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West Nile Virus

West Nile Virus (WNV) is an arbovirus belonging to the flavivirus family that also includes dengue, yellow fever, St. Louis encephalitis and Japanese encephalitis. WNV is an enveloped virus of about 40-60 nm. in diameter with a single-stranded RNA genome of approximately 10,000-11,000 bases. It is an arthropod-borne virus that is transmitted between susceptible hosts by blood-feeding mosquitoes. Birds are the mosquitoes preferred target, and subsequently act as sentinels of the virus’ presence within a geographic area. Birds and mammals can become infected when an infected mosquito bites them to take a blood meal. Although humans can be infected and can become ill from the virus, they are a “dead end” host since they normally do not participate in the life cycle of the virus. WNV cannot be spread from one human to another by casual contact.

The first North American cases occurred in New York City during the summer of 1999. The virus is endemic in Africa & the Middle East and may have reached this continent by migrant or smuggled birds. More than 4,000 individuals in 39 states were infected with WNV in 2002. There were 9858 total human WNV infections reported to the CDC in 2003, with the majority of cases occurring in Colorado, Nebraska and South Dakota.

Methods to control the spread of the virus to humans involve the individual use of protective clothing and mosquito repellants, public health measures to reduce the mosquito population in areas where the virus is prevalent, and implementation of routine testing of the blood supply to limit transfusion transmitted disease.

Although most WNV infections are asymptomatic, an estimated 20% develop West Nile fever, which is a mild illness that may be accompanied by malaise, anorexia, rash, lymphadenopathy, myalgia, headache, nausea, vomiting or eye pain. Less than 1% of infections result in severe neurologic disease. The most significant risk factor for neurologic disease is advanced age.

About one in 150 people who are infected with WNV will develop more severe symptoms of meningitis or encephalitis. Patients with encephalitis often present with headache, high fever, stiff neck, stupor, disorientation, coma, tremors, convulsions, muscle weakness, and paralysis. A small number of cases have been fatal. There is no specific treatment for WNV infection. Supportive care, such as hospitalization, IV fluids, respiratory support, and aggressive treatment of secondary infections often is required for encephalitis patients.

Most severe outcomes have been seen in immunocompromised patients; particularly organ and stem cell transplant recipients, patients receiving immunosuppressive medications and patients with hematologic malignancies, myelodysplasia, and other advanced malignancies. People who are over age 65 or women who are pregnant or immediately postpartum also may be at increased risk.

The diagnostic test of choice for WNV and other arboviral infections is serologic analysis of serum or CSF for IgM and IgG antibodies. IgM antibody to WNV can be detected as early as 4 days after onset of illness and may persist for several weeks. Since IgM antibody does not cross the blood-brain barrier, its presence in CSF strongly suggests central nervous system infection. IgG antibody to WNV may be detectable one week after illness onset. Patients who have been vaccinated against, or infected with, related flaviviruses (yellow fever, dengue) may also have positive WNV antibody tests. Although PCR testing is available for WNV, it has been found to be relatively insensitive for diagnosis. Specimen requirement is one red top tube of blood or 1.0 mL CSF.

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