Equis ISSN 2398-2977

Eastern Equine Encephalomyelitis

Synonym(s): EEE, sleeping sickness

Introduction

  • Rare non-suppurative viral encephalitis that is transmitted by mosquitoes (Culiseta melanuraandAedesspp)   Equine viral encephalitides  .
  • The virus is maintained in sylvatic populations of birds, small mammals, and reptiles.  Horses are a dead end host.
  • As of the beginning of July 2003, South Carolina, in the southeastern United States had 17 confirmed cases of EEE since the beginning of June, with about 25 pending confirmation. Florida's EEE case count was up to 113 horses and Georgia had 30.
  • Cause: virus from:
    • Family:Togaviridae.
    • Genus:Alphaviridae.
    • Group A Arboviruses, transmitted from sylvatic populations to horses. Closely related antigenically to WEE   Western Equine Encephalomyelitis   and VEE.
  • Signs: biphasic fever (38-41°C, 2 and 6 days), then general depression, anorexia, stiffness, hyperesthesia, aggression, excitability, continuous chewing movements, aimless wandering, somnolence   →   head pressing, circling, twitching and eventual recumbency and death.
  • Diagnosis: paired serum titers (4-fold increase or decrease in titer over 2-4 weeks), CSF changes including initial polymorphonuclear pleocytosis, later followed by mononuclear pleocytosis and increased protein concentration, and transient peripheral lymphopenia. Occasionally, peripheral eosinophilia occurs during the early stages of viral infection.
  • Treatment: no specific antiviral treatment is available to treat EEE.  Therefore, supportive care, nursing care, prevention of self-trauma, and non-steroidal anti-inflammatory therapy, fluids and electrolytes, total and partial parental nutrition, DMSO and corticosteroids (which are controversial), and anticonvulsive agents are commonly used with limited success.
  • Prognosis: guarded to poor as case-mortality rates range from 75-100%.  Once recumbent, horses usually die within 5 days.  Horses that recover from clinical disease frequently have persistent neurologic deficits. 

Pathogenesis

Etiology

  • Virus in the Family:Togaviridae, Genus:Alphaviridae, enveloped, single-stranded RNA virus particle 60-64 nm diameter, enclosed in an icosahedral nucleocapsid and an outer envelope that is derived from host cell plasma membrane. 
  • Two antigenic variants.

Predisposing factors

General
  • Debilitated or unvaccinated horses living in epidemic or endemic areas.

Specific

  • Unvaccinated horses are most susceptible.

Pathophysiology

  • After virus inoculation via the mosquito, 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 released into the vascular system (secondary viremia) resulting in clinical signs. 
  • Infection of the CNS can occur within 3-5 days after virus inoculation.
  • Clinical signs are related to the spread of virus to the CNS. 
  • Replication in vascular endothelium of brain and spinal cord results in vascular congestion, brain and brain stem swelling and compression.

Timecourse

  • Incubation period is 3 days to 3 weeks, with CNS signs appearing in as little as 3-5 days after virus inoculation. 
  • Horses develop clinical signs that last a few days to several weeks and if the horse survives may be left with permanent neurologic deficits. 
  • Death occurs in 75-100% of clinically ill horses; horses that are recumbent frequently die within 5 days.

Epidemiology

  • Mosquitoes (Culiseta melanura) 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 rare in human beings and there have been 153 confirmed human cases in the USA since 1964. 
  • Horse-to-horse or human-to-horse transmission of EEE has not been recorded.

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, Schwermer H, Bruckner L & Leadon D (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.
  • Cantile C, Del Piero F, Guardo G et al (2001) Pathology, immunohistochemistry, and virologic findings of Eastern Equine Encephalomyelitis in two horses. Vet Pathol 38, 451-456 PubMed.
  • Ross W A & Kaneene J B (1996) Evaluation of outbreaks of disease attributable to Eastern Equine Encephalitis virus in horses. JAVMA 208 (12), 1988-1997 PubMed.

Other sources of information

  • Centers for Disease Control (2003) Fact Sheet: Eastern Equine Encephalitis. Division of Vector-Born Infectious diseases. Website: www.cdc.gov/ncidod/dvbid/arbor/eeefact.htm.
  • Bertone J E (1992) Togavirus encephalitides (Eastern and Western) Equine Encephalitis. In: Current Therapy in Equine Medicine. Ed: Robinson N E. 3rd edn. W B Saunders, USA. pp 547-550.


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