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Infectious Diseases > MEDICAL TOPICS
Lymphocytic Choriomeningitis
Article Last Updated: Aug 25, 2006
AUTHOR AND EDITOR INFORMATION
Section 1 of 9  
Author: Rupal M Mody, MD, Fellow, Department of Infectious Diseases, Walter Reed Army Medical
Rupal M Mody is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America
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
Editors: Mark Raymond Wallace, MD, Chief, Clinical Professor, Department of Internal Medicine, Division of Infectious Disease, Naval Medical Center at San Diego; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; John L Brusch, MD, FACP, Assistant Professor of Medicine, Harvard Medical School; Consulting Staff, Department of Medicine and Infectious Disease Service, Cambridge Health Alliance; Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital; 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
Author and Editor Disclosure
Synonyms and related keywords:
LCM, lymphocytic choriomeningitis virus, LCMV
Background
Lymphocytic choriomeningitis virus (LCMV) is a single-stranded RNA virus, which belongs to the family Arenaviridae (so named because of its electron microscopic appearance, which resembles grains of sand). Other members of this family include Lassa virus and the Tacaribe group. LCMV produces a febrile, self-limited, biphasic disease, called lymphocytic choriomeningitis (LCM), which often is complicated by aseptic meningitis. Asymptomatically infected (carrier state) rodents, which most commonly are house mice, domestic mice, and hamsters, serve as the reservoirs for human infection. LCMV most commonly is transmitted by inhalation of infected excreta. Contamination of scratches on the skin is an important route of infection in pet handlers and laboratory technicians.
Pathophysiology
The initial viremia (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 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. Cytotoxic T cells follow with their production of interferon. Additionally, LCMV can suppress the production of acetylcholine neuronal cells in cell culture.
LCM may affect the autonomic nervous system, various sensory modalities, and cranial nerves. Meningitis occasionally may become chronic and may lead to hydrocephalus. Other organs, especially the testes, heart, and joints, may be involved. Orchitis usually is 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.
Frequency
United States
The exact incidence is unknown, although seroprevalence is approximately 5%. Variations in frequency occur locally and depend on rodent populations. Illness is more common during the fall and winter months.
International
LCM only has been definitely proven to occur in North America, South America, and Europe.
Mortality/Morbidity
Death occurs in less than 1% of cases and may be secondary to the complications of encephalitis or to a massive hemorrhagic syndrome.
Race
No racial differences exist in incidence of infection.
Sex
No sexual predilection exists in incidence of infection.
Age
Young adults are infected with LCMV more commonly, although illness may occur in any age group.
History
Clinical manifestations range from a flulike illness to severe CNS involvement with encephalitis. The typical patient in phase 1 of LCM complains of fever and headache, often with lymphadenopathy and a maculopapular rash. These signs and symptoms resolve after 3-5 days. In many patients, a more severe headache returns within 4 days. This may be associated with typical signs of viral meningoencephalitis.
- Patients may have a history of exposure to rodents, hamsters, or the excreta of these animals 1-3 weeks before onset of symptoms.
- Approximately one third of persons infected with LCMV are asymptomatic.
- As many as one half of patients 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 symptoms, nonspecific
- Fever
- Malaise
- Myalgias
- Nausea or vomiting
- Retro-orbital headache
- Anorexia
- Weakness
- Sore throat
- Nonproductive cough
- 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:
- Altered mentation
- 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
Causes
- LCMV, a member of the family Arenaviridae, causes LCM.
- Infection is contracted through contact with excretions or secretions from chronically infected mice. Viral particles are inoculated through the skin or mucous membranes or by inhaling infected aerosols.
- High-risk populations
- 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 2005
Enteroviruses
Other Problems to be Considered
See Table 1 for the differential diagnosis of LCM.
Other viral meningitides
Mumps
Arboviral encephalitis
Lab Studies
- Diagnosis initially is made by a suggestive history that is confirmed by various laboratory investigations.
- Leukopenia and thrombocytopenia may be observed early in the course of illness.
- LCMV can be isolated from the blood early in the course and, later, from the cerebrospinal fluid (CSF). LCMV may be isolated from the blood or CSF in either cell culture or the intracerebral inoculation of weanling mice (the most reliable method).
- Immunohistochemical staining and reverse transcription-polymerase chain reaction (RT-PCR) of tissues may be useful.
Other Tests
- Acute LCM infection also can be diagnosed through detection of immunoglobulin M (IgM) antibodies by enzyme-linked immunosorbent assay (ELISA) from serum or CSF. This is the preferred diagnostic test.
- Depressed CSF glucose levels have been observed in less than 25% of patients.
Procedures
- Lumbar puncture: In patients with meningeal signs, CSF frequently is abnormal, consisting of an increased opening pressure, increased protein levels, and a lymphocytic pleocytosis, usually in the range of several hundred WBCs.
Medical Care
- No antiviral agents have undergone clinical trials for the treatment of LCMV disease. Ribavirin has in vitro activity against LCMV and has been used with success in a renal transplant recipient with severe disease.
- No specific drug treatment is indicated in most cases.
- Administer analgesics as needed for symptomatic relief.
Further Inpatient Care
- Patients with severe meningoencephalitis usually are hospitalized.
Deterrence/Prevention
- Rodent control measures decrease occurrence.
- Laboratory personnel who handle mice or hamsters are at increased risk for infection with LCM. No established method of preventing infection in these situations exists. Prudence dictates the use of gloves when handling these animals, especially if the person's hands are abraded. If the risk of infection is high, consider the use of a personal respirator.
- No method is effective to prevent transmission by organ transplantation since determination of pet rodent ownership by the donor is neither sensitive or specific. Testing tissue with RT-PCR and immunohistochemical analysis is extremely expensive and may not necessarily be effective.
Prognosis
- LCM rarely is fatal; the overall prognosis is excellent.
- Patients with encephalitis are at higher risk for neurologic sequelae.
- Convalescence may be prolonged, with continuing dizziness, somnolence, and fatigue.
- Severe disease leading to death has been reported in immunocompromised patients and organ transplant recipients (7 of 8 infected patients died).
Patient Education
- Avoid exposure to rodent secreta and excreta.
Special Concerns
- LCM in pregnancy may result in fetal loss or congenital malformations, including hydrocephalus, microcephaly, or chorioretinitis.
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- Peters CJ. Lymphocytic choriomeningitis virus--an old enemy up to new tricks. N Engl J Med. May 25 2006;354(21):2208-11.
Lymphocytic Choriomeningitis excerpt Article Last Updated: Aug 25, 2006
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