Page 58 - 2020 Stallion Register
P. 58

 Understanding
EQUINE VIRAL ARTERITIS
By Megan Petty, DVM
Those of us in New Mexico who are associated with breeding stallions are likely familiar with Equine Viral Arteritis, or EVA, because we receive our reminder in the fall that it’s time for our stallion to get his annual EVA vaccine. However, many do not fully understand the significance of this disease, or why this annual vaccination for our stallions is of any importance. You aren’t alone if you don’t know much about EVA, though. It wasn’t until a huge outbreak in 1984 in Kentucky that we gained a greater understanding of how EVA works and the potential ramifications of the disease.
EVA is caused by the Equine Arteritis
Virus (EAV) which is a small RNA virus that replicates in the cells in the walls of arteries
in the equine body. This replication causes inflammation of the vessels, or vasculitis. Vasculitis manifests in many clinical symptoms which occur as a direct result of the compromise of the vessels throughout the body. The symptoms commonly seen with EVA include fever; edema of the lower limbs, scrotum, udder, or ventral midline; conjunctivitis and tearing; skin lesions; inflammation of the nasal passages
and nasal discharge. Additionally, abortion in pregnant mares can be a hallmark of the disease as well. Unfortunately for those of us in the horse industry, EVA also often occurs with ZERO clinical symptoms. This not-so-unusual subclinical infection is part of the reason this disease flew under the radar for so long.
THERE ARE 2 PRIMARY ROUTES OF TRANSMISSION OF EVA:
1. Aerosol-inhaled viral particles transmitted
through infective nasal secretions or urine 2. Venereal-which was the lesson learned from
the 1984 Kentucky outbreak.
Mares and geldings who are exposed to
EVA generally clear the infection in 60
days with little lasting effect except long-term immunity to the virus. Sexually mature colts and stallions, on the other hand, aren’t so lucky. 30-60% of acutely infected stallions become persistently infected and maintain the virus
in their reproductive tract, specifically in the ampullae and vas deferens. These stallions will continuously shed viral particles in their semen,
making them a dangerous source of infection. Mares who become infected via the venereal route may not display any clinical symptoms, but will shed large amounts of the virus from nasal secretions and urine, leading to lateral infections through the aerosol route of transmission.
The presence of testosterone is critical for the maintenance and persistence of the infection in stallions, thus why mares and geldings are able
to clear the infection and not become carriers themselves. Three stallion carrier states have been identified which include short-term (several week duration), medium term (3-9 months duration), and long-term (chronic, years of duration). These variable periods of carrier state likely depend on multiple factors including host immune response and the individual infecting viral strains. The reason this carrier state is so important, in addition to the insidious nature of infection, is that the semen remains infective whether fresh, cooled, or frozen. 85-100% of previously EAV negative mares will become positive when bred with infected semen, but the presence of the virus does not have a negative effect on fertility or conception rates. Mares who are infected between 3-10 months of
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