographically restricted to the areas where their host species live. Humans are not the natural reservoir for any of these viruses. Humans are infected when they come into contact with infected hosts. However, with some viruses, after the accidental transmission from the host, humans can transmit the virus to one another. Human cases or outbreaks of hemorrhagic fevers caused by these viruses occur sporadically and irregularly. The occurrence of outbreaks cannot be easily predicted. With a few noteworthy exceptions, there is no cure or established drug treatment for VHFs.

In rare cases, other viral and bacterial infections can cause a hemorrhagic fever; scrub typhus is a good example. Outbreaks | Viral Special Pathogens Branch (VSPB) | CDC Viral Special Pathogens Branch (VSPB) ShareCompartir Outbreaks This page lists outbreaks for diseases monitored by the Viral Special Pathogens Branch (VSPB) since the year 2000. Detailed outbreak information can be found on the disease site. 2014 2013 Crimean-Congo Hemorrhagic Fever Outbreak in Uganda As of August 29, 2013, the Uganda Ministry of Health reported 5 laboratory-confirmed cases of Crimean-Congo Hemorrhagic Fever, including 3 cases (no deaths) from Agago District and 2 cases (1 death) from Wakiso District. CDC is assisting the Ministry of Health in the epidemiologic and diagnostic aspects of the outbreak. Testing of samples by CDC's Viral Special Pathogens Branch is taking place at the Uganda Virus Research Institute in Entebbe.

For more information, see: 2012 Ebola Hemorrhagic Fever Outbreak in the Luwero District of Uganda As of December 2, 2012, the Ugandan Ministry of Health reported 7 cumulative cases (probable and confirmed) of Ebola virus infection, including 4 deaths, in the Luwero District of central Uganda. CDC is assisting the Ministry of Health in the epidemiologic and diagnostic aspects of the outbreak. Testing of samples by CDC's Viral Special Pathogens Branch is taking place at the Uganda Virus Research Institute in Entebbe. For more information, see: Ebola virus disease Marburg Hemorrhagic Fever Outbreak in Uganda As of November 29, 2012, the Ugandan Ministry of Health reported 15 confirmed and 8 probable cases of Marburg virus infection, including 15 deaths, in the Kabale, Ibanda, Mbarara, and Kampala Districts of Uganda. Testing of samples by CDC's Viral Special Pathogens Branch is ongoing at the Uganda Virus Research Institute in Entebbe. Working with the Ministry's National Task Force, a CDC team is assisting in the diagnostic and epidemiologic aspects of the outbreak.

Note that Kabale District, on the border with neighboring Rwanda, is distinct from Kibaale District, the site of the recently-ended Ebola outbreak; both districts are in Uganda's Western Region. A recent history of Marburg cases and outbreaks in Uganda includes: a fatal case in 2008 of a Dutch tourist who visited the Python Cave, a bat cave in Queen Elizabeth National Park (QENP); a non-fatal case in 2008 of an American tourist who visited the same cave in QENP; and, a 2007 small outbreak of Marburg HF among miners working in the Kitaka lead and gold mine in Kamwenge District. For more information, see: Marburg hemorrhagic fever Ebola Hemorrhagic Fever Outbreak in Democratic Republic of Congo The DRC Ministry of Health has declared an end to the most recent Ebola outbreak in DRC's Province Orientale. The November 26 Press Release reports a final total of 77 cases, including 36 laboratory-confirmed cases, 17 probable and 24 suspect cases, with a total of 36 deaths. CDC assisted the Ministry of Health in the epidemiologic and diagnostic aspects of the investigation.

Laboratory support was provided both through CDC's field laboratory in Isiro, and through the CDC/UVRI lab in Uganda. The Public Health Agency of Canada (PHAC) also provides diagnostic support through its field lab in Isiro. The outbreak in DRC has no epidemiologic link to the near contemporaneous Ebola outbreak in the Kibaale district of Uganda. For more information, see: Ebola virus disease Outbreak of Hantavirus Infection in Yosemite National Park As of November 1, 2012, the National Park Service (NPS) has announced a 10 confirmed cases (including 3 deaths) of hantavirus infection to visitors to Yosemite National Park since June of this year. Nine of the ten individuals with hantavirus infection stayed in Yosemite's Signature Tent Cabins in Curry Village. The tenth person hiked and camped in Tuolumne Meadows and the High Sierra Camps, located about 15 miles from Curry Village.

For more information, see: Hantavirus pulmonary syndrome (HPS) Lymphocytic choriomeningitis virus (LCMV) at a rodent breeding facility in Indiana In late April 2012, CDC was notified about a patient with aseptic meningitis who worked at a rodent breeding facility in Indiana. Testing revealed that the cause of the patient's illness was Lymphocytic choriomeningitis virus (LCMV). Further testing at the rodent breeding facility showed evidence of current or past LCMV infection in 13 out of 52 employees. Of the five employees who sought medical treatment, four were diagnosed with aseptic meningitis. The rodent breeding facility bred and raised mice and rats primarily for sale as frozen feeder animals for reptiles or birds of prey, with regular shipments of live mice. Testing at CDC of frozen mice from the facility indicated evidence of LCMV infection in 20.8 percent of the mice. Rats sampled for testing showed no signs of LCMV infection.

