Transmission occurs by inhalation (aerosol and droplet), fomites, or direct contact with excreta or blood from infected rodents. Human-to-human transmission has been reported during pregnancy from infected mothers to the fetus (5) and through solid organ transplantation (6). The incubation period is 1–2 weeks. Infections in persons with an intact immune system are often asymptomatic or result in a mild self-limiting illness including fever, chills, myalgia, and headache. Photophobia, anorexia, testicular or parotid pain, pharyngitis, and cough have also been noted (1). Leukopenia, thrombocytopenia, and mild liver function abnormalities are common and may last 1–3 weeks. Central nervous system invasion is seen only in a few patients either after an initial febrile illness or, less commonly, without any early symptoms. During this neurologic phase, most patients have aseptic meningitis and a peripheral leukocytosis (1). Cerebrospinal fluid (CSF) leukocyte cell counts often exceed 1,000/μL, and glucose levels are low. Infection is rarely fatal, although ascending paralysis, transverse myelitis, or encephalitis may develop (1).

Critical or even fatal outcomes from LCMV are usually associated with transplacental infections, and, more recently, solid organ transplantation. Congenital LCMV can result in hydrocephalus, chorioretinopathy, macrocephalopathy, or microcephalopathy and can mimic the classic TORCH (toxoplasmosis/Toxoplasma gondii, other infections, rubella, cytomegalovirus, herpes simplex virus) pathogens. In 1 study of 26 infants with congenital LCMV, 9/26 (35%) died and 10/16 (63%) survivors had severe neurologic sequelae (7). Transplacental infection presumably occurs after maternal viremia during the first and second trimesters (8). In 2003 and 2005, the first reports of infection after solid organ transplantation were reported in which 7 of 8 patients receiving LCMV infected organs, kidney, liver, and lung, died (6). Therapy for LCMV is supportive, although limited data support the use of ribavirin in immunosuppressed patients. We report a case of meningitis caused by LCMV in New York City.

Because of the patient’s hypoglycorrachia, pronounced CSF leukocytosis, and negative CSF cultures, acute infection with LCMV was considered. Serum tested at a commercial laboratory was positive for LCMV (immunoglobulin [Ig] G titer >256 (reference <16) and IgM titer 80 (reference <20) by immunofluorescence assay. CSF collected on day 1 and serum collected on days 7 and 15 was tested for LCM antibodies by the Centers for Disease Control and Prevention’s Special Pathogens Branch using ELISA. CSF and serum were both IgM and IgG positive and a 4-fold rise in acute-phase and convalescent-phase serum titers indicated the patient had a recent infection with LCMV (Table). The patient improved with supportive care, recovered fully, and was discharged on day 12.

Our patient denied both hamster and mouse exposure. His corneal transplant had occurred >1 year before, and was unlikely to be the source of infection. A definitive diagnosis was difficult, but testing by Centers for Disease Control and Prevention confirmed the diagnosis.

New York City Health Department officials attempted an investigation of the patient’s home and surroundings to look for evidence of rodents or rodent excreta, but were unable to do so due to the patient’s noncompliance. Several clues have assisted clinicians in the identification of patients with acute LCMV infection: 1) aseptic meningitis or encephalitis during the fall–winter season, 2) a febrile illness followed by brief remission before onset of neurologic illness, and 3) CSF with a lymphocytosis and hypoglycorrachia. Patients with suspected LCMV should be asked about potential rodent exposure (1). Patients with a history of organ transplantation within the preceding 3 months should be fully evaluated to determine whether infected organs were the source of LCMV.

We recommend enzyme immunoassay-based testing of CSF and serum when LCMV is considered. Public health surveillance, rodent control, healthcare provider education, and improved laboratory testing can enhance recognition of illness.