Pediatric Lymphocytic Choriomeningitis Virus

Updated: Aug 24, 2023
  • Author: J Michael Klatte, MD; Chief Editor: Russell W Steele, MD  more...
  • Print

Practice Essentials

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, 4]



Exposure to the virus in feces, urine, semen, saliva, rodent blood, or transplanted organs may result in human infection. [5] Those with occupational exposure to mice are at risk for infection. [6]

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. [7] 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. [8]



United States statistics

Seroprevalence was found to be 5% among adults at a sexually transmitted disease clinic in Baltimore, Maryland [9] ; 5.4% among those older than 30 years in Birmingham, Alabama [10] ; and 0.3% among those younger than 30 years in Birmingham, Alabama. [10] Seroprevalence in upstate New York was 0.4%. [11] 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 statistics

Disease has been reported in North and South America and Europe. Seroprevalence was 4% in Nova Scotia, [12] 1-3.6% in Argentina, [13] and 1.7% in Spain. [14]  Infections have also been reported in Australia and Japan. [15]

Race-, sex-, and age-related demographics


LCMV has no racial predilection.


LCMV has no gender predilection.


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



Prognosis is excellent for recovery in almost all cases (except congenital or transplant-associated cases). However, patients may have a period of fatigue, dizziness, and headache that lasts weeks to months following acute disease. [16]


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. [17]

Vertical transmission of LCMV during pregnancy has been associated with increased risk for spontaneous abortion and severe birth defects, which can result in fetal death. It also can cause a syndrome of hydrocephalus, chorioretinitis, and perivascular calcifications similar to that seen in congenital CMV infection and toxoplasmosis, potentially leading to mental retardation, microcephaly, seizures, and blindness. [18]


Congenital infection is a significant complication of the disease in pregnant women. For example, LCMV is likely an underrecognized cause of nonimmune hydrops. [8]

CNS manifestations of the disease may include encephalitis, Guillain-Barré syndrome, transverse myelitis, paralysis, seizures, and hydrocephalus. [19]

Rare complications of acquired infection include deafness, parotitis, myocarditis, and pneumonitis.


Patient Education

Pregnant women should be warned about contact with rodents and rodent excreta.

Laboratory personnel should use barrier precautions when they handle rodents or are exposed to rodent excreta.