eMedicine Specialties > Infectious Diseases > Viral Infections

Lymphocytic Choriomeningitis

Author: Rupal M Mody, MD, Fellow, Department of Infectious Diseases, Walter Reed Army Medical
Coauthor(s): Diane H Johnson, MD, Assistant Director, Assistant Professor, Department of Internal Medicine, Division of Infectious Diseases, Winthrop-University Hospital, State University of New York at Stony Brook School of Medicine
Contributor Information and Disclosures

Updated: Feb 6, 2009

Introduction

Background

Lymphocytic choriomeningitis virus (LCMV) is a single-stranded RNA virus that belongs to the family Arenaviridae (so named because of its appearance on electron microscopy, which resembles grains of sand). Other members of this family include Lassa virus and the Tacaribe group. Infection with LCMV results in a febrile, self-limited, biphasic disease called lymphocytic choriomeningitis (LCM), which is often complicated by aseptic meningitis. Infected but asymptomatic (carrier state) rodents, most commonly house mice, domestic mice, and hamsters, serve as reservoirs for LCMV.1,2 LCMV is most commonly transmitted via inhalation of infected excreta. Contamination of skin scratches is an important route of LCMV infection in pet handlers and laboratory technicians.2

Pathophysiology

The initial viremia of LCMV infection (phase 1) extensively seeds extra-CNS tissue. The secondary viremia (phase 2) infects the meninges and, less commonly, the cortical tissue. The leptomeninges are infiltrated mainly by lymphocytes and histiocytes, with few neutrophils. In LCMV encephalitis, the same type of inflammatory cells is observed in the perivascular Virchow-Robin spaces. LCMV is not cytotoxic. It appears that the host's immune response to the infected cells produces the various manifestations of this disease. Natural killer (NK) cells are first to respond, followed by the production of interferon by cytotoxic T cells. In addition, LCMV can suppress the production of acetylcholine neuronal cells in cell culture.3,4,6,7

LCM may affect the autonomic nervous system, various sensory modalities, and cranial nerves. Some cases of LCM become chronic, potentially resulting in hydrocephalus. Other organs, especially the testes, heart, and joints, may be involved. Orchitis is usually unilateral. Cardiac involvement is typical of viral myocarditis. The metacarpal phalangeal joint and the proximal interphalangeal joint are the most common sites of arthritis caused by LCM. The objective swelling, redness, and pain resolve within a few weeks.6,7

Frequency

United States

The exact incidence of LCMV infection is unknown, although the seroprevalence is approximately 5%. Local variations in the frequency of LCMV infection depend on the rodent populations. LCMV infection in humans is most common in autumn.7

International

North America, South America, and Europe are the only continents where LCM has been definitively proven to occur.7

Mortality/Morbidity

LCMV infection carries a mortality rate of less than 1%. Death may be attributable to complications of encephalitis or to a massive hemorrhagic syndrome. As with other arenaviruses, immunosuppression may predispose to a fatal hemorrhagic fever syndrome.8

Race

LCMV infection has no racial predilection.

Sex

LCMV infection has no sexual predilection.

Age

LCMV infection is more common in young adults, although illness may occur in any age group.7

Clinical

History

Clinical manifestations of lymphocytic choriomeningitis virus (LCMV) infection range from a flulike illness to severe CNS involvement with encephalitis. Phase 1 of LCM typically manifests as fever and headache, often with lymphadenopathy and a maculopapular rash, resolving after 3-5 days. In many patients, a more-severe headache returns within 4 days, possibly associated with typical signs of viral meningoencephalitis.3,6,7,8

Patients with LCMV infection may report a history of exposure to rodents, hamsters, or the excreta of these animals 1-3 weeks before the onset of symptoms. Infection is most common in the fall. Approximately one third of LCMV infections cause no symptoms, and up to one half of infected individuals have a nonspecific febrile illness without neurologic involvement. The remainder of patients experiences classic biphasic symptoms associated with LCMV infection and meningitis or encephalitis.
  • Initial nonspecific symptoms of LCMV infection include the following:
    • Fever
    • Malaise
    • Myalgias
    • Nausea or vomiting
    • Retro-orbital headache
    • Anorexia
  • Symptoms may subside for 2-4 days and then recur with the following:
    • Increased headache
    • Stiff neck
    • Lethargy (usually mild) ranging to encephalitis
    • Occasionally, patients develop the following:
      • Orchitis
      • Parotitis
      • Myocarditis
      • Paresis or paralysis (extremely rare)
      • Alopecia
      • Arthritis of the hand
  • Immunosuppressed individuals may develop hemorrhagic fever syndrome (seen in organ transplant recipients); symptoms include the following:5,8
    • Altered mentation/seizures
    • Respiratory insufficiency
    • Leukopenia
    • Thrombocytopenia
    • Coagulopathy
    • Renal/liver dysfunction
    • Hemorrhagic foci in multiple tissues
  • Neurologic sequelae are rare.
  • Complete recovery is the rule, although convalescence may be prolonged.

