Lymphocytic choriomeningitis
Lymphocytic choriomeningitis (LCM) is a rodent-borne viral infectious disease that presents as aseptic meningitis, encephalitis or meningoencephalitis.
During the initial or prodromal phase, which may last up to a week, common symptoms include fever, lack of appetite, headache, muscle aches, malaise, nausea, and/or vomiting.
Underreported complications include myelitis, Guillain–Barré-type syndrome, cranial nerve palsies, transient or permanent hydrocephalus, sensorineural hearing loss, orchitis, arthritis and parotitis.
[7] The entire illness usually lasts 1 to 3 weeks;[7] nonetheless, temporary or permanent neurological damage is possible in all central nervous system infections, especially in cases of meningoencephalitis.
[8] On the other hand, Clone 13 is a variant of the Armstrong viral strain, isolated from the spleen and is consequently tropic for visceral organs.
The RNA-dependent, RNA-polymerase[11] brought along with the virus initially binds to a promoter on the L and S segments and begins transcription from negative-stranded to a positive-stranded mRNA.
[citation needed] In 1996, Peter Doherty and Rolf Zinkernagel shared the Nobel Prize in Medicine and Physiology,[8] for their work with LCMV which led to a fundamental understanding of the adaptive immune response, MHC restriction.
Other modes of mouse-to-mouse transmission include nasal secretions, milk from infected dams, bites, and during social grooming within mouse communities.
[13] The virus seems to be relatively resistant to drying and therefore humans can become infected by inhaling infectious aerosolized particles of rodent urine, feces, or saliva, by ingesting food contaminated with virus, by contamination of mucous membranes with infected body fluids, or by directly exposing cuts or other open wounds to virus-infected blood.
Infants who survive may have severe neurological defects including epilepsy, impaired coordination, visual loss or blindness, spastic diplegia or quadriparesis/quadriplegia, delayed development and intellectual disability.
[7] If a woman has come into contact with a rodent during pregnancy and LCM symptoms are manifested, a blood test is available to determine previous or current infection.
A PCR assay has been recently developed which may be used in the future for prenatal diagnosis; however, the virus is not always present in the blood or CSF when the affected child is born.
[7] Studies have indicated that human infection of the virus occurs primarily during the fall and winter months, presumably due to the movement of mice indoors.
Products include devices that emit ultrasonic sound that allegedly irritates mice and drives them away, and more swift, painless means of death such as mini electrocution or gas chambers.
[7] Temperature and time of year is also a critical factor that contributes to the number of LCMV infections, particularly during fall and winter[7] when mice tend to move indoors.
[7] The probability that a woman will become infected after being exposed to rodents, the frequency with which LCMV crosses the placenta, and the likelihood of clinical signs among these infants are still poorly understood.
In 1989, an outbreak among humans occurred in a US cancer research institute that studied the effects of various therapeutic and diagnostic agents in animal models.
Clare A. Dykewicz, et al. recommend vigilant screening laboratory animals to be used in research facilities either through serum samples or cell line aliquots, as well as ensuring adequate ventilation in housing areas and use of appropriate sanitation products.
[7] A study conducted by John Hotchin and Heribert Weigand, of the New York State Department of Health, concluded, "The age of the mouse when first exposed to the virus determines its immune response."
If LCMV infection occurs in utero or within the first few hours of life, during the immunologically unresponsive period, the mouse will develop immune tolerance.
[32] Post mortem lesions in mice show signs of hepatomegaly, splenomegaly, lymphadenopathy, and swollen or shrunken and pitted kidneys due to glomerulonephritis.
[7] In these mice, and some hamsters, vasculitis and lymphocytic infiltrates in many organs and tissues including the liver, spleen, lung, kidneys, pancreas, blood vessels, meninges and brain are present.
[34] Experimental intracerebral infection of suckling rats results in microcephaly, retinitis and the destruction of several brain regions,[7] leading to permanent abnormalities of movement, coordination, vision and behavior.
[7] Necropsy lesions in primates with callitrichid hepatitis show signs of jaundice, hepatomegaly, splenomegaly, and subcutaneous and intramuscular hemorrhages.
For laboratory purposes, immunohistochemistry staining of tissues and virus isolation are used for more accurate testing, but this is unnecessary for the general house pet.
[6] The National Center for Infectious Disease suggests the following precautions to reduce the risk of LCMV infection: Rodent owners who no longer wish to keep their pet should consult a veterinarian.
[8] LCMV is already identified as the best model to examine the difference between acute and persistent infection in its natural host Mus musculus, the common house mouse.
[8] In addition, a better understanding of CD4+ T cell memory is also a result of studies with LCMV and will continue to contribute to a more efficient mechanism of vaccine formation.
Furthermore, the United States National Institute of Allergy and Infectious Diseases (NIAID)[8] has appointed the family of arenaviridae to be "Category A Priority Pathogens".
[8] This translates to the highest level of importance for the high potential for morbidity and mortality from an infectious agent which is relatively easy to produce and transmit.
