Equine Infectious Anemia

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Equine Infectious Anemia: Etiology

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1) enveloped RNA virus
2) Retroviridae
3) Lentivirus
4) other members of this genus: FIV, HIV, and CAEV
5) gp 45 and gp90: mutations result in appearance of novel antigenic variants--> recrudescence
6) most abundant core protein is p26

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Equine Infectious Anemia: Acute phase

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1) Fever*
2) thrombocytopenia*
3) depression
4) mild to moderate anemia 7-30 days post-infection
5) virus titer in serum increases in parallel w/ the febrile response
6) virus replication takes place in almost all tissues, especially in tissue macrophages
7) few horses die, most recover by have recurrences

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Equine Infectious Anemia: Recurrent phase (growing, subacute)

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1) Recurrences are associated w/ fever, cell-free viremia, thrombocytopenia and depression
2) most recurrent episodes happen in first year following acute phase. Intervals btwn fever peaks increase w/ time
3) recurrent phase--> chronic debilitating infx in some horses--> mostly goes to carrier phase
4) most severe anemia in this phase

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Equine Infectious Anemia: Inapparent carrier phase

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1) horse clinically normal
2) low level of virus in bloodstream
3) low chance of transmission
4) stress can lead to higher level of viremia
5) Horses are sero+ for life

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Exposure to less virulent strain or lower innoculum

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1) mild fever
2) mild thrombocytopenia
3) sero- until 30-45 days post-exposure

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Equine infectious anemia: Transmission

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1) interrupted feeding by horseflies and dderflies
2) contaminated needles/instruments
3) transplacental-colostral (uncommon)
4) venereal (uncommon)

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Factors influencing transmission

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1) distance btwn horses
2) stage of infection: a) febrile horses have 1,000 to 100,000 more virus in blood stream, b) virus is cell-associated in inapparent carriers
3) Vector size

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Viremia

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result of replication of the virus in tissue macrophages of liver, spleen, lymph nodes, lung, and adrenal glands and subsequent release of virus from these cells

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Persistance

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1) Occurs in a subpop of tissue macrophages
2) virus isolates from sequential febrile episodes show that each isolate is unique w/ random variation in structural glycoproteins
3) moe feasible due to chromosomal integration of cDNA

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Antibody-dependent enhancement

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1) most virus in serum consists of infectious antigen-Ab complexes: a) called antibody dependent enhancement (ADE), b) enhances pathogenicity of virus by entering macrophages by uptake via Fc receptor

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Equine Infectious Anemia: Fever

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High fever (106-107) results form release of inflam cytokines (IL 1 and 6; TNF-alpha)

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Thrombocytopenia

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1) infectious immune complexes attach to circulating platelets via Fc or complement receptors
2) coated platelets removed from circulation by tissue macrophages

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Anemia

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1) virus can attach directly to RBCs via env. glycoprotein-- attracts Ab and complement--> intravascular lysis
*2) virus-antibody complexes attach to RBC via Fc receptors-- complement activated--> intravascular hemolysis
*3) Macrophages and neutrophils phagocytose coated RBCs--> extravascular hemolysis
4) hemolytic anemia + impaired bone marrow response

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Glomerulonephritis

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IgG and C3 are present in glomerular basement membrane in ~75% of EIAV-infected horses

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Diagnosis

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1) Clinical signs-- recurrent fever, thrombocytopenia, anemia, ventral edema, weight loss
2) Coggins test-- tests for antibodies to p26 core antigen. Only detectable after 45 days post-exposure
3) ELISA

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Control

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1) most states require a negative EIA w/in 6 or 12 mos of travel into that state
2) Permanent ID of + horses
3) Life-long quarantine at least 200 yds away from other equidae
4) interstate travel regs