The virus can also be transmitted vertically and through infected organ transplantation. Transplacental infection of the fetus presumably occurs during maternal viremia, and it leads to fetal infection with resultant spontaneous abortion or severe birth defects (hydrocephalus, micro- or macrocephaly, intellectual disability, cerebral palsy, seizures, chorioretinitis, blindness, nystagmus, cataract, microphthalmia, or hepatosplenomegaly). In transplant recipients, infection is life-threatening; it can cause multi-organ failure or fatal meningoencephalitis.
LCMV-infected patients classically present with a biphasic pattern of the disease with initial presentation as an influenza-like non-specific systemic febrile illness occasionally associated with headache, rash, and lymphadenopathy. The fever subsides after 3-5 days and is followed by the second febrile phase 2-4 days later (thought to be immunopathologic phenomena, coincides with detection LCMV antibodies). When fever reappears, headache usually becomes more severe and is associated with signs or symptoms of meningismus. In patients with LCMV-associated encephalomyelitis, the disease usually presents as psychosis, paraplegia, cranial nerve dysfunction (sixth cranial nerve palsy), or autonomic dysregulation. Transient aqueductal stenosis could result from ependymal inflammation.
Other notable clinical presentations in the second phase of the disease are alopecia, orchitis (usually unilateral), myocarditis (electrocardiogram [ECG] changes and labile tachycardia), and arthritis (metacarpophalangeal and proximal interphalangeal joints are commonly affected).
Clinical recovery is spontaneous and usually complete, though it may require months to achieve. Overall mortality rate is usually low (<1%), except in organ transplant recipients in which case fatality rate is approximately 90%.
Common laboratory abnormalities include leukopenia, thrombocytopenia, and elevated liver enzymes. Cerebrospinal fluid (CSF) findings are usually compatible with those in viral (aseptic) meningitis, except hypoglycorrhachia in 25% of the patients. CSF protein concentration ranges from 50 to 300 mg/dL. CSF white blood cell (WBC) count shows several hundred lymphocytes per cubic millimeter.
Diagnosis is confirmed by detection of IgM and IgG antibodies for LCMV in serum or CSF.
- Reports associated with mice – An LCMV outbreak associated with laboratory nude mice occurred among employees of a US cancer research institute (1992). More recently, an outbreak of LCMV aseptic meningitis (May-June 2011) involving 9 employees from a rodent-breeding facility in Indiana was reported by the CDC.
- Several reported outbreaks of LCMV associated with hamsters – LCMV was transmitted through laboratory hamsters to laboratory personnel at National Institutes of Health, Bethesda, Maryland (1965), and through Syrian hamsters to University of Rochester Medical Center personnel in New York (1973). A nationwide outbreak of LCMV occurred in the United States (December 1973 through April 1974) totaling at least 181 cases in 12 US states; all were associated with pet hamsters from a single breeder in Birmingham, AL. In Europe, there were reported LCMV outbreaks associated with the domestic Syrian hamsters (Mesocricetus auratus) in Germany (November 1963 through May 1971) and France (1993).
- Reports of LCMV transmission through solid organ transplantation – As of 2012, 5 clusters of solid organ transplant-associated LCMV infections have been identified, 4 in the United States (2003, 2005, 2008, and 2011) and 1 in Australia (2008). A total of 17 recipients of solid organ transplantation (kidney, liver, and lung) have been involved, and a total of 14 deaths from multi-organ failure (82% mortality) have occurred.
A87.2 – Lymphocytic choriomeningitis
398136003 – Lymphocytic Choriomeningitis
For congenital LCMV infection, parvovirus B19 and TORCHES (toxoplasmosis, rubella, cytomegalovirus [CMV], herpes simplex virus, enteroviruses, syphilis) should be considered. (Barton and Mets provide a detailed comparison; see References.)