INTRODUCTION

IMMUNOLOGY

BACTERIOLOGY

VIROLOGY

PARASITOLOGY

MYCOLOGY

In May 2005, the Rhode Island and Massachusetts Departments of Health and CDC reported three deaths from an lymphocytic choriomeningitis virus (LCMV) infection. LCMV is an arenavirus. The deaths were in organ transplant recipients. It appears that the originally infected person obtained the virus from the urine or feces of house mice or a pet hamster. A recently purchased pet hamster owned by that person was found to be infected with LCMV. This person died of unrelated causes and donated organs were used for transplant in four recipients in April 2005. All four developed similar symptoms and tested positive for LCMV. Three died. This is the second time that LCMV has been known to be transmitted via organ transplantation. Lymphocytic choriomeningitis usually only has a fatality rate of 1% and most patients clear the virus and recover completely. It is likely that the transplant patients died because immuno-suppressive drugs are used to counter organ rejection and therefore they could not mount an immune response to the virus.

Arenaviridae are RNA viruses whose particles are spherical and have an average diameter of 110-130 nanometers. Arenaviridae members are zoonotic, which means that in nature they are found in reservoir animal hosts.  CDC
 

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 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.

Host

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.

Infection

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.

Epidemiology

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%.

Symptoms

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.

Course of the disease

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.

LCM is usually not fatal. In general, mortality is less than 1%.

Treatment

Aseptic meningitis, encephalitis, or meningoencephalitis requires hospitalization and supportive treatment based on severity. Anti-inflammatory drugs, such as corticosteroids, may be considered under specific circumstances. Although studies have shown that ribavirin, a drug used to treat several other viral diseases, is effective against LCMV in vitro, there is no established evidence to support its routine use for treatment of LCM in humans.

Individuals at risk

Individuals of all ages who come into contact with urine, feces, saliva, or blood of the house mouse are potentially at risk for infection. Laboratory workers who work with the virus or handle infected animals are also at risk. However, this risk can be minimized by utilizing animals from sources that regularly test for the virus, wearing proper protective laboratory gear, and following appropriate safety precautions. Owners of pet mice or hamsters may be at risk for infection if these animals originate from colonies that have become contaminated with LCMV, or if the animals become infected from other wild mice. Human fetuses are at risk of acquiring infection vertically from an infected mother.

 

LCMV infection can be prevented by avoiding contact with house mice and taking precautions when handling pet rodents (i.e. mice, hamsters, or guinea pigs).

Although rare, pet rodents may become infected with LCMV from wild rodents. Breeders, pet stores, and pet owners should take measures to prevent infestations of wild rodents. Pet rodents should not come into contact with wild rodents.

If you have a rodent infestation in and around your home, take the following precautions to reduce the risk of LCMV infection:

 

• Seal up rodent entry holes or gaps with steel wool, lath metal, or caulk.
• Trap rats and mice by using an appropriate snap trap.
• Clean up rodent food sources and nesting sites and take precautions when cleaning rodent-infected areas.
• If you have a pet rodent, wash your hands with soap and water (or waterless alcohol-based hand rubs when soap is not available and hands are not visibly soiled) after handling rodents or their cages and bedding.

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