In May 2012, a quarantine prohibiting shipping of mice and rats from the facility was enacted and all live mice at the facility were subsequently depopulated; all frozen product was safely disposed of. Shipping records indicate that live mice were shipped to distributors, pet stores, breeders and individuals in 21 states. The affected states are currently conducting traceout activities to detect any infected mice that were shipped to purchasers before the quarantine. To date, no subsequent human cases of LCMV infection have been reported. People using frozen or live rodents for feeding to other animals should always follow safety precautions, including wearing gloves when handling animal product, and washing hands with soap and water after handling animal products. For more information, see: Information for Pet Owners: Reducing the Risk of Becoming Infected with LCMV from Pet Rodents Ebola Hemorrhagic Fever Outbreak in Uganda On July 28, 2012, the Uganda Ministry of Health reported an outbreak of Ebola Hemorrhagic Fever in the Kibaale District of Uganda. A total of 24 human cases (probable and confirmed only), 17 of which were fatal, have been reported since the beginning of July.

Laboratory tests of blood samples, conducted by the Uganda Virus Research Institute (UVRI) and the U.S. Centers for Disease Control and Prevention (CDC), confirmed Ebola virus in 11 patients, four of whom have died. On October 4, 2012, the Uganda Ministry of Health declared the outbreak ended. For more information, see: Marburg hemorrhagic fever Ebola-Reston Virus Detected in Pigs in Philippines On October 25, 2008, CDC received samples of pig tissues, sera and cell cultures from FADDL, the Foreign Animal Disease Diagnostic Laboratory on Plum Island, NY. The samples, originally collected from pig farms outside Manila, were initially tested at the Plum Island facility, which identified multiple swine pathogens, including Porcine Reproductive and Respiratory Syndrome (PRRS) virus and porcine circovirus type 2. Additional testing by molecular analysis also tentatively identified, for the first time in pigs, Ebola-Reston virus. Further testing of the samples at CDC's Viral Special Pathogens Branch and Infectious Diseases Pathology Branch confirmed the presence of Ebola-Reston virus.

Sequence analysis conducted at FADDL and CDC revealed that the virus is similar to the Ebola-Reston virus that infected macaques from the Philippines imported into the U.S. for research in 1989, 1990 and 1996, and into Italy in 1992. The clinical significance of Ebola-Reston in pigs is unknown, since many of the samples were obtained from pigs with dual PRRSV and Ebola-Reston virus infections. Epidemiologic investigations by Philippine authorities are continuing to look for evidence of human disease associated with infected pigs. Ebola-Reston virus is of unknown pathogenicity in humans. Recent studies of small numbers of Philippine slaughterhouse workers revealed antibodies to Ebola-Reston virus, with no clinical disease.

For more information, see: FAO (UN Food and Agricultural Organization) information on Ebola-Reston virus in pigs, Philippines Hemorrhagic Fever due to Novel Old World Arenavirus, Zambia and South Africa On October 2, 2008, CDC-Zambia notified CDC's Viral Special Pathogens Branch about a cluster of 2 cases of a fatal febrile illness suspected to be a viral hemorrhagic fever, with probable person-to-person transmission. Both patients were medevac'd from Zambia to South Africa and died shortly thereafter. During hospitalization, further transmission occurred in three other hospital workers, two of whom also subsequently died. Further investigation revealed the causative agent to be a novel Old World arenavirus, genetically distinct from other arenaviruses such as Lassa and LCM. The novel arenavirus has been named Lujo virus. CDC's Viral Special Pathogens Branch and Infectious Diseases Pathology Branch worked closely with colleagues in CDC-Zambia, the Viral Special Pathogens Unit, National Institute of Communicable Diseases (NCID) in South Africa, and CDC-South Africa, as well as the respective National Ministries of Health, to provide laboratory and epidemiologic support.

For more information, see: WHO information about new Arenaviridae family virus in South Africa and Zambia Marburg Hemorrhagic Fever, Imported Case - Netherlands ex Uganda, July On July 10, 2008 CDC was notified by the European Centre for Disease Control (ECDC) about a case of Marburg Hemorrhagic Fever in a woman from The Netherlands. The woman had recently returned from traveling in Uganda. On one occasion the woman had contact with a bat in a cave in the Maramagambo forest in Western Uganda (at the southern edge of Queen Elizabeth National Park), and became ill after returning to The Netherlands. Laboratory testing at the Bernhard Nocht Institute in Hamburg, Germany revealed evidence of Marburg virus infection by polymerase chain reaction (PCR). The patient died on Thursday July 11, 2008 in the morning. ECDC is working with health authorities in The Netherlands and the World Health Organization (WHO) to respond to the situation.

For more information, see: Ebola virus disease Ebola Hemorrhagic Fever Outbreak in the Democratic Republic of Congo (DRC) On August 28, 2007, CDC was notified of cases of an unidentified disease in a remote area of Kasai Occidental Province in the Democratic Republic of Congo (DRC). Clinical samples were sent to CDC's Viral Special Pathogens Branch laboratory for testing, as well as to the Centre of International de Recherches Médicales de Franceville (CIRMF) laboratory in Gabon. Results obtained by both Real Time PCR and viral antigen assay were positive for infection with Ebola virus. The presence of other diseases in the same area of the country contributing to the outbreak cannot be ruled out. At the invitation of the DRC Ministry of Health, CDC, WHO, MSF and other collaborators have deployed field investigators to the region. The onset of the latest laboratory-confirmed case was on September 29, 2007. On October 1, 2007, the total of suspected cases was 249 with 183 deaths.

