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        Western Equine Encephalitis Virus
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        View All Western Equine Encephalitis Virus
June 6, 2024
  Clinical Features, Diagnosis, and Treatment of Western Equine Encephalitis
          Key points
            * Western equine encephalitis (WEE) is a mosquito-borne illness endemic to parts of North, Central, and South America.
            * No human cases of WEE have been reported in the United States since 1999.
            * Contact your state or local health department to request testing for patients suspected of having WEE.
            * There are no vaccines to prevent or medicine to treat WEE in people. Clinical management is supportive.
            * Counsel patients about using personal protective measures to prevent mosquito bites.
        Epidemiology
        WEE virus is an alphavirus in the Togaviridae family. The primary mosquito vectors for WEE virus are Culex tarsalis in North America and Aedes species in South America.
        Historically, WEE virus has been found in parts of North America, Central America, and South America. WEE virus was first identified in horses with encephalitis in the San Joaquin Valley, California in 1930. There has not been a human case of WEE identified in the United States since 1999.
        In late 2023 an outbreak of western equine encephalitis was identified in Argentina and Uruguay affecting people and horses. This outbreak ended in April 2024. Learn more about this WEE outbreak in South America and ways people can prevent mosquito bites while traveling.
        Clinical features
        The incubation period for WEE is 5–10 days. Infection with WEE virus can range from asymptomatic infection to severe encephalitic disease. Individuals most at risk of severe disease from WEE are children aged 2 years and younger and adults aged older than 60 years. Infants 1 year and younger are more likely to develop severe disease.
        Symptoms of WEE are similar to many other viral infections and can include fever, chills, malaise, weakness, and myalgias. The symptoms and illness can progress to aseptic meningitis or encephalitis and lead to coma or even death.
        There can be neurologic sequelae following WEE, with fatigue, irritability, headache, and tremors being most common. Young children are most likely to have a permanent neurologic disability, and older adults are most likely to die from complications.
        The case-fatality rate of people with WEE is 3–15%.
        Diagnosis
        The primary method to diagnose WEE is serological testing of serum or cerebrospinal fluid (CSF). Testing for WEE virus-specific immunoglobulin (Ig) M antibodies is available commercially at some state public health laboratories and at CDC. Positive IgM test results should be confirmed by neutralizing antibody testing, available at CDC.
        Contact your state or local health department if you have a patient with compatible symptoms and a travel history to an area with possible WEE virus transmission. They can assist you with determining if samples should be sent to the CDC Arbovirus Diagnostic Laboratory for further testing. Specimens should be submitted to CDC through state health departments. All results will be sent from CDC to the appropriate state health department.
        Treatment and Prevention
        There are no approved or recommended treatments for WEE. 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. Patients with encephalitis require close monitoring for the development of elevated intracranial pressure, seizures, and inability to protect their airway.
        There is no vaccine or medicine to prevent WEE in humans. Counsel patients about using personal protective measures to decrease their exposure to infected mosquitoes. This includes using EPA-registered insect repellent, wearing long-sleeved shirts and pants, and treating clothing and gear with 0.5% permethrin. Travelers to affected areas should choose a hotel or lodging with air conditioning or screens on windows and doors. Visit the CDC Mosquitoes website for more information about preventing mosquito bites.
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  June 6, 2024
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          Content Source:
        National Center for Emerging and Zoonotic Infectious Diseases (NCEZID)
        Sources
          * Bergren NA, Haller S, Rossi SL, Seymour RL, Huang J, Miller AL, et al. "Submergence" of western equine encephalitis virus: evidence of positive selection argues against genetic drift and fitness reductions. PLoS Pathog. 2020;16(2):e1008102. doi: 10.1371/journal.ppat.1008102
          * Calisher CH. Medically important arboviruses of the United States and Canada. Clinical Microbiology Reviews. 1994;7(1):89-116. doi: 10.1128/CMR.7.1.89
          * Centers for Disease Control and Prevention. Western equine encephalitis--United States and Canada, 1987. MMWR Morb Mortal Wkly Rep. 1987;36(39):655-659.
          * Gould CV, Fischer M. Arboviral central nervous system infections. In: Hasbun R, Bloch KC, Bhimraj A (Eds.). Neurological Complications of Infectious Diseases (pp. 133-151). Springer, 2021.
          * Luethy D. Eastern, Western and Venezuelan equine encephalitis and West Nile viruses: clinical and public health considerations. Vet Clin North Am Equine Pract. 2023;39(1):99-113. doi: 10.1016/j.cveq.2022.11.007
          * Reimann CA, Hayes EB, DiGuiseppi C, Hoffman R, Lehman JA, Lindsey NP, et al. Epidemiology of neuroinvasive arboviral disease in the United States, 1999–2007. Am J Trop Med Hyg. 2008;79(6):974-979.
          * Reisen WK, Monath TP. Western equine encephalomyelitis. In: Monath TP (Ed), The arboviruses (Vol. V, pp. 89-138). CRC Press, 1988.
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