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Miscellaneous Systemic Viral Syndromes

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).

LASSA

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

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