For more information, see: Ebola virus disease Marburg Hemorrhagic Fever Outbreak in Uganda On July 27, 2007, CDC was notified of a suspect case of Marburg Hemorrhagic Fever in Uganda by the Uganda Virus Research Institute (UVRI). A blood specimen taken from the only fatal patient, a miner at a local lead and gold mine, was received by CDC on Friday, July 27, 2007. The specimen tested positive for Marburg virus. A 6-person CDC team consisting of three medical officers, a mammologist, and two microbiologists arrived in Uganda on August 10, traveling to the town of Ibanda in Kamwenge province, near the site of the mine where the exposures are believed to have occurred. WHO, the Ugandan Minsistry of Health, and other collaborators have also deployed personnel. The team has initiated an investigation by capturing bats and other animals at the site of the mine in an effort to further identify the animal host of the Marburg virus, and by tracing human contacts in communities near the mine.

For more information, see: WHO | Ebola virus disease Ebola virus disease Updated January 2016 Key facts Ebola virus disease (EVD), formerly known as Ebola haemorrhagic fever, is a severe, often fatal illness in humans. The virus is transmitted to people from wild animals and spreads in the human population through human-to-human transmission. The average EVD case fatality rate is around 50%. Case fatality rates have varied from 25% to 90% in past outbreaks. The first EVD outbreaks occurred in remote villages in Central Africa, near tropical rainforests, but the most recent outbreak in West Africa has involved major urban as well as rural areas. Community engagement is key to successfully controlling outbreaks. Good outbreak control relies on applying a package of interventions, namely case management, surveillance and contact tracing, a good laboratory service, safe burials and social mobilisation. Early supportive care with rehydration, symptomatic treatment improves survival. There is as yet no licensed treatment proven to neutralise the virus but a range of blood, immunological and drug therapies are under development. There are currently no licensed Ebola vaccines but 2 potential candidates are undergoing evaluation.

Background The Ebola virus causes an acute, serious illness which is often fatal if untreated. Ebola virus disease (EVD) first appeared in 1976 in 2 simultaneous outbreaks, one in what is now, Nzara, South Sudan, and the other in Yambuku, Democratic Republic of Congo. The latter occurred in a village near the Ebola River, from which the disease takes its name. The current outbreak in West Africa, (first cases notified in March 2014), is the largest and most complex Ebola outbreak since the Ebola virus was first discovered in 1976. There have been more cases and deaths in this outbreak than all others combined. It has also spread between countries starting in Guinea then spreading across land borders to Sierra Leone and Liberia, by air (1 traveller) to Nigeria and USA (1 traveller), and by land to Senegal (1 traveller) and Mali (2 travellers). The most severely affected countries, Guinea, Liberia and Sierra Leone, have very weak health systems, lack human and infrastructural resources, and have only recently emerged from long periods of conflict and instability.

On August 8, the WHO Director-General declared the West Africa outbreak a Public Health Emergency of International Concern under the International Health Regulations (2005). The virus family Filoviridae includes three genera: Cuevavirus, Marburgvirus, and Ebolavirus. There are five species that have been identified: Zaire, Bundibugyo, Sudan, Reston and Taï Forest. The first three, Bundibugyo ebolavirus, Zaire ebolavirus, and Sudan ebolavirus have been associated with large outbreaks in Africa. The virus causing the 2014 West African outbreak belongs to the Zaire species. Transmission It is thought that fruit bats of the Pteropodidae family are natural Ebola virus hosts. Ebola is introduced into the human population through close contact with the blood, secretions, organs or other bodily fluids of infected animals such as chimpanzees, gorillas, fruit bats, monkeys, forest antelope and porcupines found ill or dead or in the rainforest.

Ebola then spreads through human-to-human transmission via direct contact (through broken skin or mucous membranes) with the blood, secretions, organs or other bodily fluids of infected people, and with surfaces and materials (e.g. bedding, clothing) contaminated with these fluids. Health-care workers have frequently been infected while treating patients with suspected or confirmed EVD. This has occurred through close contact with patients when infection control precautions are not strictly practiced. Burial ceremonies in which mourners have direct contact with the body of the deceased person can also play a role in the transmission of Ebola. People remain infectious as long as their blood contains the virus. Sexual transmission More surveillance data and research are needed on the risks of sexual transmission, and particularly on the prevalence of viable and transmissible virus in semen over time. In the interim, and based on present evidence, WHO recommends that: All Ebola survivors and their sexual partners should receive counselling to ensure safe sexual practices until their semen has twice tested negative. Survivors should be provided with condoms.

Male Ebola survivors should be offered semen testing at 3 months after onset of disease, and then, for those who test positive, every month thereafter until their semen tests negative for virus twice by RT-PCR, with an interval of one week between tests. Ebola survivors and their sexual partners should either: abstain from all types of sex, or observe safe sex through correct and consistent condom use until their semen has twice tested negative. Having tested negative, survivors can safely resume normal sexual practices without fear of Ebola virus transmission. Based on further analysis of ongoing research and consideration by the WHO Advisory Group on the Ebola Virus Disease Response, WHO recommends that male survivors of Ebola virus disease practice safe sex and hygiene for 12 months from onset of symptoms or until their semen tests negative twice for Ebola virus. Until such time as their semen has twice tested negative for Ebola, survivors should practise good hand and personal hygiene by immediately and thoroughly washing with soap and water after any physical contact with semen, including after masturbation. During this period used condoms should be handled safely, and safely disposed of, so as to prevent contact with seminal fluids. All survivors, their partners and families should be shown respect, dignity and compassion.

