St. Louis encephalitis
- Thomas P Monath, MD, FACP, FASTMH
Thomas P Monath, MD, FACP, FASTMH
- Adjunct Professor (Emeritus)
- Harvard School of Public Health
St. Louis encephalitis (SLE) is an acute, mosquito-borne viral illness characterized by meningeal and brain parenchymal inflammation and injury. The disease occurs in endemic and epidemic form in North and South America. Epidemics of SLE in the United States have been responsible for at least 1,000,000 mild or subclinical infections, 10,000 clinical cases, and 1000 deaths since SLE virus was first isolated in 1933 during an outbreak in St. Louis, Missouri .
Studies of SLE virus evolution indicate that the virus was introduced into North America from tropical America in the late 19th Century . There is evidence that West Nile virus, which was introduced into the United States in 1999, has displaced SLE by more efficient transmission and cross-protective immunity in wild birds . The annual incidence of SLE and the occurrence of epidemics have substantially declined as West Nile virus has spread throughout North America. In contrast, there are increasing reports of SLE infections in tropical America.
St. Louis encephalitis (SLE) virus is a member of the family Flaviviridae, a group of small (40 to 60 nm), enveloped, positive-sense, single-stranded RNA viruses that replicate in the cytoplasm of infected cells. Other members of this virus family include West Nile virus, Japanese encephalitis virus, Murray Valley encephalitis virus, yellow fever virus, and dengue virus. St. Louis encephalitis virus grows in a wide variety of avian and mammalian cell cultures and causes lethal encephalitis in infant mice or hamsters after intracerebral inoculation. SLE virus is antigenically closely related to Japanese encephalitis and West Nile virus, which cause a similar disease (see "Arthropod-borne encephalitides"). This may result in diagnostic confusion, particularly if non-specific serological tests are used. (See 'Diagnosis' below.)
SLE virus strains from the eastern and western United States and from tropical America are distinguishable at the nucleotide sequence level into at least eight lineages and multiple clades [2,4-6], which differ with respect to the mosquito vectors responsible for transmission and the virulence for animal models . The SLE virus Lineage II, which is present east of the Mississippi river, has been associated with severe epidemics, has the highest virulence for laboratory animals, and has the highest case-fatality rate for humans. Although there is evidence for geographic separation and local persistence of strains (eg, Lineage I in California), analyses of SLE virus evolution suggest flow of neotropical strains, particularly from northern Central America, Mexico, and the Caribbean, into the United States by the agency of migratory birds [5,8]. As an example, one analysis identified circulation of an ancestral genotype of SLE circulating in Culex nigripalpus in southern Mexico, which may have given rise to cosmopolitan virus genotypes .
After inoculation of St. Louis encephalitis (SLE) virus into the human host via mosquito saliva, viral replication is initiated in local tissues and regional lymph nodes. Subsequent spread occurs initially to extraneural tissues via the lymphatics and blood. SLE virus replicates in a wide array of cell types, including connective tissue, skeletal muscle, exo- and endocrine glands, and reticuloendothelial tissues. Viremia is terminated approximately one week after infection by neutralizing antibodies and cytotoxic T cells.
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- TRANSMISSION CYCLE
- CLINICAL FEATURES
- Prodromal symptoms
- Neurologic signs
- Laboratory findings
- Cerebrospinal fluid analysis
- OUTCOME OF INFECTION
- DIFFERENTIAL DIAGNOSIS
- SOCIETY GUIDELINE LINKS
- SUMMARY AND RECOMMENDATIONS