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Equine viral arteritis (EVA)


Synonym(s): EVA, infectious cellulitis, pink eye, equine typhoid


  • A contagious disease of equids associated with a panvasculitis and viral replication in cells of blood vessel walls and reticuloendothelial system.
  • Cause: equine arteritis virus (EAV) Equine viral arteritis virus spread by the respiratory or venereal route.
  • Signs: respiratory, conjunctivitis; dependent, especially limb edema, abortion, neonatal pneumonia, enteritis.
  • Diagnosis: virus isolation detection, antigen detection, serology, paired sera.
  • Treatment: not indicated except in severely affected animals, especially stallions.
  • Prognosis: uneventful recovery in majority of adult horses; can cause abortion and mortality in neonatal foals; carrier stallions shed virus in semen.
Print off the Owner factsheet on Equine viral arteritis - EVA to give to your clients.



Predisposing factors


  • Severity of clinical signs can be exacerbated in horses kept under poor management, of advanced age or undergoing physical stress, eg in training, or under harsh climatic conditions.



  • Viral replication occurs in cells of the reticuloendothelial system, most components of the cardiovascular system and in parts of the reproductive tract in the carrier stallion, especially certain areas of the accessory sex glands.
  • Initial replication → dissemination → panvasculitis.
  • Virus enters lung in droplet form → initial replication in bronchial and alveolar macrophages → satellite lymph nodes, especially bronchial nodes → leukocyte-associated viremia → secondary replication in endothelial cells → endothelial damage → neutrophil infiltration and penetration of virus to medial cells → vascular damage → lung edema, pleural effusions → virus disseminates throughout the cardiovascular system → panvasculitis.
  • Virus is eliminated by mares, geldings and immature colts within a few weeks of infection and they do not become carriers.

EAV abortion

  • Myometrial necrosis and edema → placental detachment → fetal death.

Carrier stallions

  • Virus persistence is mediated directly or indirectly by testosterone → virus persists in certain accessory sex glands → shed constantly in semen → venereal spread/artificial insemination → susceptible mare → respiratory spread.
  • Frequency of the carrier rate in stallions can be very variable; it can be as high as 70% in naturally infected stallions of certain breeds.
  • Shedding may cease within 12 months, but has been reported to continue for 12 years or longer.
  • Development of the carrier state following vaccination with a modified live virus vaccine has never been reported.


  • Incubation period: 2-13 days.


  • Respiratory transmission: most frequent.
  • Venereal transmission by acute or chronically infected stallions which shed the virus in semen.
  • From semen and semen products used in artificial insemination - neither, chilling, freezing nor antibiotics used in semen extenders inactivate the virus.
  • Congenital infection of foal where mare exposed to infection very late in pregnancy.
  • Venereal transmission of the virus can also occur in the case of the acutely infected mare.


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Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Bażanów B A et al (2014) Abortogenic viruses in horses. Equine Vet Educ 26 (1), 48-55 VetMedResource.
  • Balasuriya U R R, Go Y Y & Maclachlan N J (2013) Equine arteritis virus. Vet Microbiol 167 (1-2), 93-122 PubMed.
  • Chung C C et al (2013) Comparison of an improved competitive enzyme-linked immunosorbent assay with the World Organization for Animal Health-prescribed serum neutralization assay for detection of antibody to Equine arteritis virus. J Vet Diag Invest 25 (2), 182-188 PubMed.
  • Pronost S et al (2010) Description of the first recorded major occurrence of equine viral arteritis in France. Equine Vet J 42 (8), 713-720 PubMed.
  • Duthie S, Mills H & Allen W R (2008) The efficacy of a commercial ELISA as an alternative to virus neutralisation test for the detection of antibodies to EAV. Equine Vet J 40 (2), 182-183 PubMed.
  • Barbacini S (2005) An outbreak of equine arteritis virus infection in a stallion at a Trakehner studfarm. Equine Vet Educ 17 (6), 294-296 VetMedResource.
  • Wood J L N & Newton J R (2005) The continuing challenge of EVA. Equine Vet Educ 17 (6), 297-298 VetMedResource.
  • Cullinane A A (2004) Testing for equine arteritis virus (Letter). Vet Rec 155 (20), 647-648 PubMed.
  • Del Piero F (2000) Equine viral arteritis. Vet Pathol 37 (4), 287-296 PubMed.
  • Newton J R, Wood J L, Castillo-Olivares F J & Mumford J A (1999) Serological surveillance of equine viral arteritis in the United Kingdom since the outbreak in 1993. Vet Rec 145 (18), 511-516 PubMed.
  • Parker J (1999) Control of equine viral arteritis. Vet Rec 144 (7), 186 PubMed.
  • Glaser A L, de Vries A A, Rottier P J, Horzinek M C & Colenbrander B (1996) Equine arteritis virus - a review of clinical features and management aspects. Vet Q 18 (3), 95-99 PubMed.
  • Chirnside E D (1995) Equine viral arteritis - A free market threat. Equine Vet Educ 5 (3), 137-139 VetMedResource.
  • Wood J L N (1994) Equine viral arteritis - progress in the last 100 years? Equine Vet Educ 6 (6), 348-350 VetMedResource.

Other sources of information

  • Horserace Betting Levy Board (2019) Codes of Practice. 5th Floor, 21 Bloomsbury Street, London WC1B 3HF, UK. Tel: +44 (0)207 333 0043; Fax: +44 (0)207 333 0041; Email:; Website:
  • Timoney P J (2002) Equine Viral Arteritis. In: Equine Respiratory Diseases. Ed: Lekeux P.
  • British Equine Veterinary Association (1999) Equine Viral Arteritis. In: Newsletter No. 98. April 1999. Website:
  • British Equine Veterinary Association (1999) Code of Practice on the use of AI in the UK. 5 Finlay Street, London SW6 6HE, UK. Website:
  • Wood J L N Diagnosis and Control of Equine Viral Arteritis. Animal Health Trust Virology Insights No. 1.

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