For more, read the Guidance on clinical care for survivors of Ebola virus disease Symptoms of Ebola virus disease The incubation period, that is, the time interval from infection with the virus to onset of symptoms is 2 to 21 days. Humans are not infectious until they develop symptoms. First symptoms are the sudden onset of fever fatigue, muscle pain, headache and sore throat. This is followed by vomiting, diarrhoea, rash, symptoms of impaired kidney and liver function, and in some cases, both internal and external bleeding (e.g. oozing from the gums, blood in the stools). Laboratory findings include low white blood cell and platelet counts and elevated liver enzymes. Diagnosis It can be difficult to distinguish EVD from other infectious diseases such as malaria, typhoid fever and meningitis. Confirmation that symptoms are caused by Ebola virus infection are made using the following investigations: antibody-capture enzyme-linked immunosorbent assay (ELISA) antigen-capture detection tests reverse transcriptase polymerase chain reaction (RT-PCR) assay electron microscopy virus isolation by cell culture. Samples from patients are an extreme biohazard risk; laboratory testing on non-inactivated samples should be conducted under maximum biological containment conditions.

Treatment and vaccines Supportive care-rehydration with oral or intravenous fluids- and treatment of specific symptoms, improves survival. There is as yet no proven treatment available for EVD. However, a range of potential treatments including blood products, immune therapies and drug therapies are currently being evaluated. No licensed vaccines are available yet, but 2 potential vaccines are undergoing human safety testing. Prevention and control Good outbreak control relies on applying a package of interventions, namely case management, surveillance and contact tracing, a good laboratory service, safe burials and social mobilisation. Community engagement is key to successfully controlling outbreaks. Raising awareness of risk factors for Ebola infection and protective measures that individuals can take is an effective way to reduce human transmission. Risk reduction messaging should focus on several factors: Reducing the risk of wildlife-to-human transmission from contact with infected fruit bats or monkeys/apes and the consumption of their raw meat. Animals should be handled with gloves and other appropriate protective clothing. Animal products (blood and meat) should be thoroughly cooked before consumption. Reducing the risk of human-to-human transmission from direct or close contact with people with Ebola symptoms, particularly with their bodily fluids. Gloves and appropriate personal protective equipment should be worn when taking care of ill patients at home.

Regular hand washing is required after visiting patients in hospital, as well as after taking care of patients at home. Reducing the risk of possible sexual transmission, based on further analysis of ongoing research and consideration by the WHO Advisory Group on the Ebola Virus Disease Response, WHO recommends that male survivors of Ebola virus disease practice safe sex and hygiene for 12 months from onset of symptoms or until their semen tests negative twice for Ebola virus. Contact with body fluids should be avoided and washing with soap and water is recommended. WHO does not recommend isolation of male or female convalescent patients whose blood has been tested negative for Ebola virus. Outbreak containment measures, including prompt and safe burial of the dead, identifying people who may have been in contact with someone infected with Ebola and monitoring their health for 21 days, the importance of separating the healthy from the sick to prevent further spread, and the importance of good hygiene and maintaining a clean environment. Controlling infection in health-care settings: Health-care workers should always take standard precautions when caring for patients, regardless of their presumed diagnosis. These include basic hand hygiene, respiratory hygiene, use of personal protective equipment (to block splashes or other contact with infected materials), safe injection practices and safe burial practices.

Health-care workers caring for patients with suspected or confirmed Ebola virus should apply extra infection control measures to prevent contact with the patient’s blood and body fluids and contaminated surfaces or materials such as clothing and bedding. When in close contact (within 1 metre) of patients with EBV, health-care workers should wear face protection (a face shield or a medical mask and goggles), a clean, non-sterile long-sleeved gown, and gloves (sterile gloves for some procedures). Laboratory workers are also at risk. Samples taken from humans and animals for investigation of Ebola infection should be handled by trained staff and processed in suitably equipped laboratories. WHO response WHO aims to prevent Ebola outbreaks by maintaining surveillance for Ebola virus disease and supporting at-risk countries to developed preparedness plans. The document provides overall guidance for control of Ebola and Marburg virus outbreaks: When an outbreak is detected WHO responds by supporting surveillance, community engagement, case management, laboratory services, contact tracing, infection control, logistical support and training and assistance with safe burial practices. WHO has developed detailed advice on Ebola infection prevention and control: VHF | CIDRAP Pathogenesis Agents A wide range of viruses can cause viral hemorrhagic fever (VHF) and hence are designated as hemorrhagic fever viruses.

All possess single-stranded RNA (which requires reverse transcriptase for multiplication or amplification by polymerase chain reaction [PCR]) All possess a lipid envelope Hemorrhagic fever viruses belong to four taxonomic families, only one of which, Filoviridae, has been assigned to an order (Mononegavirales): Filoviridae Bunyaviridae Flaviviridae Specific hemorrhagic fever viruses in each of the four families and key characteristics are included in the table below. The table includes the predominant hemorrhagic fever viruses but is not a comprehensive list. For example, a new arenavirus (Lujo virus) was identified in 2008 as a cause of illness in humans in Africa (Peters 2010: Lymphocytic choriomeningitis, Lassa virus, and South American hemorrhagic fevers).

