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Pediatric Lymphocytic Choriomeningitis Virus

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


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]



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]




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.


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]


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]


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.

Contributor Information and Disclosures

J Michael Klatte, MD Assistant Professor of Pediatrics, Tufts University School of Medicine; Pediatric Infectious Diseases Division, Baystate Medical Center

J Michael Klatte, MD is a member of the following medical societies: American Academy of Pediatrics, Infectious Diseases Society of America, Massachusetts Medical Society, Pediatric Infectious Diseases Society, Society for Healthcare Epidemiology of America

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Chief Editor

Russell W Steele, MD Clinical Professor, Tulane University School of Medicine; Staff Physician, Ochsner Clinic Foundation

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, Southern Medical Association

Disclosure: Nothing to disclose.

Additional Contributors

Itzhak Brook, MD, MSc Professor, Department of Pediatrics, Georgetown University School of Medicine

Itzhak Brook, MD, MSc is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians-American Society of Internal Medicine, American Medical Association, American Society for Microbiology, Association of Military Surgeons of the US, Infectious Diseases Society of America, International Immunocompromised Host Society, International Society for Infectious Diseases, Medical Society of the District of Columbia, New York Academy of Sciences, Pediatric Infectious Diseases Society, Society for Experimental Biology and Medicine, Society for Pediatric Research, Southern Medical Association, Society for Ear, Nose and Throat Advances in Children, American Federation for Clinical Research, Surgical Infection Society, Armed Forces Infectious Diseases Society

Disclosure: Nothing to disclose.


Leslie L Barton, MD Professor Emerita of Pediatrics, University of Arizona College of Medicine

Leslie L Barton, MD is a member of the following medical societies: American Academy of Pediatrics, Association of Pediatric Program Directors, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

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