Transmission of the virus occurs by either sexual contact or inhalation.  The virus is shed in the semen of carrier stallions, which are the reservoir for EVA in the equine population.  The carrier state can last months to years.  Fresh, chilled, and frozen semen from a carrier stallion can infect mares bred by artificial insemination.  Infected horses also transmit the virus through aerosolization and subsequent inhalation by a susceptible horse.

   EVA can be a diagnostic challenge because the clinical signs are variable and non-specific.  Some horses are very mildly affected while others are so severely affected that the disease is fatal.  Interestingly, there is breed-specific variation in EVA seroprevalence.  Standardbred seroprevalence has been reported to be as high as 80%, although no breed-specific disease susceptibility has been discerned.  There are differences based upon the signalment of the animal in question as well.  A racehorse may manifest EVA as one or more of the following signs: pyrexia (up to 105°F),  anorexia, depression, nasal and ocular discharge, coughing, skin rashes, and/or edema, with dependent and periorbital edema being the most common.  Some of the less common clinical signs include ataxia, papules on mucosal surfaces, severe respiratory distress, and lymphadenopathy.  Abortion may be the only clinical sign of EVA infection in a pregnant mare, although they can also have the aforementioned clinical signs followed by abortion.  A neonatal foal infected with EVA will usually show severe respiratory distress and die within 24 hours.  All of the clinical signs seen are related to the panvasculitis that occurs when the horse is infected with EVA.  The virus replicates within macrophages, mesothelium, and endothelium.

   If there is suspicion of Equine Viral Arteritis, standard blood work will not provide much helpful information.  The only parameter that may be useful  is the evidence of leukopenia seen on the CBC.  The next best step would be to submit paired serology samples, one acute and the other convalescent.  A fourfold increase in the EVA titer would be highly suggestive of infection.  A single serology test for EVA titer is of limited usefulness as horses can be exposed and seroconvert without becoming clinically ill.  In an outbreak situation, the best samples to collect from exposed horses that may be early in the disease process are nasopharyngeal swabs or washes, conjunctival swabs, and blood samples collected in EDTA tubes.  In mares that abort, the virus can sometimes be isolated from the placenta or fetal tissues.  Additionally, the mare can be evaluated for seroconversion and an endometrial biopsy can be tested by Polymerase Chain Reaction (PCR) and virus isolation.  At necropsy, immunohistochemistry and virus isolation are useful diagnostic tools.  There has also been a report of an antemortem diagnosis of EVA using immunohistochemistry on skin biopsy samples although, to date, this method is not widely used.

  Prevention of Equine Viral Arteritis can be accomplished through proper testing and vaccination protocols.  There are both modified live and killed vaccines available.  The modified live vaccine only protects against clinical signs of EVA, and may only be partially effective.  The killed vaccine protects against infection.  The immune response produced by the vaccines may be protective for up to two years, although annual boosters are recommended at least 21 days before the start of the breeding season.  All breeding stallions should be tested for carrier status.  If the stallion is a known carrier, the mares to which he is bred should be seropositive before coitus or artificial insemination, either via natural infection or vaccination.  If the stallion is EVA negative, this should be documented; the stallion should then be vaccinated annually 28 days prior to the start of each breeding season.  Young colts that may be used as breeding stallions in the future should be vaccinated after the maternal antibodies have declined, typically between two and six months of age.  To be certain that there will be no maternal antibody interference, the colts are usually given the first vaccine between 6-12 months of age and then annually thereafter.  It is worthwhile to note that animals that are vaccinated may not be eligible for export to certain countries because it is not possible to differentiate natural infection from vaccine seroconversion.

  Although Equine Viral Arteritis is not a widely prevalent disease, it can cause significant problems on breeding farms and racetracks in the event of an outbreak.  It is important that this disease remains on the differential list, and that equine practitioners are aware of the best samples to submit for EVA testing.  Proper testing and vaccination strategies could effectively eliminate this disease from the equine population.

-by Amber Boring, Class of 2009
-edited by Dr. Ryan Jennings, ADDL Graduate Student

References

1. Smith BP: 2002.  Large Animal Internal Medicine. 3^rd ed.

2. DelPiero F: 2006.  Equine Viral Arteritis: Signs, Lesions, Pathogenesis, and Diagnoses.  Proceedings of the annual meeting of the American College of Veterinary Pathologists and the American Society of Veterinary Clinical Pathology.