Characteristics of Hemorrhagic Fever Viruses Familya Back to top Pathogenesis The pathogenesis of hemorrhagic fever viruses is not completely understood; however, key points include the following ( Peters 2002 ): Hemorrhagic fever viruses enter the bloodstream through various mechanisms (eg, the bite of a mosquito or tick, inhalation, mucous membrane exposure, parenteral exposure), and all (except hantaviruses) cause disease during the period of viremia. The infectious dose for hemorrhagic fever viruses appears to be low (1 to 10 organisms) ( Franz 1997 ). Endothelial infection occurs with most hemorrhagic fever viruses and may be limited or widespread, depending on the virus. Hemorrhagic manifestations occur as a result of thrombocytopenia or severe platelet dysfunction along with endothelial dysfunction. Increased vascular permeability is common and may result in periorbital edema and hemoconcentration. Vascular dysregulation also often occurs, manifested by flushing of the face and chest. Hemorrhagic fever viruses can cause necrosis and hemorrhage in most organs; however, hepatic involvement often is particularly prominent.

Hantaviruses, New World arenaviruses, and Ebola, Marburg, and Lassa viruses cause cytokine activation ( Gomez 2011 ; Feldmann 2011 ; Peters 2010: Lymphocytic choriomeningitis virus, Lassa virus, and the South American hemorrhagic fevers; Peters 2010: Marburg and Ebola virus hemorrhagic fevers). The relative lack of histologic lesions in fatal cases and the lack of immunopathology suggest that cytokines are the primary mediators of hemorrhagic fever in arenavirus infections and that they play a major role in the clinical features of filovirus infections as well Studies in primates demonstrate that Ebola and Marburg viruses lead to a dysregulation of the immune response, with elevated circulating levels of cytokines and chemokines ( Geisbert 2003 : Pathogenesis of Ebola hemorrhagic fever in primate models; Hensley 2011 ). Ebola, Marburg, yellow fever, and Rift Valley fever viruses have a marked cytopathic effect (ie, are highly destructive to the cells they infect).

Ebola and Lassa viruses also appear to infect monocyte-derived dendritic cells; dendritic cells exposed to these viruses do not up-regulate, fail to secrete pro-inflammatory or immunoregulatory cytokines, and do not effectively stimulate T cells ( Bosio 2003 , Mahanty 2003 ). These changes delay an effective early host response. Ebola, Marburg, Rift Valley fever, and Crimean-Congo hemorrhagic fever viruses can cause disseminated intravascular coagulation (DIC); the other hemorrhagic fever viruses generally do not. Coagulation abnormalities noted with Ebola virus infection appear to be triggered by immune-mediated mechanisms rather than occurring as the result of direct cytolysis of endothelial cells ( Geisbert 2003 : Pathogenesis of Ebola hemorrhagic fever in primate models). Findings from a study in rhesus macaques suggest that a mixed anti-inflammatory response syndrome (MARS) occurs following Ebola virus infection, similar to what is seen in severe sepsis and septic shock ( Ebihara 2011 ).

Suppression of the host antiviral response appears to play a critical role in the pathogenesis of Ebola virus infection (Peters 2010: Marburg and Ebola virus hemorrhagic fevers; Ebihara 2006 ). Failure to mount an effective immune response may be related to an immunosuppressive amino acid sequence in the filovirus glycoprotein or the secretion of a soluble glycoprotein by infected cells (Peters 2010: Marburg and Ebola virus hemorrhagic fevers). In addition, extensive lymphoid necrosis (in the spleen, thymus, and lymph nodes) and lymphocyte depletion through apoptosis also may play a role in suppression of the immune response ( Feldmann 2011 ); however, one report suggests that lymphocyte apoptosis may be not be essential for disease progression ( Bradfute 2010 ).

A model of the pathogenesis of Ebola virus based on observations of infection in cynomolgus monkeys is as follows ( Geisbert 2003 : Pathogenesis of Ebola hemorrhagic fever in cynomolgus macaques): Ebola virus spreads from the initial site of infection via monocytes and dendritic cells to lymph nodes (likely via the lymphatics) and to the liver and spleen (via blood). At these sites, the virus infects tissue macrophages, dendritic cells, and fibroblastic reticular cells. A series of events then occur that lead to virus-induced immunosuppression and apoptosis of T lymphocytes. As the disease progresses, apoptosis of natural killer cells also occurs, which limits the innate immune response. Unchecked viral replication then leads to increased levels of additional proinflammatory cytokines, chemokines, and possibly other mediators, which cause vascular impairment and trigger the coagulation cascade, ultimately leading to DIC. DIC then results in hemorrhagic shock, failure of multiple organs, and death. Characteristic pathologic features of selected hemorrhagic fever viruses are shown in the table below. Pathologic Features of Selected Hemorrhagic Fever Virusesa Agent Abbreviation: DRC, Democratic Republic of the Congo.

