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Pathology => Human Diseases => Hemorrhagic Fever
Hemorrhagic Fever
INTRODUCTION
Hemorrhagic Fever, common name for a group of acute viral diseases, the symptoms of which usually begin with fever and muscle aches and progress to dizziness, collapse, swelling, and shock. Depending upon the particular virus, hemorrhagic fevers may progressively produce respiratory problems, internal bleeding, kidney problems, and death. Most hemorrhagic fever viruses have only been recognized within the past 50 years and new hemorrhagic fever viruses are identified each year.
Hemorrhagic fevers are caused by more than 20 known viruses from four different families: Arenaviridae, Bunyaviridae, Flaviviridae, and Filoviridae. The viruses are often named for the region, town, or geographic feature where they were first identified. The Arenaviridae family includes Lassa, Junín (the cause of Argentine hemorrhagic fever), Machupo (the cause of Bolivian hemorrhagic fever), and Guanarito (the cause of Venezuelan hemorrhagic fever) viruses. While these viruses are usually transmitted to humans by rodents, human-to-human transmission can occur, particularly with Lassa fever.
The Bunyaviridae family includes Rift Valley fever virus, a notable mosquito-borne virus in Africa, and the hantaviruses. During the Korean War (1950-1953), thousands of American troops developed mysterious symptoms including high fevers, headaches, internal bleeding, and kidney failure. It was not until 1976 that the viral cause of the disease was identified as Hantaan virus, a hantavirus. The disease is now recognized as one of a group of diseases called hemorrhagic fever with renal syndrome. A related virus, named Sin Nombre, was discovered in the United States in 1993. Sin Nombre was found to cause severe respiratory distress syndrome, which starts with flulike symptoms followed by respiratory failure and often death. The original 1993 outbreak struck New Mexico, Colorado, Arizona, and Utah, killing 58 people. Today, Sin Nombre virus is known to exist in deer mice in more than 30 American states, and similar viruses have been found in South America and Canada.
The Flaviviridae family includes the viruses that cause dengue hemorrhagic fever and yellow fever. These viruses are transmitted by the bites of infected mosquitoes. Dengue hemorrhagic fever occurs mostly in children under the age of ten who live in areas where milder dengue fever is common. Dengue fever resembles the flu with fever, tiredness, and muscle aches from which patients recover in about a week, but dengue hemorrhagic fever is also accompanied by internal hemorrhaging and shock and may cause death. Yellow fever, found mostly in Africa and South America, is spread in urban areas by the bite of the mosquito, Aedes aegypti. In the jungle, yellow fever is carried by various mosquito species and monkeys that live high in the tree canopy, the uppermost layer of spreading branches in the forest.
The Filoviridae family includes Marburg and four strains of Ebola viruses. Ebola hemorrhagic fever was first recognized in Zaire (now the Democratic Republic of the Congo, or DRC) and the Sudan in 1976 where it caused deadly epidemics. The virus reemerged in Kikwit, Zaire, in 1995 and Gabon in 1996, causing additional, frightening epidemics. Persons infected with the Ebola virus experience headache, high fever, muscle pain, vomiting, and internal and external bleeding. The mortality rate of Ebola hemorrhagic fever ranges from 50 to 90 percent.
HOW INFECTION OCCURS
Viruses that cause hemorrhagic fever are zoonotic-they carry out life cycles within multiple animal reservoir hosts (organisms in which viruses normally live but do not harm) and only infect humans incidentally. When these viruses infect humans, they can replicate well and cause severe, even lethal, disease. In some cases other animals, such as birds, monkeys, sheep, goats, and cattle, are also infected incidentally, like humans.
For some viruses, such as the hantaviruses, human exposure occurs by contact with a reservoir host's feces or urine. In the case of Sin Nombre virus, rodent feces containing the virus dry out, turn into dust, become airborne, and are inhaled by humans.
