West Nile Virus: A Primer for the Clinician

Abstract

This paper provides the clinician with an understanding of the epidemiologic and biological characteristics of West Nile virus in North America, as well as useful information on the diagnosis, reporting, and management of patients with suspected West Nile virus infection and on advising patients about prevention. Information was gathered from the medical literature and from national surveillance data through May 2002. Since the identification of West Nile virus in New York City in 1999, enzootic activity has been documented in 27 states and the District of Columbia. Continued geographic expansion is likely. Overall, one in 150 infections results in severe neurologic illness. Advanced age is by far the most important risk factor for neurologic disease and, once disease develops, for worse clinical outcome. Surveillance has identified 149 persons with West Nile virus-related illness in 10 states. Encephalitis is more commonly reported than meningitis, and concomitant muscle weakness and flaccid paralysis may provide a clinical clue to the presence of West Nile virus infection. Peak incidence occurs in late summer, although onset has occurred from July through December. Immunoglobulin M antibody testing of serum specimens and cerebrospinal fluid is the most efficient method of diagnosis, although cross-reactions are possible in patients recently vaccinated against or recently infected with related flaviviruses. Testing can be arranged through local, state, or provincial (in Canada) health departments. Prevention rests on elimination of mosquito breeding sites; judicious use of pesticides; and avoidance of mosquito bites, including mosquito repellent use.

West Nile Virus-Associated Meningoencephalitis in Two Chronically Immunosuppressed Renal Transplant Recipients

“…The detection of IgM antibodies by the capture enzyme immunoassay to West Nile virus in serum or CSF collected at least 8 days after onset of illness is currently the most efficient diagnostic method for West Nile virus (6). IgM antibodies do not cross the blood-brain barrier; therefore the finding of virus-specific IgM antibodies in the CSF is strongly associated with CNS infection (3,6,7). Nucleic acid amplification tests were not performed in our patients.…”

“…Nucleic acid amplification tests were not performed in our patients. Viral culture and nucleic acid amplification tests have low sensitivities and should not be used routinely (3,6).…”

“…In healthy individuals, symptoms typically include 3-6 days of malaise, anorexia, arthralgia, vomiting, nausea, rash, and lymphadenopathy. In elderly or immunocompromized individuals, more severe neurological symptoms including mental status changes, muscle weakness, and flaccid paralysis may occur (3). Although most patients are asymptomatic, approximately 1 in 150 patients who have serologic evidence of West Nile virus infection develop encephalitis or meningitis, which may be associated with ataxia, myelitis, seizures or optic neuritis (3,4).…”

Recent progress in West Nile virus diagnosis and vaccination

“…The human incubation period of West Nile virus is 2 to 14 days [53]. The majority (~75 to 80%) of humans infected with WNV usually have no or very mild symptoms.…”

A new era of uveitis: impact of polymerase chain reaction in intraocular inflammatory diseases

“…This virus is a member of the Japanese encephalitis virus serocomplex and has widely spread from Africa to other continents [110]. It is mainly transmitted by Culex mosquitoes, but other transmission routes, such as through blood transfusion and organ transplantation, transplacental transmission, laboratory transmission, and breast feeding, have recently been recognized [111].…”