Physical

  • Typical clinical features of LCMV infection3,6,7   
    • Fever (generally 39-40°C)
    • Relative bradycardia
    • Nonexudative pharyngitis
    • Papilledema (rare)
    • Nuchal rigidity (mild)
    • Erythematous maculopapular rash (rare)
    • Lymphadenopathy
  • Atypical clinical features of LCMV infection
    • Psychosis
    • Paralysis
    • Alterations in function of cranial, sensory, or autonomic nerves
    • Encephalitis rarely observed but may present as psychosis and paraplegia

Causes

  • LCM is caused by infection with LCMV, a member of the family Arenaviridae.
  • LCMV infection is contracted through contact with excretions or secretions from chronically infected rodents. Viral particles are inoculated through the skin or mucous membranes or inhalation of infected aerosols.7
  • Populations at high risk of LCMV infection include the following:
    • Laboratory workers involved in the handling of mice or hamsters
    • Individuals who inhabit locales with large mouse populations
    • Reported in organ transplant recipients (liver, lung, kidney) in 2003 and 20055

More on Lymphocytic Choriomeningitis

Overview: Lymphocytic Choriomeningitis
Differential Diagnoses & Workup: Lymphocytic Choriomeningitis
Treatment & Medication: Lymphocytic Choriomeningitis
Follow-up: Lymphocytic Choriomeningitis
References
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References

  1. Brown D, Lloyd G. Zoonotic virus. In: Infectious Diseases. Philadelphia, Pa: Mosby; 1999:11.1-11.14.

  2. Childs JE, Glass GE, Korch GW, et al. Lymphocytic choriomeningitis virus infection and house mouse (Mus musculus) distribution in urban Baltimore. Am J Trop Med Hyg. Jul 1992;47(1):27-34. [Medline].

  3. Cunha BA. Meningitis. In: Schlossberg D, ed. Central Nervous System Infections. New York, NY: Springer-Verlag; 1990.

  4. Farmer TW, Janeway CA. Infection with the virus of lymphocytic choriomeningitis. Medicine (Baltimore). 1942;2:11.

  5. Fischer SA, Graham MB, Kuehnert MJ, Kotton CN, Srinivasan A, Marty FM. Transmission of lymphocytic choriomeningitis virus by organ transplantation. N Engl J Med. May 25 2006;354(21):2235-49. [Medline].

  6. McKee KT Jr. Hemorrhagic fever virus. In: Infectious Diseases. 2nd ed. Philadelphia, Pa: WB Saunders Co; 1998:2249-65.

  7. Peters CJ. Lymphocytic choriomeningitis virus, Lassa Virus, and the South American Hemorrhagic Fevers. In: Mandell, Douglas, Bennett, eds. Principles and Practice of Infectious Diseases. 6th ed. New York, NY: Churchill Livingstone; 2005:2090-6.

  8. Peters CJ. Lymphocytic choriomeningitis virus--an old enemy up to new tricks. N Engl J Med. May 25 2006;354(21):2208-11. [Medline].

  9. Barton LL. LCMV transmission by organ transplantation. N Engl J Med. Oct 19 2006;355(16):1737; author reply 1737-8. [Medline].

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Further Reading

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Keywords

lymphocytic choriomeningitis, LCM, lymphocytic choriomeningitis virus, LCMV, LCM virus

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Contributor Information and Disclosures

Author

Rupal M Mody, MD, Fellow, Department of Infectious Diseases, Walter Reed Army Medical
Rupal M Mody, MD is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Coauthor(s)

Diane H Johnson, MD, Assistant Director, Assistant Professor, Department of Internal Medicine, Division of Infectious Diseases, Winthrop-University Hospital, State University of New York at Stony Brook School of Medicine
Diane H Johnson, MD is a member of the following medical societies: American College of Physicians, American Medical Association, American Medical Women's Association, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Medical Editor

Mark Raymond Wallace, MD, Infectious Disease Fellowship Director, Orlando Regional Healthcare; Clinical Professor of Medicine, Florida State University
Mark Raymond Wallace, MD is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Tropical Medicine and Hygiene, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

John L Brusch, MD, FACP, Assistant Professor of Medicine, Harvard Medical School; Consulting Staff, Department of Medicine and Infectious Disease Service, Cambridge Health Alliance
John L Brusch, MD, FACP is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

 
 
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