Transmission
St. Louis encephalitis virus (SLEV) is maintained in a mosquito-bird-mosquito cycle, with periodic amplification by peridomestic birds and Culex species mosquitoes. Wild birds are the primary vertebrate hosts. Birds sustain inapparent infections but develop viremias (i.e., virus in their blood) sufficient to infect the mosquito vectors. Birds that are abundant in the urban-suburban environment, such as the house sparrow, pigeon, blue jay, and robin, are principally involved. The principal vectors are Cx pipiens and Cx quinquefasciatus in the east, Cx nigripalpus in Florida, and Cx tarsalis and members of the Cx pipiens complex in western states. Humans and domestic mammals can acquire SLEV infection, but are dead-end hosts.

Less than 1% of St. Louis encephalitis virus (SLEV) infections are clinically apparent and the vast majority of infections remain undiagnosed. The incubation period for SLEV 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 SLEV disease develop only fever and headache or aseptic meningitis; almost 90% of elderly persons with SLEV disease develop encephalitis. The overall case-fatality ratio is 5 to 15%. The risk of fatal disease also increases with age.

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

In acute SLEV neuroinvasive disease cases, cerebrospinal fluid (CSF) examination shows a moderate (typically lymphocytic) pleocytosis. CSF 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.
SLEV is difficult to isolate from clinical samples and almost all isolates have come from brain tissue or CSF. In the absence of a sensitive and non-invasive virus detection method, serologic testing is the primary method for diagnosing SLEV infection. Combined with a consistent clinico-epidemiologic presentation, a rapid and accurate diagnosis of acute neuroinvasive SLEV disease can be made by the detection of SLEV-specific IgM antibody in serum or CSF. SLEV IgM tests are available commercially, in some state health department laboratories, and at CDC. A positive SLEV 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 SLEV disease cases should be reported to local public health authorities.