Treatment of West Nile virus is primarily supportive care. MRI may show abnormalities after several weeks of acute neuroinvasive disease. Imaging: CT of the brain will typically not show any acute findings of the disease. In patients with a high suspicion of viral infection and an initial negative test, a repeat should be performed 10 days later as IgM levels may take time to elevate to the levels necessary to be detectable. For neuroinvasive disease, the CSF should also be tested using the ELISA test. Analysis of CSF shows elevated protein and leucocyte levels, with a possible predominance of neutrophils early, transitioning to a lymphocytic predominance accompanied by normal glucose levels. Neuroinvasive West Nile virus will typically have findings consistent with viral meningitis on lumbar puncture. Hyponatremia may be seen when the CNS is involved. A plaque reduction neutralization test (PRNT) can distinguish serologic cross-reactions. The diagnosis is via serologic detection of West Nile virus using an enzyme-linked immunosorbent assay (ELISA) for the IgM antibody in blood or CSF samples. Routine labs may reveal leukocytosis and other non-specific findings secondary to the viral infection. The typical infection includes a fever for five days, headache for 10 days and fatigue for around a month. The West Nile virus incubation period is two to 14 days. However, this includes areas on most continents, as listed in the epidemiology section. Most people infected with West Nile virus have a history of travel to an area where the virus is endemic during the summer or fall. Even with aggressive supportive treatment, the mortality rate following a case of neuroinvasive West Nile infection is high. These patients initially present with features of encephalitis and/or meningitis that progresses rapidly, and they require ICU care. However, in rare cases, the virus can cause neurologic symptoms, including severe muscle weakness, changes in mental status, seizures, or flaccid paralysis. Other associated symptoms include headache, eye pain, vomiting, anorexia, and up to 50% may have a maculopapular rash on the trunk appearing upon defervescence. The clinical presentation of West Nile virus in most cases include myalgia, malaise, and a low-grade fever. The incubation period of the West Nile virus varies from 4-14 days.Symptoms tend to last 5-7 days and include fever in at least 1/4th of patients. This data extrapolates to an estimated 3 to 5 million cases of infection. Serologic surveys and blood donor screening data shows a rate of neuroinvasive disease of around 0.5% of infected patients and an infection rate of 10% in areas of outbreak. The number of neuroinvasive cases varies heavily year to year, ranging from 386 to 2946. In the US from 1999 to 2015, there have been almost 44000 confirmed and probable cases of West Nile virus with over 20000 cases of neuroinvasive disease. In warmer climates, cases can occur throughout the year. Outbreaks tend to be associated late summer and fall due to the mosquito vector’s life cycle and the amplification from the bird-mosquito-bird cycle. This fact leads to the likely vast underreporting of West Nile virus infections. West Nile fever is present in 25% of those infected the remaining 75% show few to no symptoms.
Based on a comprehensive literature review in 2013, meningitis and encephalitis (neuroinvasive disease) were present in less than one percent of infected patients with a mortality of 10 percent. In the mid-1990s West Nile virus became correlated with severe neurologic disease. The original outbreaks of the virus showed a typically self-limited and minor illness. As of today, the West Nile virus is found in Africa, Europe, Asia, North America, Australia, and the Middle East. It resurfaced in 1999 when there were reports of seven deaths and 62 cases of encephalitis in New York this was the first presentation of the virus in the western hemisphere. The first reports of West Nile virus were in Uganda in 1937.
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