Pediatric Lymphocytic Choriomeningitis Virus

Updated: Jan 12, 2015
  • Author: J Michael Klatte, MD; Chief Editor: Russell W Steele, MD  more...
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Overview

Background

Lymphocytic choriomeningitis virus (LCMV) is a single-stranded RNA virus of the family Arenaviridae. Other members of Arenaviridae include Lassa, Argentine hemorrhagic fever, Bolivian hemorrhagic fever, and Venezuelan hemorrhagic fever viruses. LCMV causes an asymptomatic infection in its rodent reservoir (eg, mice) and has variable effect on hamster health. It is passed to humans when they inhale, consume, or otherwise contact infected excreta. Typically a febrile, self-limited, biphasic disease, LCMV is a significant teratogen, whose role in congenital infections has only recently gained appreciation. [1] Individuals who are exposed to rodents from living conditions or other exposure, such as pet handlers and laboratory personnel, are at particular risk for infection. Transmission of infection during organ transplantation has been documented. [2, 3]

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Pathophysiology

After transmission of LCMV via inhalation, consumption, cutaneous or mucosal exposure, or organ transplantation, a primary viremia ensues, resulting in extra–CNS seeding and an initial, nonspecific, febrile illness. Several days later, secondary viremia follows and frequently results in CNS involvement and typical meningitis/meningoencephalitis.

The manifestations of the disease are thought to result from the host response to the virus as natural killer cells and cytotoxic T cells respond to infection with the production of interferon and additional inflammatory mediators. No human-to-human transmission occurs, except in congenital disease or organ transplantation. Congenital LCMV infection is typically much more serious than the acquired disease. It can mimic toxoplasmosis and cytomegalovirus (CMV) congenital infection. As in acquired infection, congenital disease is thought to result from T-cell and B-cell–mediated injury to the fetal host. LCMV transmitted in utero likely demonstrates selective neurotropism, targeting the developing fetal brain and retina. [4]

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Epidemiology

Frequency

United States

Seroprevalence was found to be 5% among adults at a sexually transmitted disease clinic in Baltimore, Maryland; [5] 5.4% among those older than 30 years in Birmingham, Alabama; [6] and 0.3% among those younger than 30 years in Birmingham, Alabama. [6] Seroprevalence in upstate New York was 0.4%. [7] Disease is more common in the fall and winter months (when rodents seek shelter indoors), and depends on rodent populations. Prevalence of intrauterine infections is unknown.

International

Disease has been reported in North and South America and Europe. Seroprevalence was 4% in Nova Scotia, [8] 1-3.6% in Argentina, [9] and 1.7% in Spain. [10]

Mortality/Morbidity

Less than 1% of patients with acquired infection have fatal disease, usually encephalitis or massive hemorrhage. By contrast, 35% of congenital infections are believed to result in fetal loss, and mortality in transplant-acquired infection is substantial. Most surviving infants (84%) have neurodevelopmental sequelae, including cerebral palsy, seizures, decreased visual acuity, mental retardation, and progressive hydrocephalus. [11]

Race

LCMV has no racial predilection.

Sex

LCMV has no gender predilection.

Age

Disease is most common among young adults, although infection may occur in individuals of any age.

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