West Nile virus (WNV) is a flavivirus related to Japanese encephalitis and St. Louis encephalitis viruses that affects humans, horses, birds, and other vertebrates. The clinical presentation cannot reliably be distinguished from other causes of viral encephalitis. In fall 2002, WNV was detected in a crow, a raven, and two horses in Washington State. There is currently significant WNV activity in California and the disease may occur locally this summer. The following information summarizes the clinical manifestations, diag-nosis and laboratory testing, and reporting for WNV infections in King County.

General Information: WNV is transmitted by the bite of one of a number of mosquito species (primarily Culex species in Washington) that become infected after feeding on birds carrying WNV. It is not transmitted person-to-person, or to humans directly from dead or living animals other than mosquitoes, with the following exceptions. WNV can be transmitted via body fluids, and in 2002, transfusion of blood products, organ transplantation, transplacental transmission, and trasmission via breast milk were identified as potential routes of infection with WNV. Two cases of blood product associated trasmission, one case of transplacental trans-mission, and one case of transmission via breast-milk have been reported.

Clinical presentations: WNV infection should be con-sidered in persons of all ages (particularly between May and November) with unexplained encephalitis, aseptic meningitis, acute flaccid paralysis, presumed Guillain-Barré Syndrome, or other neurological presentations described below. Because WNV transmission can occur year-round in some areas, obtaining a recent travel history is always important.

Most WNV infections are mild or clinically unapparent. Approximately 20% of infected persons develop West Nile fever, a less severe form of infection. The incubation period is thought to range from 3 to 14 days, and symptoms last 3 to 6 days or longer. Symptoms of West Nile fever may include fever, malaise, anorexia, nausea, vomiting, eye pain, head-ache, body aches, skin rash, and swollen lymph glands.

Approximately 1 in 150 infections cause the more severe neurological forms of disease including encephalitis and meningitis. Neuro-invasive disease is associated with a range of neurologic and systemic manifestations including headache, high fever, gastrointestinal symptoms, neck stiffness, stupor, disorientation, cranial nerve abnormalities, ataxia, coma, tremors, convulsions, muscle weakness, paralysis, and, rarely, death. Case-fatality rates for hospitalized patients range from 3% to 15% and are highest in the elderly. Neuromuscular weakness in persons with a viral meningoencephalitis syndrome is suggestive of WNV infection. Other neurological presentations include acute flaccid paralysis (which may present without meningitis or encephalitis), ataxia and extrapyramidal signs, tremor and Parkinson-like syndrome, cranial nerve abnormalities, myelitis, optic neuritis, polyradiculitis, and seizures.

There is no vaccine or specific therapy for WNV in humans. In severe cases, intensive supportive therapy is indicated including hospitalization, intravenous fluids, airway management, respiratory support, prevention of secondary infections and good nursing care.

Laboratory Diagnosis
The most efficient method for diagnosis of WNV is through detection of IgM antibody to WNV in serum collected 8-14 days after illness onset, or in CSF collected within 8 days of illness onset, using the IgM antibody capture enzyme-linked immunosorbent assay (MAC-ELISA).

Because WNV cannot be distinguished from other causes of meningoencephalitis on clinical grounds, concurrent testing for other common causes of aseptic meningitis/encephalitis syndrome, (including cultures and/or PCR testing for enteroviruses and herpes viruses) is encouraged.

Test Interpretation: IgM antibody develops by day 8 and IgG antibody within 3 weeks after illness onset. When indicated, convalescent serum specimens should be drawn about 3-4 weeks after acute specimens. Negative results on any specimen obtained <8 days after onset of illness should be considered inconclusive and a convalescent serum specimen, obtained at least 2 weeks after the first specimen, is needed to make a final determination. Cross-reactions may occur among patients who have had yellow fever, Japanese encephalitis vaccination, a previous history of arboviral encephalitis, or dengue fever.

For complete information on WNV, see the Public Health - Seattle & King County WNV web site: www.metrokc.gov/health/westnile