West Nile Virus Identified in Spokane-area Mosquitoes

Posted Aug. 17, 2018. Past health advisories and alerts are archived for historical purposes and are not maintained or updated.

Overview

Earlier this month, two separate mosquito pools in Spokane County tested positive for West Nile Virus.  While no human, bird, or horse cases of West Nile Virus (WNV) cases have been identified to date in Spokane, mid-August marks the first symptom onset of human cases in 2016 and 2017 (the first years in which locally-acquired WNV cases were identified). While we expect mosquito populations to dwindle as the weather gets cooler, continued mild weather will contribute to prolonged mosquito activity and thus, prolonged risk for acquiring WNV.  

Symptoms & Clinical Management

The incubation period is usually two to 14 days.  While most (80%) of WNV infections are asymptomatic, symptomatic persons can experience an acute systemic febrile illness that often includes headache, weakness, myalgia, and/or arthralgia.  Gastrointestinal symptoms and a transient maculopapular rash are less common symptoms.  Less than 1% of infected persons develop neuroinvasive disease, which typically manifests as meningitis, encephalitis, or acute flaccid paralysis. Neuroinvasive disease is more likely to occur in immunocompromised individuals and/or those over age 60.

  • WNV meningitis is clinically indistinguishable from viral meningitis due to other etiologies and typically presents with fever, headache, and nuchal rigidity.
  • WNV encephalitis is a more severe clinical syndrome that usually manifests with fever and altered mental status, seizures, focal neurologic deficits, or movement disorders, such as tremor or parkinsonism.
  • WNV acute flaccid paralysis is usually clinically and pathologically identical to poliovirus-associated poliomyelitis, with damage of anterior horn cells, and may progress to respiratory paralysis requiring mechanical ventilation. WNV poliomyelitis often presents as isolated limb paresis or paralysis and can occur without fever or apparent viral prodrome. WNV-associated Guillain-Barre syndrome and radiculopathy have also been reported and can be distinguished from WNV poliomyelitis by clinical manifestations and electrophysiological testing.

Rarely, cardiac dysrhythmias, myocarditis, rhabdomyolysis, optic neuritis, uveitis, chorioretinitis, pancreatitis, and hepatitis have been described in patients with WNV disease. The case fatality rate for neuroinvasive disease is around 10%.

Routine clinical laboratory studies are generally nonspecific. In patients with neuroinvasive disease, CSF examination generally shows lymphocytic pleocytosis, but neutrophils may predominate early in the illness. Brain MRI is frequently normal, but signal abnormalities in the basal ganglia, thalamus, and brainstem may be seen in patients with encephalitis, and in the anterior spinal cord in patients with poliomyelitis.

There is no specific treatment for WNV; clinical management is supportive. Patients with severe meningeal symptoms often require pain control for headaches and antiemetic therapy and rehydration for associated nausea and vomiting.  Treatment for neuroinvasive disease often involves hospitalization, intravenous fluids, respiratory support, and prevention of secondary infection.

Diagnostic Testing

The most efficient diagnostic method for WNV infection is detection of virus using the IgM antibody-capture enzyme immunoassay (MAC-EIA) or microsphere immunoassay (MIA) of IgM antibody to WNV in serum collected eight to 14 days after onset or CSF collected within eight days of illness onset. More than 90% of those infected have detectible serum IgM eight days after onset; serum collected within eight days of illness onset may not have detectable IgM and testing should be repeated on a convalescent-phase sample. The EIA can exhibit serologic cross-reactivity in patients who have been recently vaccinated against or recently infected with related flaviviruses. In addition, since most WNV infections are asymptomatic and IgM can persist in the serum for up to 500 days, the presence of IgM in residents from an endemic area may indicate a previous rather than current infection.

The diagnosis can also be confirmed by a four-fold rise in antibody titer between acute and convalescent (14 to 21 days after acute) sera. Since serum IgM does not cross the blood-brain barrier, IgM in the CSF strongly suggests central nervous system infection.

Reverse transcription polymerase chain reaction (RT-PCR) assay to detect WNV nucleic acid in serum or CSF is useful for patients with immune dysfunction but is not recommended for routine diagnosis of WNV disease.

Testing should be done at commercial laboratories.

Prevention

The primary route of transmission is through the bite of an infected mosquito.  WNV is not transmitted through casual contact.  In very rare cases, it has been transmitted through blood transfusions, organ transplants, percutaneous injuries in the laboratory, and from mother to baby via the placenta and possibly breastmilk.

There is no vaccine for humans. WNV prevention depends on mosquito bite prevention. Personal protective measures include use of mosquito repellants, wearing long-sleeved shirts and long pants, and limiting outdoor exposure from dusk to dawn. Using air conditioning, installing window and door screens, and reducing mosquito breeding sites can further reduce the risk for WNV exposure. To reduce mosquito breeding sites around the home, advise patients to twice weekly drain and routinely empty anything that holds water, such as gutters, pet bowls, tires, bird baths, etc. Keep water moving in ornamental ponds by recirculating water or by installing a fountain.