Lymphocytic Choriomeningitis Virus Infection
Lymphocytic choriomeningitis virus (LCMV) is an “Old World” arenavirus with a wide host range, including rodents and human and nonhuman primates. Its principal natural reservoir host is the wild house mouse (Mus musculus).
Although originating in the Old World, LCMV occurs worldwide, largely due to colonization of M. musculus.Epidemics of LCM have occurred among laboratory personnel exposed either to hamsters shedding virus or to infected cell lines. Pet hamsters are also the recognized source of virus in some human cases. In one outbreak in Europe, there were approximately 200 reported cases of LCM in humans after contact with subclinically infected pet hamsters. It was suggested that there may have been up to 4,000 additional cases of exposure in pet owners after hamsters were distributed to homes nationwide from the supplier of infected animals. In human cases, signs of infection may vary from subclinical infections to influenza-like symptoms. On rare occasions, viral meningitis or encephalomyelitis may occur. One report documented infection of 4 patients receiving solid-organ transplants from a single donor, of which 3 died due to LCMV infections. The source of the infection was traced to a pet store hamster recently purchased by the organ donor. These fatal cases serve to emphasize the increased risk to immunocompromised patients exposed to this virus.
Epizootiology and Pathogenesis
Infection with LCMV may occur by exposure to saliva or urine from animals shedding the virus. Portals of entry include the oronasal route and skin abrasions. Cage-to- cage transmission via aerosols (or transmission through soiled bedding) does not appear to play an important role in spread. Congenital infections also occur in hamsters. Cell cultures or transplantable tumors contaminated with the virus are an important source of the virus in the laboratory. The patterns of disease that occur in hamsters postexposure depend on the age of the animal, strain and dose of the virus, and route of administration.
In 1 study, newborn hamsters were inoculated subcutaneously with LCMV. Approximately half of the recipients cleared the virus, with minimal to moderate lymphocytic infiltration in the viscera. In the remaining inoculated animals, viremia and viruria persisted for approximately 3 and 6 months, respectively. In addition, there was chronic wasting, and lymphocytic infiltration was observed in tissues such as liver, lung, spleen, meninges, and brain. Vasculitis and glomerulitis were present in hamsters examined histologically at 6 or more months postinoculation. Antigen-antibody complexes were demonstrated in arterioles and glomerular basement membranes.Diagnosis
Pathology is varied, and seldom useful for definitive diagnosis. Serology is the recognized method for detecting infection among infected populations. Sera collected from hamsters infected early in life may have a high percentage of samples with anticomplementary activity, but the complement fixation test is generally not used any more. Antigen-antibody complexes may also obscure serologic detection. Hamsters that acquire LCMV infections as adults usually seroconvert early in the infection and remain seropositive for a long period of time. Immunohistochemistry can be used to demonstrate viral antigen during the acute stages of the disease, and PCR is now the method of choice for definitive diagnosis. The Mouse Antibody Production (MAP) test has been shown to be equally or more sensitive than PCR.
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