Equis ISSN 2398-2977

Equine infectious anemia (EIA)

Synonym(s): EIA, Swamp fever

Contributor(s): Christopher Brown, Susan Dawson, Melissa Kennedy, Prof Derek Knottenbelt, Ruth Morgan, Vetstream Ltd

Introduction

  • Widespread virus infection within relatively defined geographical areas transmitted by transfer of blood (especially by biting flies) or blood products.
  • Cause: equine infectious anemia virus - a lentivirus which replicates and persists in tissue macrophages from where it is released intermittently to cause recurrent bouts of disease Equine infectious anemia virus.
  • Signs: highly variable - acute, subacute, chronic and subclinical syndromes all resulting in progressive anemia.
  • Diagnosis: clinical signs, hematologic changes, enzyme-linked immunosorbent assay (ELISA) or agar gel immunodiffusion test (Coggins test).
  • Treatment: no specific treatment available.
  • Prognosis: most recover from acute/subacute syndromes but all are permanently infected; many chronic cases die/euthanized; asymptomatic carriers common following subclinical infections.
  • Carrier horses are of serious concern to State Veterinary Health Authorities, and is a notifiable disease in the US.
  • In the UK, EIA is notifiable by law under the Infectious diseases of Horses Order 1987.
Print off the Owner factsheet on Equine infectious anaemia - EIA to give to your clients.

Pathogenesis

Etiology

  • EIA virus Equine infectious anemia virus - is a lentivirus of the retrovirus family which contains reverse transcriptase, allowing conversion of the viral RNA into complimentary DNA, which can be inserted into the host DNA and persist indefinitely.

Predisposing factors

General

  • Presence of carrier animals.
  • Low immunity to the disease (outside endemic areas).
  • Stressors in carriers with subclinical infection.

Specific

Pathophysiology

  • Virus transmitted between horses by transfer of blood or blood products. Other transmission methods have also been suggested.
  • Biting flies often involved.
  • Iatrogenic, transplacental and colostral transmission can occur.
  • Subclinical carrier animals act as an important source.
  • Virus replicates in macrophages → released into circulation → recurrent bouts of pyrexia and disease.
  • The virus is protected from the host's immune response whilst in the macrophages.
  • Anemia is due to hemolysis of RBCs, to which IgG/IgM or complement is bound.
  • Eventually post-immune responses are stimulated sufficiently to prevent bouts of viremia.
  • Antigenic drift is probably the reason for undulant fever and episodes of disease.
  • Disease may be eliminated or persist as a carrier infection. Carriers may be/are seropositive.
  • Bone marrow suppression is also involved - possibly similar to the anemia of chronic inflammation.
  • Replication of virus within macrophages of liver, spleen and lymph nodes → release into circulation → clearance by cell-mediated and humoral immune responses.
  • Virus persists in macrophages and undergoes rapid antigenic variation allowing recurrent replication and release of large quantities of virus.
  • When sufficient host immune response is stimulated recurrent bouts of disease cease.
  • Necrotizing vasculitis Vasculitis affecting a variety of organ systems including heart, kidney and CNS may accompany infection.
  • Lesions are attributable in part to immune-mediated tissue damage, eg immune complex deposition.

Timecourse

  • The first acute stage lasts from 103 days.
  • The second chronic stage can last up to 12 months.
  • The chronic subclinical stage can last indefinitely.

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.
  • van Maanen C (2013) Progressive control of equine infectious anaemia through more accurate diagnosis. Vet Rec 172 (8), 208-209 PubMed.
  • Issel C Jet al (2013) Challenges and proposed solutions for more accurate serological diagnosis of equine infectious anaemia. Vet Rec 172 (8), 210 PubMed. 
  • Murakami K, Konishi M, Kameyama K & Shibahara T (2012) Detection of equine infectious anaemia virus in native Japanese ponies. Vet Rec 171 (3), 72 PubMed.
  • Brangan P, Bailey D C, Larkin J F, Myers T & More S J (2008) Management of the national programme to eradicate equine infectious anaemia from Ireland during 2006: A review. Equine Vet J 40 (7), 702-704 PubMed.
  • More S J, Aznar I et al (2008) An outbreak of equine infectious anaemia in Ireland during 2006: Investigation methodology, initial source of infection, diagnosis and clinical presentation, modes of transmission and spread in the Meath cluster. Equine Vet J 40 (7), 706-708 PubMed.
  • More S J, Anzar I et al (2008) An outbreak of equine infectious anaemia in Ireland during 2006: The modes of transmission and spread in the Kildare cluster. Equine Vet J 40 (7), 709-711 PubMed.
  • 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.
  • Cullinane A et al (2007) Diagnosis of equine infectious anemia during the 2006 outbreak in Ireland. Vet Rec 161 (19), 647-652 PubMed.
  • Lucas M H & Davies T H R (1995) Exotic disease series - equine infectious anemia. Equine Vet Educ (2), 89-92 VetMedResource.
  • Tashjian R J (1984) Transmission and clinical evaluation of an equine infectious anemia herd and their offspring over a 13 year period. JAVMA 182, 298-304 VetMedResource.

Other sources of information

  • Horserace Betting Levy Board (2016) 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:enquiries@hblb.org.uk; Website:http://codes.hblb.org.uk.


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