bubble_chart Overview

Lymphocytic choriomeningitis (LCM) is an acute infectious disease caused by the LCM virus. The clinical course of the disease can range from flu-like symptoms to meningitis and encephalitis of varying severity. The disease is self-limiting with a good prognosis. It is essentially a zoonotic infectious disease, and the natural host of the LCM virus is the brown rat.

bubble_chart Epidemiology

This disease is distributed worldwide, generally sporadic, with a higher incidence in autumn and winter. Laboratory-acquired external contraction can lead to outbreaks of the disease. There are few reports of this disease domestically.

The pestilence sources of this disease are mainly small brown rats and field mice, while wild rodents can also serve as pestilence sources. The urine, feces, saliva, and nasal secretions of infected rats all contain the virus, contaminating dust or food, which can infect humans through the respiratory and digestive tracts. Contact with the skin and hair or excreta of infected rats can also lead to infection. People of all ages and genders are susceptible, with higher incidence rates among older children and young adults. Laboratory workers, animal handlers, and others have a higher mechanism of disease. A single infection (including latent infection) can confer lasting immunity. There have been no reports of human-to-human transmission of this disease.

bubble_chart Pathogen

The LCM virus is an RNA-type virus, approximately 50 nm in size. Morphologically and serologically, it resembles viruses such as Lassa, Machupo, and Tacaribe, hence it is also classified as an arenavirus. The pathogen has multiple strains with varying disease characteristics (such as tissue tropism and virulence), yet all share the same group-specific antigen. The virus can be inactivated at 56°C within one hour and is easily destroyed by ether, formaldehyde, ultraviolet light, or pH below 7. It can be preserved long-term in 50% glycerol at -70°C. This virus can grow in chicken embryo or mouse embryo fibroblast tissue cultures and is pathogenic to mice, rats, guinea pigs, hamsters, rabbits, monkeys, and other animals.

bubble_chart Pathogenesis

The exact pathogenesis of the disease remains incompletely understood. When the virus initially invades the respiratory tract, it can proliferate extensively within epithelial cells, leading many patients to exhibit symptoms of upper respiratory tract infection or "flu-like" symptoms. After entering the bloodstream, the virus causes viremia and may cross the blood-brain barrier to infect meningeal cells. Fatalities from this disease are extremely rare, so reports on its pathological changes are scarce. The main findings include brain swelling, lymphocyte and mononuclear cell infiltration in the meninges and choroid plexus, capillary hemorrhage, necrosis, etc. However, there have also been reports of no pathological changes in the central nervous system, with lesions only observed in organs such as the lungs, liver, kidneys, and adrenal glands.

bubble_chart Clinical Manifestations

The incubation period of this disease ranges from 6 days to several weeks, with diverse clinical manifestations.

(1) Influenza-like Type: The onset is mostly abrupt, with fever reaching above 39°C, accompanied by back pain, headache, and general muscle soreness. Some patients report nausea, vomiting, photophobia, swollen and painful lymph nodes, diarrhea, rash, or symptoms such as sore throat, stuffy nose, runny nose, and cough. The course of the illness lasts about 2 weeks, with occasional relapses. A sense of lack of strength may persist for 2 to 4 weeks after the illness.

(2) Meningitis Type: This may occur after "influenza-like" symptoms (often following a brief stage of remission) or begin directly as meningitis. The onset is acute, presenting with fever, headache, vomiting, meningeal irritation signs, etc. Convulsions are rare except in young children. Consciousness generally remains unaffected. The course lasts about 2 weeks.

(3) Others: Rare types such as meningoencephalitis or encephalomyelitis manifest as severe headache, delirium, unconsciousness, convulsions, paralysis, mental disturbances, etc. Some cases may leave neurological sequelae, such as aphasia, deafness, arachnoiditis, varying degrees of paralysis, ataxia, diplopia, strabismus, etc.

The disease may occasionally complicate with orchitis, parotitis, pneumonia, arthritis, late abortion in pregnant women, etc.

bubble_chart Auxiliary Examination

The peripheral blood picture shows a normal or decreased total white blood cell count, with a relative increase in lymphocytes, often accompanied by the appearance of abnormal lymphocytes. In patients with encephalitis, the cerebrospinal fluid cell count may increase to 100–3000/mm³, with over 90% being lymphocytes; protein levels are elevated but generally do not exceed 100 mg/dl; glucose is normal or slightly reduced, and chloride levels are normal. Pressure is normal or slightly elevated.

In the acute phase, inoculation of the patient's blood or cerebrospinal fluid into the brain or abdominal cavity of mice can isolate the pathogen. Serum immunofluorescence tests may turn positive as early as the first week of the disease course, aiding in early diagnosis. Complement fixation tests become positive 10–14 days into the disease course, with titers peaking at 5–8 weeks and disappearing within 4–6 months. Neutralization tests are used only for epidemiological investigations.

bubble_chart Diagnosis

A history of contact with field mice or white mice, or residence in an area with rodents and nearby cases of similar illness, followed by a brief relief of "influenza-like" symptoms and subsequent signs of meningeal irritation, with cerebrospinal fluid showing predominantly lymphocytes, normal chloride levels, and relatively decreased sugar, are all of significant diagnostic value. Confirmation relies on serological tests or virus isolation.

This disease is easily confused with influenza, other viral respiratory infections, various types of viral meningitis, and subcutaneous nodular meningitis. Differentiation should be based on epidemiological data, serological tests, and virus isolation. Since small numbers of abnormal cells may appear in peripheral blood, it can also be mistaken for infectious mononucleosis complicated with meningitis. However, in the latter, the total number of abnormal lymphocytes may exceed 10%, heterophil agglutination tests are often strongly positive, and EB virus antibodies (IgM-type membrane capsid antibodies) are mostly positive.

bubble_chart Treatment Measures

There is no specific treatment for this disease. Symptomatic treatment is given for severe headaches, and dehydration agents such as mannitol can be used for those with increased intracranial pressure.

bubble_chart Prognosis

The vast majority recover smoothly, with rare fatalities; those accompanied by encephalitis recover more slowly and may experience neurological sequelae.

bubble_chart Prevention

The main preventive measures include eliminating house mice, avoiding consumption of food that may be contaminated by rodents, and laboratory workers should enhance personal protection. Patients do not need to be isolated.