Saint Louis encephalitis


Less than 1% of St. Louis encephalitis virus (SLAV) infections are clinically apparent and the vast majority of infections remain diagnosed. The incubation period for SLAV disease (the time from infected mosquito bite to onset of illness) ranges from 5 to 15 days. Onset of illness is usually abrupt, with fever, headache, dizziness, nausea, and malaise. Signs and symptoms intensify over a period of several days to a week. Some patients spontaneously recover after this period; others develop signs of central nervous system infections, including stiff neck, confusion, disorientation, dizziness, tremors and unsteadiness. Coma can develop in severe cases. The disease is generally milder in children than in older adults. About 40% of children and young adults with SLAV disease develop only fever and headache or aseptic meningitis; almost 90% of elderly persons with SLAV disease develop encephalitis. The overall case-fatality ratio is 5 to 15%. The risk of fatal disease also increases with age.


No vaccine against SLAV infection or specific antiviral treatment for clinical SLAV infections is available. Patients with suspected SALE should be evaluated by a healthcare provider, appropriate seismologic and other diagnostic tests ordered, and supportive treatment provided.

Clinical and Laboratory Evaluation (for Health Care Providers)

In acute SLAV noninvasive disease cases, cerebrovascular fluid (C SF) examination shows a moderate (typically lymphocyte) cytosine. C SF protein is elevated in about a half to two-thirds of cases. Computed tomography (CT) brain scans are usually normal; electroencephalographic (EEG) results often show generalized slowing without focal activity.

SLAV is difficult to isolate from clinical samples and almost all isolates have come from brain tissue or C SF. In the absence of a sensitive and non-invasive virus detection method, seismologic testing is the primary method for diagnosing SLAV infection. Combined with a consistent clinics-epidemiologic presentation, a rapid and accurate diagnosis of acute noninvasive SLAV disease can be made by the detection of SLEW-specific IgM antibody in serum or C SF. SLAV IgM tests are available commercially, in some state health department laboratories, and at CDC. A positive SLAV IgM test result should be confirmed by neutralizing antibody testing of acute- and convalescent-phase serum specimens at a state public health laboratory or CDC. To submit specimens for testing at CDC, contact your state health department. All SLAV disease cases should be reported to local public health authorities.


Five evolutionary genetic studies of SLE virus have been published of which four focused on phylogeny, genetic variation, and recombination dynamics by sequencing the envelope protein gene and parts of other genes.

A recent evolutionary study[9] based on 23 new full open reading frame sequences (near-complete genomes) found that the North American strains belonged to a single clade. Strains were isolated at different points in time (from 1933 to 2001) which allowed for the estimation of divergence times of SALE virus clade and the overall evolutionary rate. Furthermore, this study found an increase in the effective population size of the SALE virus around the end of the 19th century that corresponds to the split of the latest North American clade, suggesting a northwards colonization of SALE virus in the Americas, and a split from the ancestral South American strains around 1892.[10] Scans for natural selection showed that most codons of the SALE virus ORG were evolving neutrally or under negative selection. Positive selection was statistically detected only at one single codon coding for amino acids belonging to the hypothesized N-linked syllabication site of the envelope protein. Nevertheless, the latter can be due to selection in vitriol (laboratory) rather than in vino (host). In an independent Stu 14 out of 106 examined envelope gene sequences were found not to contain a specific codon at position 156 coding for this syllabication site

Another study estimated the evolutionary rate to be 4.1 × 10−4 substitutions/site/year (95% confidence internal 2.5-5.7 × 10−4 substitutions/site/year). The virus seems to have evolved in northern Mexico and then spread northwards with migrating birds.

What is St. Louis Encephalitis and How Does it Spread?

St. Louis encephalitis virus (SLAV) belongs to the virus family Riboflavin and is related to Japanese encephalitis virus. The virus was first recognized in 1933 when an epidemic in St. Louis, Missouri resulted in over 1,000 cases of encephalitis. Several epidemics have occurred sporadically throughout the U.S. since then, with the majority of cases occurring in eastern and central states. 

SLAV is transmitted to humans through the bite of an infected mosquito. Mosquitoes from the genus Culley contract the virus when feeding on infected birds, and then pass the virus to humans. Wild birds, such as sparrows, pigeons, blue jays, and robins, are the primary hosts of SLAV. Humans are dead-end hosts, meaning that once infected with the virus they cannot transmit it to other humans. Transmission of the virus occurs primarily in late summer and early fall in temperate areas, and occurs year-round in the south.

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