West Nile encephalitis
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West Nile vi·rus (WNV),
First isolated in Uganda in 1937 from a patient with encephalitis, WNV has since been identified in isolated cases throughout Africa, Asia, and Europe, and has caused occasional outbreaks of febrile illness with encephalitis. The first cases of WNV infection to be recognized in North America occurred in August 1999 in New York City. Sixty-two cases of human infection were eventually identified, of which 7 were fatal. During the next 5 years, the virus spread southward along the east coast to Florida and then across the country to the west coast. By the end of 2004 human infections had occurred in all but 3 of the 48 contiguous states. WNV is transmitted by more than 20 species of North American mosquitoes, most of them belonging to the genus Culex, but also including Aedes albopictus. The chief hosts are wild corvid birds, principally crows, ravens, and jays. Seasonal avian migrations are thought to be responsible for the geographic spread of the virus. Mammals, including human beings and horses, are occasional hosts, but mammalian viremia is apparently insufficient for further transmission by a mosquito vector. A few cases of transmission by blood transfusion, organ transplantation, or accidental percutaneous inoculation of laboratory workers have been reported. Intrauterine infection has also been observed. Human infections occur during late spring, summer, and early fall, with peak incidence in the U.S. in late August and early September. Seasonal variations depend on mosquito biting seasons and hence geographic latitude. Human cases peak in southern states about 1 week earlier than in northern states. Most cases of human infection are clinically inapparent. Early symptoms are nonspecific and include fever, chills, malaise, headache, ocular pain or photophobia, myalgia, and occasionally a maculopapular rash (more common in children) and gastrointestinal upset. Encephalitis or aseptic meningitis, which occurs in fewer than 1% of those infected, may be manifested by hyperreflexia, myoclonus, tremor, drowsiness, or confusion progressing to delirium or coma, meningism, or seizures. A less common syndrome consists of muscular weakness progressing to asymmetric flaccid paralysis due to destruction of anterior spinal horn cells or demyelination of peripheral motor nerves. The case fatality rate in symptomatic patients is 5-15%. The incubation period is 3-15 days. The period of illness varies from a few days to several weeks. Severity of disease and risk of fatal outcome increase with advancing age. The average age of patients manifesting encephalitis or meningitis due to WNV is about 70. Spontaneous recovery is the rule in children, but adult infection may be followed by neurologic and muscular sequelae. More than one third of adult survivors of WNV infection continue to experience muscular weakness, cognitive impairment (for example, confusion, difficulty concentrating), or both after 12 months. The disease is diagnosed by the finding of Ig antibody to the virus in serum or CSF or by identification of viral nucleic acid in CSF or brain tissue obtained at autopsy. Treatment is purely supportive. Efforts are underway to produce a vaccine. Meanwhile, prevention depends on mosquito control, including public education, elimination of breeding places (for example, stagnant ponds and hollows or open containers that catch rain water), the use of larvicides, and avoidance of personal exposure by means of appropriate attire and application of insect repellent. see also Aedes albopictus, Culex pipiens, Culex quinquefasciatus, and Culex restuans.