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Western Equine Encephalomyelitis


Synonym(s): WEE, sleeping sickness


  • Non-supprative viral encephalitis of horses, birds and humans that is transmitted by mosquitoes (Culex tarsalisandCuliseta melanura) Equine viral encephalitides.
  • The virus is maintained in sylvatic populations of wild birds.
  • Cause: virus from:
    • Family: Togaviridae.
    • GenusAlphaviridae.
    • Group A Arboviruses (closely related EEE Eastern Equine Encephalomyelitis virus and VEE viruses). Transmitted from sylvatic populations of wild brids to hroses via blood meal from mosquito bite. Virus over winters in other mammals, birds, amphibians and reptiles (reservoir hosts).
  • Signs: biphasic fever (38-41°C, 2 and 6 days), then general depression, dullness, anorexia, stiffness, ataxia, hyperesthesia, aggression, excitability, continuous chewing movements, aimless wandering, somnolence → head pressing, circling, twitching, recumbency and death.
  • Diagnosis: paired serum titers (4-fold increase in titer over 2-4 weeks), virus isolation from brain tissue at necropsy or single high serum titer during the acute phase of the disease.
  • Treatment: no specific antiviral treatment is available to treat WEE. Therefore, supportive care, nursing care, prevention of self-trauma, and non-steroidal anti-inflammatory therapy, fluids, electrolytes, total and partial parental nutrition, DMSO and corticosteroids (controversial). Also, diazepam or phenobarbital to control convulsions.
  • Prognosis: guarded as mortality rates range from 10-50% in cases with neurologic signs.  Once recumbent, death may occur within 5 days.  Horses that recover from clinical disease frequently have persistent neurologic deficits. 



  • Virus in the Family Togaviridae, Genus Alphaviridae, enveloped, single-stranded RNA virus particle 60-64 nm diameter, enclosed in an icosahedral nucleocapsid (30-35 nm diameter) enclosed in host cell derived plasma membrane. 
  • Three antigenic variants have been isolated and are antigenically related by hemagglutination inhibition to EEE and VEE.
  • Sensitive to heating to 60°C for 30 min and can be held indefinately at 4°C in the lyophilized state.
  • Sensitive to lipid solvents, chlorine and phenol and relatively insensitive to trypsin. 

Predisposing factors


  • Debilitated or unvaccinated horses living in endemic areas.


  • Unvaccinated horses are most susceptible.


  • After virus inoculation via the mosquito (Culicine mosquitoes, especially Culex tarsalis), multiplication occurs in local muscle, followed by entry into the lymphatic circulation and localization in local and regional lymph nodes.
  • Viruses replicate in macrophages and neutrophils. 
  • Virus may be cleared and no clinical signs noted (if virus neutralizing antibodies are produced).  If virus is not cleared then replication occurs in endothelial cells and concentrates in highly vascular organs, such as the spleen and liver. Replication continues in the spleen and liver and virus is release into the vascular system (secondary viremia) resulting in clinical signs. 
  • Infection of CNS can occur within 3-5 days after secondary viremia.
  • Horses are thought to be dead end hosts.
  • Clinical signs are related to the spread of virus to and within the CNS. 
  • Replication in vascular endothelium of brain and spinal cord results in vascular congestion, brain and brain stem swelling and compression.
  • Mortality rate in horses varies from 10-50%.
  • Many infections result in subclinical disease.
  • Much of the CNS pathology is immune-mediated.
  • Necrotizing encephalitis results from WEE infection.


  • Incubation period is 1-3 weeks, with CNS signs appearing as early as 3-5 days after secondary viremia. 
  • Horses that develop clinical neurologic signs, display them for a few days to several weeks, and if the horse survives it may be left with permanent neurologic deficits.


  • Mosquitoes (primarily theCulex tarsalis) act as the biologic vector. 
  • Reservoir hosts include mammals, birds, amphibia and reptiles. 
  • Horses, human beings and domestic birds are incidental hosts and do not spread the virus to other mammals because of the short lived and minimal viremia that occurs. 
  • The disease is more common in human beings than EEE and there have been 639 confirmed cases human cases of WEE in the USA since 1964.
  • There is no horse-to-horse or horse-to-human transmission of WEE.
  • Human beings and horses are usually infected when the virus prevalence becomes high in wild mammals and birds.
  • According to the Centers for Disease Control (CDC) in the USA, there were no reported equine or human WEE cases in the USA in 2001.


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Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Herholz C, Fussel A-E, Timoney P et al (2008) Equine travellers to the Olympic Games in Hong Kong 2008: A review of worldwide challenges to equine health, with particular reference to vector-borne diseases. Equine Vet J 40 (1), 87-95 PubMed.
  • Lambert A J, Martin D A & Lanciotti R (2003) Detection of North American eastern and Western equine encephalitis viruses by nucleic acid amplification assays. J Clin Microbiol 41 (1), 379-385 PubMed.
  • Walton T E, Jochim M M, Barber T L et al (1989) Cross-protective immunity between equine encephalomyelitis viruses in equids. Am J Vet Res 50 (9), 1442-1446 PubMed.

Other sources of information

  • Centers for Disease Control (2003) Fact Sheet: Western Equine Encephalitis. Division of Vector-Born Infectious diseases. Website:
  • Bertone J E (1992) Togavirus Encephalitides (Eastern and Western) Equine Encephalitis. In: Current Therapy in Equine Medicine. Ed: Robinson N E. 3rd edn. WB Saunders, USA. pp 547-550.

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