ISSN 2398-2977      

Eastern Equine Encephalomyelitis virus


Sarah Binns




  • Family:Togaviridae.
  • Genus:Alphaviridae.
  • Originally Group A Arboviruses.


  • L:tegere- to cover ('toga').
  • Gk:alpha- first letter of alphabet.

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Clinical Effects



  • Mosquitoes are biologic vectors.
  • Seasonality of infections corresponds to mosquito activity.
  • Reservoir (overwintering) hosts may be other mammals, birds, amphibia and reptiles.


  • Mosquito vector ingests infective blood meal.
  • Vector is infected by virus if host is sufficiently viremic. Does not act purely as mechanical vector.
  • Virus initiates infection in insect's gut, and is eventually distributed to the salivary glands.
  • Replication in salivary glands allows transmission to further hosts.
  • Vector remains infected for life.


  • Primary transmission cycle of EEE involves swamp mosquitoes and birds, with occasional spillover into horses, human beings, and domestic birds, especially pheasants.
  • Horses and human beings have minimal viremia, and are therefore not an important source of virus.
  • Transmission may also occur directly between birds via pecking.

Pathological effects

  • Inflammatory response occurs within 4-5 days of infection.
  • Response involves antibody production, production of interferon, and activation of natural killer cells. These may limit virus replication and spread, and prevent reinfection.
  • Peak antibody titers develop within 2 weeks, against all virus proteins.
  • Antibodies may neutralize virus, enhance virus clearance, and mediate complement or killer-cell-dependent lysis.
  • Local antibodies may also be produced in the CNS.
  • Cell-mediated immunity may aid in virus clearance and protective immunity. Cytotoxic T-cells may appear 3-4 days post-infection.
  • Most equine, human and avian infections with EEE are severe, in horses the disease is often fatal (mortality rates of 75-98% have been reported)   Equine viral encephalitides  .
  • Infection follows the bite of an infected insect.
  • Primary virus replication occurs locally and in adjacent lymph nodes. Accompanied by fever, which may be subclinical.
  • Primary viremia persists for several days and infects target organs, and is followed by secondary viremia.
  • If viremia sufficiently severe, virus enters central nervous system via exposed nerve endings or neuromuscular junctions.
  • Necrotizing encephalitis results 1-3 weeks post-infection. Clinical signs begin as behavior change, progressing to dementia.
  • Lesions may develop throughout grey matter of brain, and include neuronal degeneration, vascular cuffing, neutrophil and lymphocyte infiltration, microglial proliferation, and hemorrhage.
  • Much of the CNS pathology may be immune-mediated.
  • Necrotic lesions may also be found in lymphoid tissues (myeloid depletion of bone marrow, spleen and nodes), pancreas, adrenal cortex, liver, myocardium, and small blood vessels.
  • Death is usually due to respiratory arrest 2-3 days after onset of CNS signs.
  • Surviving horses may have residual CNS damage, eg visual deficits, behavioral or learning disabilities. They are often called 'dummies' or 'sleepers'.

Other Host Effects

  • Subclinical infection of horses is rare with EEE.
  • Species other than horses, human beings and birds may show subclinical infection, eg cats, dogs, hamsters, mice, squirrels, amphibians and reptiles. These animals, together with wild swamp birds, may form the overwinter reservoir of EEE.


Control via animal

  • Treatment is rarely successful; supportive and symptomatic therapy may be attempted.
  • In early cases, ensure adequate food and water supply, using tube feeding   Gastrointestinal: nasogastric intubation  or intravenous fluids   Fluid therapy: overview  if necessary.
  • Nursing to minimize effects of recumbency and self-inflicted trauma.

Control via chemotherapies

  • No specific antiviral agents currently available.
  • Intravenous dimethylsulfoxide   Dimethyl sulfoxide  (not licensed for this use) or mannitol   Mannitol  may have diuretic and anti-inflammatory effects. Alternatively, furosemide   Furosemide  can be used.
  • Anti-inflammatories   Therapeutics: anti-inflammatory drugs  , eg dexamethasone   Dexamethasone  , may be indicated to reduce inflammation.
  • High fevers can be treated with antipyretics.
  • Seizure control may be attempted with barbiturates, diazepam   Diazepam  , chloral hydrate or guaifenesin   Guaifenesin  .

Control via environment

  • Mosquito control measures are important.
  • Eliminate mosquito breeding sites by water control or spraying programmes.


  • Vaccination may be beneficial in the face of an outbreak.
  • As the duration of immunity is unknown, recovered animals should also be vaccinated.
  • Protective levels of antibody may develop as early as 3 days after vaccination.
  • For routine protection, horses should be given 2 doses of vaccine 3-4 weeks apart, with inactivated vaccine one month before the mosquito season followed by annual boosters.
  • Both intradermal and intramuscular vaccines are available.
  • Inactivated vaccines are safe for use in pregnant mares.
  • Maternal antibodies usually decline by 2 months of age, but may persist, therefore foals of vaccinated mares should be given a series of 2-3-monthly vaccinations beginning at 2-4 months of age. They should then be re-vaccinated at 6 and 12 months.


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Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Linssen B et al (2000) Development of reverse transcription-PCR assays specific for detection of equine encephalitis viruses. J Clin Microbiol 38 (4), 1527-1535 PubMed.
  • Patterson J S, Mes R K, Mullaney T P & Benson C L (1996) Immunohistochemical diagnosis of eastern equine encephalomyelitis. J Vet Diagn Invest (2), 156-160 VetMedResource.
  • Gregory C R, Latimer K S, Niagro F D et al (1996) Detection of eastern equine encephalomyelitis virus RNA in formalin-fixed, paraffin-embedded tissues using DNA in situ hybridization. J Vet Diagn Invest (2), 151-155 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.

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