A common feature of the arenaviruses is their zoonotic reservoir, particularly small ro-dents, in which they may be sustained for long periods. Primary infection (horizontal transmission) in mature rodents often results in disease and death, whereas intrauterine or perinatal infection (vertical transmission) usually leads to chronic lifelong viremia with persistent shedding of virus into the feces, urine, and respiratory secretions. Although chronically infected rodents are somewhat tolerant to the virus (ie, infection is persistent without causing illness), they produce antibodies, and evidence of deleterious effects can be found in older hosts, usually in the form of immune complex glomerulonephritis. The viruses are perpetuated by vertical transmission from infected mothers to their offspring. When environmental contact becomes close, spread from the rodent reservoir to humans (and, in some instances, subhuman primates) can occur via aerosols; through exposure to infective urine, feces, or tissues; or directly by rodent bites. This is in contrast to the arthropod spread of arboviruses.
The agents of arenavirus hemorrhagic fevers are transmitted from infected rodents to hu-mans in the manner described above, although person-to-person spread by contact with secretions and body fluids also occurs readily. The viruses in this group include the South American hemorrhagic fever agents (Junin virus, the cause of Argentinean hemorrhagic fever, and Machupo virus, the cause of Bolivian hemorrhagic fever) and Lassa virus, the cause of Lassa fever in West Africa.
These viruses have pathogenic and pathologic features similar to those described for the arboviruses that cause hemorrhagic fevers; however, the mechanism involved in the coagulation abnormalities is not understood. All are characterized by fever, usually ac-companied by hemorrhagic manifestations, shock, neurologic disturbances, and bradycar-dia. Lassa fever also frequently causes hepatitis, myocarditis, exudative pharyngitis, and acute deafness. The last deficit may persist after recovery. Mortality is estimated to be 10 to 50% for Lassa fever and 5 to 30% for the others. All are considered highly dangerous in terms of infectivity. Importation of cases to nonendemic areas has occurred, with sig-nificant risk of spread to medical and laboratory personnel.
The diagnosis is suggested primarily by the recent travel history of the patient and the clinical syndromes. Although virus isolation and serologic diagnosis may be performed, these procedures should not be attempted in a hospital diagnostic laboratory. Any patient suspected of having such an infection should be immediately isolated and public health authorities notified. Because of the high risk of spread of infection from body fluids and excreta, even routine laboratory studies are best deferred until the diagnosis and proper disposition of specimens can be resolved. Viremia can persist 1 month, and virus shed-ding in the urine may continue more than 2 months after the onset of illness. Treatment is primarily supportive; however, intravenous ribavirin, if begun within 6 days of illness on-set, has been shown to be helpful in Lassa fever.
Infection with lymphocytic choriomeningitis virus is particularly common in hamsters and mice. In the United States, most human illnesses have been traced to contact with ro-dent breeding colonies in research or pet supply centers and to pet hamsters in the home. The illness usually consists of fever, headache, and myalgia although meningitis or meningoencephalitis also occurs occasionally. Such CNS infections may persist as long as 3 months. There is also evidence that transplacental infection can occur in humans, re-sulting in fetal death, hydrocephalus, or chorioretinitis. No person-to-person transmission of infection has been documented.
The diagnosis is suggested by a history of rodent contact. The virus may be isolated in the early stages of disease by cell culture or intracerebral inoculation of blood or CSF into weanling mice or young guinea pigs. Serologic testing of acute and convalescent sera is usually performed by indirect immunofluorescence.