Tuesday 28 October 2014

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hemorrhagic fevers

any of a variety of highly fatal viral diseases that are characterized by massive external or internal bleeding or bleeding into the skin. Other symptoms vary by the type of viral hemorrhagic fever but often include fever, malaise, muscle aches, vomiting, and shock. Most viral hemorrhagic fevers are geographically restricted because they are transmitted by specific animal or insect hosts (reservoirs) that occupy narrow and sometimes localized ecological niches. Viral hemorrhagic fevers are caused by viruses of four families: Flaviviridae, Arenaviridae, Bunyaviridae, and Filoviridae.

The most common viral hemorrhagic fevers are dengue and yellow fever, caused by related mosquitoborne flaviviruses. In the late 18th century, yellow fever epidemics in American coastal cities caused widespread panic, but the disease currently occurs only in developing countries of Africa and South America. It is the only major viral hemorrhagic fever for which an effective preventive vaccine exists and is widely used. Most cases of dengue, seen in tropical areas, are mild and influenza-like, but all four dengue viruses may produce dengue hemorrhagic fever or its severe form, dengue shock syndrome. Unlike yellow fever, which affects the liver and causes severe bleeding, dengue involves the liver only minimally and tends to induce only minor bleeding that is rarely fatal. However, if dengue shock syndrome occurs, patients may die when fluids and electrolytes in their vascular compartments shift into tissues, collapsing the blood volume and precipitating low blood pressure and shock. Dengue is unique among the fatal hemorrhagic fevers in that even severe cases can be effectively treated with simple fluid administration.

The arenaviruses are highly adapted to specific rodent hosts, which may become silently infected and excrete the virus in feces, urine, and saliva. However, when humans come into contact with food or soil contaminated by these rodent excreta, disease may result. The arenaviruses cause the diseases Lassa fever (occurring in Africa), Argentine hemorrhagic fever, Bolivian hemorrhagic fever, Brazilian hemorrhagic fever, and Venezuelan hemorrhagic fever.

Hantaviruses, Rift Valley fever virus (genus phlebovirus), and Crimean-Congo hemorrhagic fever virus (genus nairovirus) belong to the family Bunyaviridae. The hantaviruses, like the arenaviruses, are spread to humans by rodent contact. Hantaviruses cause Korean hemorrhagic fever and hantavirus pulmonary syndrome, which is highly fatal owing to accumulation of fluid in the lungs but features only minor hemorrhagic manifestations. Rift Valley fever, a mosquitoborne disease that is fatal in sheep and cattle, occurs in East and Southern Africa and the Middle East. Most people who contract Rift Valley fever survive, but a minority develop fatal hemorrhagic fevers, encephalitis, or severe eye disease. Crimean-Congo hemorrhagic fever, found in East and Southern Africa, the Middle East, and Russia, is a tickborne disease of cattle and other farm animals that is occasionally transmitted to humans.

The filoviruses, seen in Central and East Africa, include Ebola virus and Marburg virus. These are among the most highly fatal of the hemorrhagic fevers; some strains of Ebola cause death in up to 90 percent of victims. The filoviruses may also cause disease in primates. Marburg virus was discovered when it was transported with imported monkeys to Marburg, Germany, and caused a fatal outbreak. The origin of filovirus epidemics remains unclear; however, the virus has been found in the Old World fruit bat Rousettus aegypticus, which lives in areas throughout sub-Saharan Africa. Scientists suspect that these bats may be responsible for outbreaks of Marburg disease.


David Morens
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ALL YOU NEED TO KNOW ABOUT EBOLA VIRUS

Introduction

hemorrhagic fever

virus of the family Filoviridae that is responsible for a severe and often fatal viral hemorrhagic fever; outbreaks in primates, including gorillas, chimpanzees, and humans, and domestic pigs have been recorded. The disease is characterized by extreme fever, rash, and profuse hemorrhaging. In humans, certain strains of the virus can cause fatality in 50 to 90 percent of cases.


Strains of Ebola

The virus takes its name from the Ebola River in the northern Congo basin of central Africa, where it first emerged in 1976. Ebola is closely related to the Marburg virus, which was discovered in 1967, and the two are the only members of the Filoviridae that cause epidemic human disease. Five strains of Ebola virus, known as Ebola-Zaire, Ebola-Sudan, Ebola-Côte d'Ivoire, Ebola-Reston, and Ebola-Bundibugyo, named for their outbreak locations, have been described.