Another means of transmission to humans is by direct contact with infected human blood, urine, feces, or saliva. There is a high risk of infection for health care providers who care for patients suffering from Ebola hemorrhagic fever or Lassa fever. Gloves, gowns, and eye shields are necessary when caring for hemorrhagic fever patients.
Once inside the body, many of the hemorrhagic fever viruses attack white blood cells called macrophages (cells of the immune system that normally protect the body against infection). Macrophages carry these viruses through the bloodstream, distributing them to tissues and organs that are most susceptible to infection.
SYMPTOMS
Once infection occurs, the time it takes symptoms to develop, known as the incubation period, depends upon the virus and its rate of growth in human tissues. For example, humans develop symptoms 3 to 6 days after being bitten by a mosquito carrying yellow fever virus, 5 to 7 days after direct contact exposure to Ebola virus, 10 to 14 days after exposure to dried rodent excretions containing Lassa virus, and 14 to 30 days after exposure to rodent excretions containing Hantaan virus, the cause of hemorrhagic fever with renal syndrome.
In addition to fever and severe muscle pain, persons with hemorrhagic fever often develop bloodshot eyes and redness of the face and upper body. They may experience vomiting, diarrhea, and mild, general edema (swelling caused by accumulation of fluids in tissue spaces). Tiny, pinpoint-sized purple or red spots on the skin, known as petechiae, are also common. As the infection progresses, it often impairs the blood's ability to clot. The walls of the capillaries (smallest blood vessels) may be damaged, permitting blood to escape and causing hemorrhaging (excessive bleeding). The amount of blood circulating through the body is reduced, sometimes producing shock, characterized by pale, cold extremities; a rapid, weak pulse; and falling blood pressure. Arenavirus infections may cause severe encephalopathy (any of various diseases of the brain) with convulsions, deafness, or encephalitis (inflammation or swelling of the brain). Kidney failure and pulmonary edema (accumulation of fluid in the lungs) are characteristics of hantaviral diseases.
TREATMENT AND PREVENTION
There is currently no cure for any of the viral hemorrhagic fevers. Treatment consists of supportive care and prevention and treatment of shock by careful use of intravenous fluids and drugs to combat low blood pressure. Blood dialysis (mechanical process of removing waste products from blood) is used to treat kidney failure in patients with hemorrhagic fever with renal syndrome.
In Argentina, patients infected with Junín virus are treated with plasma containing antibodies from persons who have recovered from the infection. A vaccine is used to prevent Junín virus in people at high risk for infection, such as farm workers. An effective vaccine is available to prevent yellow fever, and dengue vaccines are presently under development. The only effective antiviral drug against a hemorrhagic fever virus is ribavirin, which is used for patients suffering from Lassa fever. Rodent control campaigns have been highly effective in preventing Machupo hemorrhagic fever in Bolivian villages.
Despite all these measures, fatality rates from hemorrhagic fevers range from 1 to 5 percent for Junín infection to as high as 90 percent for Ebola hemorrhagic fever. In 1998 researchers in the United States developed a vaccine that protects monkeys from the Marburg virus. In the future, scientists hope to develop vaccines to protect humans against Marburg, Ebola, and other viruses that cause hemorrhagic fevers.
HEMORRHAGIC FEVER OUTBREAKS
In many cases, the rising incidence of hemorrhagic fever outbreaks may be directly related to human activities. The cutting of rain forests in South America is bringing mosquitoes infected with yellow fever virus down from the treetops to where people live and work. Explosive population growth in Latin America, accompanied by poor sanitation and housing, is increasing the habitat for the reservoir hosts of mosquito-borne viruses. The use of broadleaf herbicides in corn fields in Argentina is leading to the dominance of the grass-loving rodent that carries Junín virus and presents a deadly risk to farm workers. The discovery of diamonds in the West African country of Sierra Leone has led to the development of housing compounds for thousands of immigrant workers and their families. The rodent that carries Lassa virus thrives in this habitat with its new source of food and shelter.
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