Clinical Pearls & Morning Reports
Acute flaccid paralysis is a well-known complication of West Nile virus infection, although it can occur with St. Louis virus infection and Jamestown Canyon virus infection. Acute flaccid paralysis has not been recently reported with eastern equine encephalitis or Powassan virus infection. Read the latest Case of the Massachusetts General Hospital.
Q: What are some general features of arbovirus infections?
A: Arbovirus infections have an incubation period of 1 to 3 weeks and then are manifested by an acute febrile illness that can progress to neuroinvasive disease, including encephalitis, meningitis, and flaccid paralysis. On magnetic resonance imaging (MRI) of the head, FLAIR and T2-weighted images typically show hyperintensity in the deep gray matter with no enhancement or diffusion restriction. In New England, mosquito-borne arboviruses include West Nile virus, eastern equine encephalitis, Jamestown Canyon virus, and St. Louis virus. Powassan virus is carried by the Ixodes scapularis tick and has increasingly been reported in New England in the spring and fall.
Q: How common is neuroinvasive disease among patients with West Nile virus infection?
A: West Nile virus remains the most common arbovirus in New England; it causes symptomatic infection in approximately 10% of affected persons. Of the symptomatic persons, only 10% have progression to neuroinvasive disease. Such progression is more common in older patients or those with immunodeficiency. West Nile encephalitis is associated with an in-hospital mortality of approximately 20%.
A: According to the available literature, prognosis in West Nile virus neuroinvasive disease, particularly West Nile virus encephalitis, is related to several factors. An age of more than 50 years and coexisting medical illnesses, factors that affect general health, are associated with increased morbidity and mortality. Coma at presentation and cranial neuropathy are each associated with brain-stem dysfunction and portend worse outcomes. Acute flaccid paralysis has historically been associated with a mortality as high as 50%, in large part because of neuromuscular respiratory failure. However, the degree of recovery in West Nile virus neuroinvasive disease is highly variable.
A: After West Nile virus is acquired from an insect vector, viremia ensues for a period of approximately 10 days, and then the virus becomes detectable in the CSF for 2 to 3 days. Viral replication in the CSF coincides with the onset of clinical symptoms. The West Nile virus–specific humoral response develops in the CSF 11 or 12 days after infection, and then antibody becomes detectable in the blood. Because viral replication in the CSF occurs for a short duration, a polymerase-chain-reaction assay for West Nile virus is often negative by the time the patient presents for clinical evaluation. However, an IgM response has developed in most patients at the time of presentation; therefore, ELISA for the detection of IgM antibody in CSF is the test of choice for West Nile virus infection.
Figure 2. Kinetics of Viral and Serologic Responses after Exposure to West Nile Virus.