Source:Enders G, Varho-Göbel M, Löhler J, et al. Congenital lymphocytic choriomeningitis virus (LCMV) infection: an underdiagnosed disease.
Ped Inf Dis J.

Enders and colleagues describe 6 children infected in utero with lymphocytic choriomeningitis virus (LCMV). This agent is in the Arenaviridae family and its reservoir is rodents, particularly mice and hamsters. Acquired human infection generally manifests as fever, headache, nausea, myalgia, meningitis, or meningoencephalitis. Fetal infection in the first trimester of pregnancy has been associated with spontaneous abortions, and in the second and third trimesters with intrauterine death, hydrocephalus, and chorioretinitis. This report presents clinical and serologic data from 6 German children (including 1 in utero death and a set of twins) studied between 1991–1997. Abnormalities noted in the 5 live-born children with congenital LCMV infection included hydrocephalus (5), chorioretinitis (4), microcephaly (3), intracranial calcifications (1), and severe developmental delay (4). The fetal death was associated with hydrocephalus and lymphocytic myocarditis. Three of the 6 pregnant women had definite contact with rodents, including one who worked in a pet store that sold mice and hamsters.

These case series demonstrate that LCMV is a cause of congenital infection with features classically associated with congenital toxoplasmosis and cytomegalovirus (CMV) infections. The authors recommend assessing IgG and IgM antibodies to LCMV (and, if feasible, polymerase chain reaction [PCR] for LCMV RNA) in the fetus or neonate with hydrocephalus or chorioretinitis, even though no specific therapy is currently available.

LCMV is an important, often unrecognized human, postnatal and fetal pathogen. Acquired infection, contracted by contact with infected rodents and their excreta, is asymptomatic in approximately one third of individuals; one half of the remainder develop “aseptic meningitis” or meningoencephalitis. A diversity of other clinical sequelae including deafness, myocarditis and parotitis have also been reported.1 

Congenital LCMV infection was first documented in England in 1955 with subsequent reports from Germany, Lithuania, and France. In the United States, recognition of in utero LCMV infection has occurred only within the last decade. Since 1993, there have been 5 reports (with 2 additional in preparation) documenting LCMV infection in American infants with chorioretinitis, hydrocephalus, intracranial calcifications, or micro- or macrocephaly. Mental retardation, seizures, and severe visual impairment have been prominent.2,3 Although differentiation from congenital CMV and rubella infections may be problematic, there have been no reports of cataracts in congenital LCMV, and hearing deficits have been reported only rarely. Congenital toxoplasmosis, however, poses an even greater differential diagnostic challenge. Serologic diagnosis of both congenital and acquired LCMV infections is currently the gold standard, utilizing the sensitive immunofluorescent antibody (IFA) test. Because virus isolation has rarely been documented, the application of PCR to the diagnosis of LCMV infection described in this report opens up exciting new avenues of investigation. The message is clear: public and physician awareness of the potential risks that rodents pose, especially to pregnant women, must be increased.

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