Ebola-Zaire causes death in 80 to 90 percent of cases, and Ebola-Sudan causes death in 50 percent of cases. Ebola-Côte d'Ivoire, found in dead chimpanzees in the Taï National Park in southwestern Côte d'Ivoire, can infect humans, although only two human cases have been documented, and both individuals survived. Ebola-Reston, which was originally discovered in laboratory monkeys in Reston, Va., in 1989, was also detected in laboratory monkeys in other locations in the United States in 1990 and 1996, as well as in Siena, Italy, in 1992. All the monkeys infected with Ebola-Reston have been traced to one export facility located in the Philippines, although the origin of the strain has not been identified. Similar to Ebola-Côte d'Ivoire, Ebola-Reston does not appear to cause death in humans. The fifth strain, Ebola-Bundibugyo, was discovered in November 2007 in an outbreak in Bundibugyo district, near the border of Uganda and Congo (Kinshasa); it causes death in about 25 percent of cases.


Outbreaks

The first outbreaks in 1976 in Zaire (now Congo [Kinshasa]) and The Sudan resulted in more than 400 deaths. A subsequent outbreak in Congo (Kinshasa) in May 1995 prompted temporary quarantine of the Kikwit region, and more than 250 people died. Later outbreaks in Uganda in 2000 and in Congo (Kinshasa) in 2002 also resulted in several hundred deaths. In September 2007 an outbreak was confirmed in Congo (Kinshasa) in the Kasai-Occidental (West Kasai) province, located in the south-central region of the country. However, while Ebola was detected in blood samples from some people that fell ill, other people were found to be infected with Shigella, the bacterium that causes dysentery—a disease whose symptoms are similar to the early symptoms of Ebola. As a result, although several hundred people became ill and more than 160 people died during the Ebola outbreak, it was unclear how many of the deaths were actually caused by Ebola. Less than two years later, in December 2008, a second outbreak of the disease was confirmed in the Kasai-Occidental province. Ebola had been detected in just four people by early 2009; however, another 42 cases were suspected, and some 200 people were under close observation for infection. Although 13 deaths had been reported in association with the outbreak, samples collected from the victims did not test positive for Ebola.

In 2008, tissue samples from pigs that died of unknown causes in the Philippines were analyzed and found to contain Ebola-Reston virus. This was the first time that the virus was found in a mammalian species other than primates. Infections in pigs were unexpected and raised concerns about transmission of the virus from pigs to humans. In January 2009, antibodies to Ebola-Reston were found in five Filipinos, four of whom worked on pig farms and one of whom worked in a slaughterhouse. All five individuals were believed to have been infected with the virus through direct contact with infected pigs. The infected people were healthy and did not show signs of infection at the time antibodies to the virus were detected. In order to stop the spread of Ebola-Reston among pigs, Philippines officials authorized the slaughter of thousands of potentially infected swine.


Course of infection

Viewed through an electron microscope, the Ebola virus appears as long filaments, sometimes branched or intertwined. The virion (virus particle) contains one molecule of noninfectious, single-stranded RNA (ribonucleic acid). It is not known how the Ebola virus attacks cells; however, it has been postulated that the virus produces proteins that suppress the immune system, allowing reproduction of the virus to continue unhindered. Viral hemorrhagic fevers similar to Ebola typically are carried by arthropods and rodents; however, the natural reservoir for the Ebola virus has yet to be discovered. Among the suspected reservoirs for Ebola are bats, primates, rodents, and insects that inhabit tropical forests in Africa and Asia. Ebola can be transmitted through contact with infected blood, bodily fluids, and possibly respiratory secretions. The virus has also been detected in the organs of patients after recovery from the fever. Unsanitary conditions and lack of adequate medical supplies may be factors in the spread of the disease.

The Ebola virus has an incubation period of 4 to 16 days. The onset is sudden and harsh. Infected persons develop fever, severe headaches and muscle aches, and loss of appetite. Within a few days the virus causes a condition known as disseminated intravascular coagulation, which is marked by both blood clots and hemorrhaging. In the case of Ebola fever, clots are concentrated in the liver, spleen, brain, and other internal organs, forcing capillaries to bleed into surrounding tissue. Nausea, vomiting and diarrhea with blood and mucus, conjunctivitis, and sore throat soon follow. A maculopapular rash (discoloured elevations of the skin) appears on the trunk and quickly spreads to the limbs and head. The patient is then beset by spontaneous bleeding from body orifices and any breaks in the skin, such as injection sites, and within the gastrointestinal tract, skin, and internal organs. Death is usually brought on by hemorrhaging, shock, or renal failure and occurs within 8 to 17 days.


Treatment

There is no known treatment for Ebola fever, although immune plasma may be beneficial. Current therapy consists of maintenance of fluid and electrolyte balance and administration of blood and plasma to control bleeding.

Drugs designed to disrupt Ebola virus replication have been developed and tested in Ebola-infected monkeys. One such therapy was found to protect more than 60 percent of rhesus monkeys infected with Ebola-Zaire when the agent was administered within 30 to 60 minutes following infection. The treatment, which in 2010 was approved for safety trials in humans, was promising for persons who become accidentally infected in laboratory or hospital settings.

The spread of Ebola virus can be contained by barrier nursing, handling of infected blood and tissue in isolated laboratory units, and proper decontamination of reusable equipment.
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