Ebola Hemorrhagic Fever Ebola hemorrhagic fever is an important emerging infection in central Africa and has received much attention in recent years owing to the documented high case-fatality rates (50% to 90%) associated with outbreaks. Ebola virus was first recognized in 1976 when two outbreaks of VHF occurred in Africa during that year (one in southern Sudan and one in northwest Zaire [now the Democratic Republic of the Congo]) ( Peters 1999 ; Pourrut 2005 ; WHO 1978: Ebola hemorrhagic fever in Zaire). Since 1976, nearly 20 outbreaks have been recognized in Equatorial Africa ( CDC 201 1: Known cases and outbreaks of Ebola hemorrhagic fever, in chronological order). Furthermore, a geographic pattern has emerged in which the Ebola-Zaire strain affects predominantly central Africa and the Ebola-Sudan strain affects Southern Sudan and East Africa. The only strain identified in West Africa is the Ivory Coast strain, although as of mid-2012, this virus had been detected only on one occasion ( Pourrut 2005 ).

The Ebola-Bundibugyo strain has been found in East Africa (in Uganda) ( McNeil 2010 , Wamala 2010 ). The incidence of filovirus infections (with Ebola virus or Marburg virus) continues to be relatively low. As of 2008, these viruses combined have caused approximately 2,317 clinical cases and 1,671 confirmed deaths ( Leroy 2011 ). In some situations, human Ebola outbreaks have occurred in conjunction with deaths in animals species (including gorillas, chimpanzees, mandrills, and bush pigs) ( Lahm 2007 ; Vogel 2007 ). Characterization of Ebola-Zaire isolates from wild ape carcasses implicated recombinant viruses from the apes as the cause of outbreaks among humans from 2003 through 2005 ( Wittmann 2007 ). During outbreaks in rural settings, multiple introductions of the virus into the human population through wildlife likely occur; whereas, during outbreaks in urban settings, a single introduction of the virus in the community appears to be more common ( Allaranga 2010 ).

A recent large serological survey of rural populations in Gabon, using a sensitive and specific enzyme-linked immunosorbent assay (ELISA), found an overall Immunoglobulin G (IgG) seroprevalence of 15.3% to the Ebola-Zaire strain ( Becquart 2010 , Nkoghe 2011 ). The survey lasted 3 years and included 4,349 adults and 362 children from 220 randomly selected villages, representing 10.7% of all villages in Gabon. These results suggest that a large portion of the population may have been exposed to low levels of the virus through a common source, such as bat saliva on contaminated fruits. The findings also indicate that mild illness or asymptomatic infection may occur with greater frequency than previously suggested and support the perspective that the Ebola-Zaire strain is endemic in Gabon.

In addition to disease occurrence in Africa, several outbreaks of Ebola virus infection have been recognized in cynomolgus macaques in the Philippines or in monkeys imported from the Philippines into the United States or Italy; these situations have all involved the Ebola-Reston strain ( CDC 1990 :Filovirus infections among persons with occupational exposure to nonhuman primates or their tissues; CDC 1990 : Filovirus infection associated with contact with nonhuman primates or their tissues; CDC 1996 : Ebola-Reston virus infection among quarantined nonhuman primates; Miranda 1999 ). The first outbreak occurred in 1989 at a primate facility in Reston, Virginia, which is why the strain associated with these outbreaks is referred to as the Ebola-Reston strain. At that time, animal cases also occurred in primate facilities in Pennsylvania and Texas. All three locations had received monkeys from the same export facility in the Philippines. Subsequently, outbreaks also occurred at the primate facility in the Philippines that exported the infected animals.

Several persons working with infected primates had serologic evidence of recent filovirus infection; however, as of mid-2012, no clinical illnesses associated with this strain have been reported in humans. In 2008, the Ebola-Reston strain was isolated from pigs in the Philippines. At the time, an increase in mortality was occurring on swine farms and samples from pigs that had died demonstrated evidence of infection with porcine reproductive and respiratory syndrome (PRRS) virus. In additions, some pigs had evidence of co-infection with the Reston-Ebola strain ( Miranda 2011 ). Several people in contact with infected pigs had serologic evidence of infection, and all were asymptomatic; these results suggest that pigs can transmit the Ebola-Reston strain to humans. The most likely routes of transmission from pigs to humans include direct contact with the blood, secretions, organs, or other bodily fluids of infected animals and possibly respiratory transmission ( WHO 2009 : WHO expert consultation on Ebola Reston pathogenicity in humans).

Ongoing circulation of the Ebola-Reston strain in the pig population provides an unusual opportunity for continued genetic evolution to occur as a result of passage, adaptation, and possible natural selection of this virus ( WHO 2009 : WHO expert consultation on Ebola Reston pathogenicity in humans). Monitoring the virus in pig populations, therefore, is appropriate. Experimental challenge studies have demonstrated that the Ebola-Reston strain can cause asymptomatic infection in pigs and that viral shedding can occur from the nasopharynx following infection. These findings suggest that infected pigs can pose a transmission risk to farm, veterinary, and abattoir workers ( Marsh 2011 ). In response to the isolation of the Ebola-Reston strain from pigs, another group of investigators challenged domesticated pigs with the Ebola-Zaire strain. They found that pigs also can be infected with the Ebola-Zaire strain and that infected pigs develop severe respiratory disease ( Kobinger 2011 ). Furthermore, infected pigs shed virus from the nasopharynx for approximately 14 days after infection and can transmit the virus to uninfected pigs.

