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9 Cards in this Set

  • Front
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Equine viral arteritis: Etiology
1) Enveloped + strand RNA virus
2) Super family nidovirales, family arteriviridae, genus arterivirus
3) Occurs worldwide
4) genetic diversity
5) breed predisposition: a) standardbreds (70-90% sero+), b) low incidence (2-3%) in Thoroughbreds
EVA: Transmission
1) Respiratory and venereal during acute phase
2) Venereal only during carrier state
EVA: Clinical signs
1) subclinical/clinical depends on dose and virulence of strain
2) more severe in young, old, and debilitated animals
3) incubation: 3-14 days (aerosol), 6-8 days (venereal)
4) fever, leukopenia, anorexia, depression, edema, rhinitis and conjunctivitis (serous--> mucopurulent), skin rash
5) abortions-- occur almost immediately after onset of respiratory signs
6) low mortality
7) acute infection--> PI in 30-60% of Standardbred stallions (not mares)
EVA: Pathogenesis of EVA
EVA infection--> 24hrs-- EAV in macrophages--> 48 hrs-- EAV in satellite lymph nodes--> 3 days-- EAV in endothelium and circulating monocytes--> Systemic distribution of EAV (male carrier state)--> 6-8 days-- EAV in blood vessel endothelium and medial myocytes--> 10 days-- severe damage to blood vessels (abortion infected newborn)--> 10-21 days-- EVA in renal tubular epithelium. Shedding of virus in urine
EVA: pathogenesis of EAV Abortion
Leukocyte associated viremia. EAV infectes urterine blood vessels and myometrium--> 1) vasculitis and myometritis w/ ischemia followed by precocious chorionic detachment--> Uninfected aborted fetus. 2) EAV infects arcolar trophoblast chorionic mesencyme and sporadically, the fetus--> Infected aborted fetus or infected newborn foal
EAV: Gross Lesions
1) Edema
2) congestion and hemorrhages in subcu tissues, lymph nodes, and viscera
3) Yellowish clear exudate in body cavities
4) affected neonates have hemorrhages and lung congestion
Histologic lesions
1) blood vessels: vasculitis w/ fibrinoid necrosis of the tunica media, perivascular infiltration and endothelium loss
2) Lungs: mild to severe interstitial pneumonia; pulmonary arteritis and phlebitis; hypertrophy and hyperplasia of pneymocytes
3) Lymphoid tissue: lymphoid follicle necrosis, edema
4) Kidnay: Interstitial nephritis, possible tubular necrosis
5) Skin: Evidence of vasculitis. Skin biopsy for histopath and or IHC
EAV: Diagnosis
1) clinical signs
2) Abortions seen shortly after respiratory phase
3) no gross lesions in aborted fetuses
4) should be differentiated from infection w/: a) EHV1,4, b) equine influenza virus, c) equine adenovirus, d) equine rhinovirus
5) Virus isolation (cumbersome): nasopharyngeal and conjunctival swabs; citrated blood
6) PCR or VI: semen, refrigerate citrated blood; send others on dry ice
7) Histopath or IHC
8) VN or paired sera
EAV: Prevention and control
1) MLV: a) safe for stallions and non-preg mares, b) don't give to mares in last 2 mos. of gestation or to foals < 6 wks
2) Segregation of pregnant mares from other horses
3) Isolation (3-4 wks): a) horses from other farms, b) horses bought at sales, c) horses returning from racetracks