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16 Cards in this Set

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  • Back
Equine Infectious Anemia: Etiology
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
Equine Infectious Anemia: Acute phase
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
Equine Infectious Anemia: Recurrent phase (growing, subacute)
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
Equine Infectious Anemia: Inapparent carrier phase
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
Exposure to less virulent strain or lower innoculum
1) mild fever
2) mild thrombocytopenia
3) sero- until 30-45 days post-exposure
Equine infectious anemia: Transmission
1) interrupted feeding by horseflies and dderflies
2) contaminated needles/instruments
3) transplacental-colostral (uncommon)
4) venereal (uncommon)
Factors influencing transmission
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
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
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
Antibody-dependent enhancement
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
Equine Infectious Anemia: Fever
High fever (106-107) results form release of inflam cytokines (IL 1 and 6; TNF-alpha)
1) infectious immune complexes attach to circulating platelets via Fc or complement receptors
2) coated platelets removed from circulation by tissue macrophages
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
IgG and C3 are present in glomerular basement membrane in ~75% of EIAV-infected horses
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
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