Ebola hemorrhagic fever cases and outbreaks identified between 1976 and mid-2012 are outlined in the table below, which can be found on the Centers for Disease Control and Prevention (CDC) Web site (CDC 2011: Known cases and outbreaks of Ebola hemorrhagic fever, in chronological order). Recognized Cases and Outbreaks of Ebola Hemorrhagic Fever, In Chronological Ordera Year(s) Abbreviation: CFR, case-fatality rate; DRC: Democratic Republic of the Congo. a CDC 201 1: Known cases and outbreaks of Ebola hemorrhagic fever, in chronological order. Marburg Hemorrhagic Fever Marburg hemorrhagic fever, like Ebola hemorrhagic fever, is an emerging disease in sub-Saharan Africa, although Marburg virus infection appears to be less common and case-fatality rates may be somewhat lower than those for Ebola virus infection. Marburg virus was first recognized in 1967 when outbreaks occurred simultaneously in laboratory workers in Marburg, Germany; Frankfort, Germany; and Belgrade, Yugoslavia (now Serbia). These outbreaks were related to contact with African green monkeys that were imported from Uganda.

The incidence of filovirus infections (with Ebola virus or Marburg virus) continues to be relatively low. As of 2008, these viruses combined have caused approximately 2,317 clinical cases and 1,671 confirmed deaths ( Leroy 2011 ). Since the initial outbreaks, several additional cases and outbreaks have been reported; all have occurred among persons living or traveling in rural southern and eastern Africa; recognized cases and outbreaks are shown in the table below ( CDC 2009 : Known cases and outbreaks of Marburg hemorrhagic fever, in chronological order). Recognized Outbreaks of Marburg Hemorrhagic Fever, in Chronological Ordera Location CBRNE - Viral Hemorrhagic Fevers: Background, Pathophysiology, Epidemiology Overview Background Viral hemorrhagic fevers (VHFs) are a group of febrile illnesses caused by RNA viruses from several viral families. These highly infectious viruses lead to a potentially lethal disease syndrome characterized by fever, malaise, vomiting, mucosal and gastrointestinal (GI) bleeding, edema, and hypotension.

The four viral families known to cause VHF disease in humans include the Arenaviridae , Bunyaviridae, Filoviridae, and Flaviviridae. General characteristics of these viral families can be found in the table below. The image below depicts palatal petechiae and hemorrhage in a patient with Ebola hemorrhagic fever. Filovirus disease - Ebola fever. Patient with Ebola hemorrhagic fever during 1976 outbreak in Zaire demonstrating palatal petechiae and hemorrhage. Photo courtesy of Joel Breman. References Simpson SQ, Spikes L, Patel S, Faruqi I. Hantavirus pulmonary syndrome. Infect Dis Clin North Am. 2010 Mar. 24(1):159-73. [Medline] . Normile D. Emerging infectious diseases. Scientists puzzle over Ebola-Reston virus in pigs. Science. 2009 Jan 23. 323(5913):451. [Medline] . Towner JS, Sealy TK, Khristova ML, et al. Newly discovered ebola virus associated with hemorrhagic fever outbreak in Uganda. PLoS Pathog.

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Feldmann H, Jones SM, Daddario-DiCaprio KM, et al. Effective post-exposure treatment of Ebola infection. PLoS Pathog. 2007 Jan. 3(1):e2. [Medline] . [Full Text] . Sarwar UN, Sitar S, Ledgerwood JE. Filovirus emergence and vaccine development: A perspective for health care practitioners in travel medicine. Travel Med Infect Dis. 2010 Jun 26. [Medline] . Tuffs A. Experimental vaccine may have saved Hamburg scientist from Ebola fever. BMJ. 2009 Mar 23. 338:b1223. [Medline] . Blaney JE, Wirblich C, Papaneri AB, et al. Inactivated or live-attenuated bivalent vaccines that confer protection against rabies and Ebola viruses. J Virol. 2011 Oct. 85(20):10605-16. [Medline] . [Full Text] . Bausch DG, Hadi CM, Khan SH, Lertora JJ.

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Vesicular stomatitis virus-based vaccines protect nonhuman primates against aerosol challenge with Ebola and Marburg viruses. Vaccine. 2008 Dec 9. 26(52):6894-900. [Medline] . Geisbert TW, Hensley LE. Ebola virus: new insights into disease aetiopathology and possible therapeutic interventions. Expert Rev Mol Med. 2004 Sep 21. 6(20):1-24. [Medline] . Geisbert TW, Jahrling PB. Towards a vaccine against Ebola virus. Expert Rev Vaccines. 2003 Dec. 2(6):777-89. [Medline] . Hartman AL, Towner JS, Nichol ST. Ebola and marburg hemorrhagic fever. Clin Lab Med. 2010 Mar. 30(1):161-77. [Medline] . Holmes GP, McCormick JB, Trock SC, et al. Lassa fever in the United States. Investigation of a case and new guidelines for management. N Engl J Med. 1990.

