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Western Equine Encephalomyelitis
Synonym(s): WEE, sleeping sickness
Introduction
- 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.
- Genus: Alphaviridae.
- 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.
Presenting signs
- Biphasic fever spikes, 2 and 6 days after infection.
- Dullness/sleepiness.
- Sternal recumbency.
- Behavior changes.
- Aggression.
- Dementia.
- Head pressing.
- Ataxia.
- Blindness.
- Circling.
- Dysphagia.
- Excessive salivation.
- Generalized weakness.
- Hyperesthesia.
- Twitching of body and muzzle.
- Recumbency.
- Death within 5 days after presentation.
- Improvement in signs after 5 days in 50-90% of cases.
- Seizures are rare.
Acute presentation
- Fever, followed by general dullness, sleepiness, dementia, listlessness, then aimless wandering, ataxia then improvement or continued worsening signs progressing to paralysis, recumbency → death.
- Clinical infection is more common than with EEE Eastern Equine Encephalomyelitis.
Geographic incidence
- Western USA, west of the Mississippi Eiver valley, and South and Central America.
- Western and Northern (Manitoba) Canada.
- Northern USA (Minnesota and North Dakota).
- Eastern USA, except Eastern Seaboard.
- Eastern Seaboard of the USA.
- Eastern Canada.
Age predisposition
- All ages affected.
- Rare in foals <3 months of age.
Breed/Species predisposition
- No breed predilection.
Public health considerations
- Transmission from horse-to-horse or horse-to-human beings is usually not a problem because the level of viremia is insufficient for transmission via mosquitoes.
- However, human beings can become infected after performing a post mortem examination on infected horses or wild animals as well as by being bitten by infected mosquitoes that have bitten an infected wild bird or wild animal.
- Human beings usually become infected as spillover from reservoir hosts.
- In humans, there have been 639 confirmed cases of WEE in the USA since 1964.
- Mild to severe neurologic deficits persist in survivors.
- Human groups at risk of infection include residents of endemic areas, visitors to endemic areas and persons working outdoors or taking part in recreational activities. Outbreaks in human beings are generally preceded by outbreaks in horses and are limited to the time of the year when mosquitoes are active.
- The total cost of treatment for human cases of WEE ranges from $21,000 (¬19,800) for transient infections to $3 million (¬2.8 million) for severe infections. Insecticide applications can cost as much as $1.4 million (¬1.2 million) depending on the size of the area treated.
Cost considerations
- Loss of horse.
- Medical treatment moderately expensive.
Special risks
- Horses may become violent and pose a danger to itself and handlers.
- Tranquilization Anesthesia: standing chemical restraint and control of seizures may be necessary during acute episode of neurologic disease.
Pathogenesis
Etiology
- 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
General
- Debilitated or unvaccinated horses living in endemic areas.
Specific
- Unvaccinated horses are most susceptible.
Pathophysiology
- 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.
Timecourse
- 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.
Epidemiology
- 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.
Diagnosis
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Treatment
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Prevention
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Outcomes
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Further Reading
Publications
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: www.cdc.gov/ncidod/dvbid/arbor/weefact.htm.
- 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.