This SITE includes a variety of viral infections that produce severe systemic syndromes (Table 1). In some cases, these infections are transmitted by arthropod vectors; in others, they are acquired by direct contact with the reservoir animal or its excreta. The illnesses may be hemorrhagic fever (eg, dengue, Marburg, Ebola, or Lassa fevers), generalized fever (yellow fever or Colorado tick fever), or pneumonia (caused by hantavirus infection). Only two of these are endemic in the United States, hantavirus infection and Colorado tick fever. All of these viruses are RNA viruses, and vaccine has been developed for one (yellow fever).
Dengue & Yellow Fever
Marburg & Ebola Virus
Hantaviruses
Colorado Tick Fever
LASSA & OTHER HEMORRHAGIC FEVERS
Lassa fever, with its focus of endemicity in West Africa, is the best known of the arenavirus hemorrhagic fevers. Other agents, such as Junin and Machupo, cause similar syndromes in different geographic areas (Argentina and Bolivia, respectively). Lymphocytic choriomeningitis virus (LCM) is an arenavirus that causes viral meningitis (see site).
Epidemiology
Each arenavirus infects specific rodents; for example, the natural host of Lassa fever virus is a small Nigerian rodent. Chronic infection is common in these animals and leads to chronic viremia and virus shedding in saliva, urine, and feces. Infection of humans is primarily from droppings and may occur by way of aerosols, contamination of food, or fomites. Bites are not a usual mechanism of spread. Persistently infected rodents do not usually exhibit illness. Human-to-human infection occurs with Lassa fever virus through contact with infected secretions or body fluids, but this mode of spread rarely if ever occurs with other arenaviruses. Arenaviruses do not require insects for spread. The incubation period for arenavirus infections averages 10-14 days.
Microbiology
Arenaviruses are pleomorphic, helical, and enveloped, with a size of 50-300 nm. They contain RNA in a linear configuration. Replication is in the cytoplasm, with budding from the host cell cytoplasm.
Pathogenesis
Arenaviruses are able to infect macrophages and possibly cause the release of mediators of cell and vascular damage. In certain laboratory animals the clinical severity of arenavirus disease appears to be directly related to the host’s immunologic response. The greater the immune (especially T lymphocyte) response, the worse the disease. Whether these mechanisms are operative in human infection is not clear. In patients with the hemorrhagic fever, petechiae and visceral hemorrhage occur, as do liver and spleen necrosis, but not vasculitis.
Clinical Findings
Clinical illness is characterized by fever and coagulopathy. Hemorrhage and shock occur and occasionally cardiac and liver damage. Pharyngitis, diarrhea, and vomiting may be very prevalent, especially in patients with Lassa fever. The diagnosis is suggested by recent travel to endemic areas.
Diagnosis
The diagnosis of arenavirus infections is usually made through serologic tests, although the virus can be recovered by inoculation of blood or cerebrospinal fluid into suckling mice or Vero monkey cells. Throat specimens can yield arenaviruses, as can urine. Substantial risk is present for laboratory workers handling body fluids. Therefore, if the diagnosis is suspected, laboratory personnel should be warned and specimens processed only in facilities specialized for the isolation of contagious pathogens.
Treatment
Only supportive therapy for patients with arenavirus infection is currently available. Uncontrolled studies suggest that ribavirin may be useful for those with Lassa fever.
Prognosis. Death occurs in = 50% of those with Lassa fever and in a smaller percentage among those infected with the other arenaviruses.
Prevention & Control
Prevention of these rodent-borne infections rests on control of the vector’s contact with humans. Laboratory-acquired cases can be reduced by processing samples for arenavirus isolation in at least P3 biosafety facilities and not in the usual clinical virology laboratory.
Table 1. Important viral fevers.
Family
Agent
Reservoir/Vector
Disease
Outbreak Locations
Route of Transmission
Mortality (%)
Arenaviridae
Machupo
Lassa
Vesper mouse (R)
Mastomys rodents (R)
Bolivian hemorrhagic fever
Lassa fever
Bolivia
West Africa including hospital workers
Inhalation of dried rodent excreta
Inhalation of dried rodent excreta plus person-to-person (body fluids)
10-20
15-25
Flaviviridae
Yellow fever virus
Dengue (1-4)
Humans, simians (R) Aedes aegypti (V)
Human (R), ?monkeys, Aedes, ticks (V)
Yellow fever
Dengue fever (DF)
Dengue hemorrhagic fever (DHF)
Equatorial Africa, South America
Tropical worldwide
Mosquito bite
Arthropod bite
10
DF = 0; DHF = 15
Bunyaviridae
Phleboviruses:
Rift Valley
Cattle, sheep (R)
Aedes, others (V)
Rift Valley fever
South Africa—sheep
Egypt-Aswan Dam
Mauritania-Senegal R. Dam
Mosquito bite
1
Hantaviruses:
Sin Nombre
Deer mouse (R)
Hantavirus pulmonary syndrome
Southwestern United States
Inhalation of dried rodent excreta
10-50
Nairoviruses:
Congo
Hares, hedgehogs, ticks (V)
Congo-Crimean hemorrhagic fever
Western Russia, Balkans, East Africa
Tick bites plus person-to-person (blood)
20-50
Filoviridae
Marburg
Unknown
Marburg virus disease
Germany, Yugoslavia—lab workers: South Africa; Kenya
Person-to-person (body fluids)
20-25
Ebola
Unknown
Ebola hemorrhagic fever
Sudan
Zaire
Person-to-person (body fluids)
70-90
Reoviridae
Coltvirus
Mammals (squirrels, chipmunks, rabbits, deer); tick (D andersoni)
Colorado tick fever
Western United States and Canada
Tick bite
<1
Virazole