ETIOLOGY

The causal agent is an arterivirus, an RNA virus of the family Togaviridae. It is the sole member of the genus.⁵ Several strains of the EVA virus with varying degrees of virulence have been reported, with only one antigenic type.^6–8 The prototype is the Bucyrus strain from the originally diagnosed outbreak,¹ and its virulence contrasts sharply with the clinically inapparent infections transmitted by many long-term carrier stallions.^6,9

EPIDEMIOLOGY

Equine viral arteritis was first recognized in 1953 following an outbreak of severe respiratory disease and abortion in Bucyrus, Ohio, and additional outbreaks occurred in Ohio, Indiana, California, and Kentucky.¹ From then to 1984 there were relatively few reports of EVA, although infection appears to be widespread.^5,10,11 Outbreaks of clinical disease are infrequent and occur mainly in mares on breeding farms where up to 50% abort.

A serologic survey revealed 70% to 90% of Standardbred mares and less than 3% of adult Thoroughbreds to be EVA seropositive.¹⁰ The first recorded outbreaks at racetracks in Standardbreds were reported in 1977. The outbreak of EVA in Kentucky in 1984 was the first reported occurrence in Thoroughbreds in North America.⁵ There was considerable variation in severity in the 1984 outbreak, with affected mares exhibiting a variety of clinical signs from commonly reported EVA lesions to inapparent infection.^5,6 There were no associated deaths or confirmed cases of abortions. All affected mares made complete, uneventful recoveries. In confirmed outbreaks of EVA since 1984, abortion occurred infrequently.⁶

Horses are the only host of EVA virus, and all ages are susceptible. EVA spreads rapidly in groups of susceptible horses. Mortality rate is low in natural outbreaks, and after recovery, affected horses have prolonged immunity. Currently, the EVA virus is so avirulent that clinical signs are not obvious or are mild when sporadic outbreaks occur.^2,6,10

TRANSMISSION

Susceptible mares can be infected by inhalation of aerosols from infected horses, and respiratory spread is a major method of transmission of EVA virus in barns, at pasture or sales, and at racetracks.^1,11 Droplets from nasal exudate of infected horses remain infectious for up to 10 days in the environment. Abortion from natural or experimental infection occurs 23 to 57 days after exposure and from 6 to 29 days after the onset of fever.¹²

Venereal transmission from infected stallions to susceptible mares played a significant role in the widespread dissemination of EVA during the 1984 outbreak.^6,9,13 Sexually infected mares transmitted EVA virus to susceptible mares by contact.^6,12 Virtually 100% transmission of EVA virus occurred in susceptible mares bred to long-term shedding stallions during the 1984 outbreak, so clinical infection must have been mild and undetected. Venereal transmission was a major method of spread of EVA on breeding farms.^5,6

The role of indirect contact with virus-contaminated fomites varied with outbreaks.⁶ The role of teaser stallions and nurse mares, although a potential risk, was apparently insignificant in the 1984 outbreaks.⁶

The EVA virus is present in fluids and tissues of aborted fetuses and placentae, which could potentially result in indirect lateral spread of infection.¹ Foals of immune mares are resistant to infection until the loss of colostral antibodies at 2 to 6 months of age.

Carriers of EVA virus are important in perpetuating infection in horse populations. The duration of the carrier state in stallions shedding the virus in semen can vary from weeks to years.^6,9 The frequency of long-term carriers is approximately 30% to 35%. Following experimental infection with EVA, the virus is shed in semen for months, and the ampulla and bulbourethral glands appear to be preferred sites for viral infection.¹³ There is little evidence, however, to indicate that mares are EVA carriers with any appreciable frequency. Evidence of congenital infection in foals is lacking.⁶