Lymphocytic Choriomeningitis

by CDC

What is lymphocytic choriomeningitis?

Lymphocytic choriomeningitis, or LCM, is a rodent-borne viral infectious disease that presents as aseptic meningitis (inflammation of the membrane, or meninges, that surrounds the brain and spinal cord), encephalitis (inflammation of the brain), or meningoencephalitis (inflammation of both the brain and meninges). Its causative agent is the lymphocytic choriomeningitis virus (LCMV), a member of the family Arenaviridae that was initially isolated in 1933. Although LCMV is most commonly recognized as causing neurological disease, as its name implies, infection without symptoms or mild febrile illnesses are common clinical manifestations. Additionally, pregnancy-related infection has been associated with congenital hydrocephalus, chorioretinitis, and mental retardation.

Where does the virus come from?

The primary host is the common house mouse, Mus musculus. Infection in house mouse populations may vary by geographic location but, about 5% of mice throughout the United States carry LCMV. The virus is found in the saliva, urine, and feces of infected mice. Infected mice carry LCMV and shed it for the duration of their lives without showing any sign of illness. Other types of rodents, such as hamsters, are not the natural reservoirs but can become infected with LCMV from wild mice at the breeder, in the pet store or home environment. Humans are more likely to contract LCMV from house mice, but infections from pet rodents have also been reported.

How do humans become infected?

Individuals become infected with LCMV after exposure to fresh urine, droppings, saliva, or nesting materials. Transmission can also occur when these materials are directly introduced into broken skin, the nose, the eyes, or the mouth, or presumably, via the bite of an infected rodent. Person-to-person transmission has not been reported, with the exception of vertical transmission from infected mother to fetus. Recent investigations indicate that organ transplantation may also be a means of transmission.

Where does the disease occur?

LCM and milder LCMV infections have been reported in Europe, the Americas, Australia, and Japan, and may occur wherever infected rodent hosts of the virus are found. However, the disease has historically been underreported, often making it difficult to determine incidence rates or estimates of prevalence by geographic region. Several serologic studies conducted in urban areas have shown that the prevalence of LCMV infection among humans ranges from 2% to 5%.

What are the symptoms of LCM?

Some people infected with LCMV do not become ill. For infected persons who do become ill, onset of symptoms usually occurs 8-13 days after being exposed to the virus. A characteristic biphasic febrile illness then follows. The initial phase, which may last as long as a week, typically begins with any or all of the following symptoms: fever, malaise, lack of appetite, muscle aches, headache, nausea, and vomiting. Other symptoms that appear less frequently include sore throat, cough, joint pain, chest pain, testicular pain, and parotid (salivary gland) pain. Following a few days of recovery, the second phase of the disease occurs, consisting of symptoms of meningitis (for example, fever, headache, and a stiff neck) or characteristics of encephalitis (for example, drowsiness, confusion, sensory disturbances, and/or motor abnormalities, such as paralysis). LCMV has also been known to cause acute hydrocephalus (increased fluid on the brain), which often requires surgical shunting to relieve increased intracranial pressure. In rare instances, infection results in myelitis (inflammation of the spinal cord) and presents with symptoms such as muscle weakness, paralysis, or changes in body sensation. An association between LCMV infection and myocarditis (inflammation of the heart muscles) has been suggested.

During the first phase of the disease, the most common laboratory abnormalities are a low white blood cell count (leukopenia) and a low platelet count (thrombocytopenia). Liver enzymes in the serum may also be mildly elevated. After the onset of neurological disease during the second phase, an increase in protein levels, an increase in the number of white blood cells or a decrease in the glucose levels in the cerebrospinal fluid (CSF) is usually found.

Are there any complications after recovery?

Previous observations have shown that most patients who develop aseptic meningitis or encephalitis due to LCMV recover completely. No chronic infection has been described in humans, and after the acute phase of illness, the virus is cleared. However, as in all infections of the central nervous system, particularly encephalitis, temporary or permanent neurological damage is possible. Nerve deafness and arthritis have been reported. Infection of the human fetus during the early states of pregnancy may lead to developmental deficits that are permanent.

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