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78(8):4330-41. [Medline] . Media Gallery Ebola virus. Electron micrograph courtesy of the Centers for Disease Control and Prevention. Marburg virus. Negative stain image courtesy of the Centers for Disease Control and Prevention. Mastomys rodent, natural host of Lassa virus. Image courtesy of the Centers for Disease Control and Prevention. Bunyavirus infection. Ecchymoses encompassing left upper extremity one week after onset of CCHF. Ecchymoses often are accompanied by hemorrhage in other locations: epistaxis, puncture sites, hematemesis, melena, and hematuria. Image provided by Robert Swaneopoel, PhD, DTVM, MRCVS, National Institute of Virology, Sandringham, South Africa. Apodemus agrarius, the vector of Korean hemorrhagic fever caused by a hantavirus. Photo courtesy of David McClain, MD. Bunyavirus infection - Hantaan virus. Patient with Korean hemorrhagic fever caused by Hantaan virus demonstrating typical 'sunburn flush' of cheeks, chin, and base of neck. Photo courtesy of John Huggins, PhD. Bunyavirus infection.

A patient with Korean hemorrhagic fever demonstrating conjunctival hemorrhages, facial petechiae, and "sunburn flush" of the cheeks. Photo courtesy of John Huggins, PhD. Filovirus disease - Ebola fever. Patient with Ebola hemorrhagic fever during 1976 outbreak in Zaire demonstrating palatal petechiae and hemorrhage. Photo courtesy of Joel Breman. Patient with morbilliform exanthem of dengue fever. Note islands of sparing characteristics for dengue. Photo courtesy Duane Gubler, PhD. Patient with dengue hemorrhagic fever complicated by ecchymoses. Photo courtesy of Duane Gubler, PhD. Dengue Virus Notice posted outside Maracanã Stadium, Rio de Janeiro, Brazil, 2012. Translation: This site is a strategic point for controlling Dengue. Mastomys natalensis, natural host of Lassa virus. Photo courtesy of BioMed Central, originally published in Kelly JD, Barrie MB, Ross RA, Temple BA, Moses LM, Bausch DG. Housing equityfor health equity: a rights-based approach to the control of Lassa fever inpost-war Sierra Leone. BMC Int Health Hum Rights.

2013 Jan 2;13:2. of 12 Haemorrhagic Diseases - London Vaccination Clinic Haemorrhagic Diseases Healthy Travel Resources David Channon About haemorrhagic fevers All viral haemorrhagic fevers, also called VHFs, are caused by a handful of virus families. The illnesses they cause can be spectacularly nasty, including Ebola , Marburg , Lassa fever and yellow fever . What do they all have in common? They all affect multiple organs, damage blood vessels and throw the body’s ability to regulate itself into chaos. Some of the diseases caused are mild, like the Scandinavian nephropathia epidemica. Others, like Ebola, are deadly more often than not. You can catch VHFs anywhere in the world, but they’re most often found where the animals that carry them live. Lassa fever, for example, is only found in rural West Africa, carried by local rats and mice. As an ordinary traveller, the risk is relatively low. But it makes a great deal of sense to avoid areas where there have been outbreaks, especially important when there are no drugs to treat VHFs. All doctors can do is treat the symptoms.

All VHF illnesses come with a fever, as the name implies, and most also come with bleeding disorders. They can all result in shock and many kill. Five kinds of RNA viruses are responsible As far as we know so far, all VHFs come from one of five families of RNA virus. Lassa fever comes from the Arenaviridae family of viruses, as does Lujo, Machupo, Sabiá and Guanarito The Bunyaviridae virus family is responsible for diseases like HFRS, Crimean-Congo haemorrhagic fever and Rift Valley fever The Filoviridae virus family includes the horrific Ebola and Marburg Flaviviridae viruses lead to dengue, yellow fever and two tick-borne encephalitis illnesses: Omsk haemorrhagic fever and Kyasanur Forest disease A newly-discovered Rhabdoviridae virus is probably responsible for two fatal cases of haemorrhagic fever in the Democratic Republic of Congo , proving that we still have a lot to learn about VHFs, where they come from, how they’re carried and how they spread What are the symptoms of haemorrhagic diseases?

Fever Increased, uncontrollable, unexplained and unusual bleeding A flushed, red face and chest Little red or purple spots on the skin Unexplained bruising Muscle pain, headache, vomiting and diarrhoea Haemorrhagic disease diagnosis Because many of the signs and symptoms can easily be mistaken for other diseases, especially in the early stages, a definitive diagnosis is usually only possible through samples diagnosed at a special lab. In general there are fewer white blood cells in infected people, fewer blood platelets, more blood serum liver enzymes and problems with blood clotting. VHF prevention – how to stay safe from viral haemorrhagic fever If you’re a regular traveller or holidaymaker, the best way to stay safe from VHFs is to stay away from affected areas altogether. If you work in healthcare or you’re a voluntary worker, it isn’t always that simple. If that’s you, here are some facts to bear in mind: With the exception of Yellow fever, there’s no vaccine for VHFs. Medics can only treat the symptoms, not the cause If you’re an aid worker or healthcare volunteer in an affected area, there are strict VHF isolation guidelines to follow.

Everyone except those with dengue should be isolated Good hand hygiene, goggles, face shields, doubled-layer gloves, gowns, covers for your shoes and legs are all vital when there’s an outbreak and you’re working with patients VHFs can easily spread in hospitals, especially Lassa, CCHF, Ebola and Marburg. If they’re around you’ll need a proven HEPA filter respirator, air-purifying respirator or a positive pressure supplied air respirator if you come within six feet of a patient Isolation and special decontamination procedures should be in place

Question: Which virus is responsible for causing the spectacularly fatal haemorrhagic fever?
Answer: Ebola Virus