Equine Viral Arteritis

CHAPTER 35 Equine Viral Arteritis

Equine viral arteritis (EVA) is an acute contagious disease of equids, characterized principally by fever, dependent edema, respiratory signs, and the potential for abortion in pregnant mares. The causal agent is equine arteritis virus (EAV), which can also persist in the reproductive tract of some infected stallions for an extended period. The disease was first etiologically defined following an extensive outbreak of respiratory disease and abortion on a Standardbred breeding farm near Bucyrus, Ohio, in 1953.

For more than 30 years after the etiology and pathologic features had been elucidated, EVA garnered little attention from the equine industry and even less from the national and international scientific community. That changed dramatically in 1984, however, when outbreaks of the disease developed on numerous Thoroughbred breeding farms in central Kentucky. Widespread concern was expressed over the likelihood of the virus becoming widely disseminated through movement of horses and the significant risk of abortion outbreaks in populations of unprotected pregnant mares. To mitigate the risk of this occurring, most countries imposed stringent requirements governing international trade in horses for breeding or performance purposes. Although most countries have since eased their import requirements regarding EAV, some continue to permit entry of horses only if they are seronegative for antibodies against the virus.

For many years, EVA was considered a disease solely of members of the family Equidae. A recent report, however, suggests that EAV can also infect certain nonequid species, specifically alpacas. There is no evidence that the virus can be transmitted to humans.

In the 50 years since its initial isolation in 1954, evidence of EAV infection has been found in equine populations in many countries. Very few countries (such as Japan and Iceland) have been confirmed to be free of the virus. The prevalence of infection can vary as widely among countries as it can among horse breeds in the same country. The prevalence of infection is frequently greater in Standardbreds and certain Warmblood breeds. A national survey conducted in the United States in 1998 revealed that only 2% of unvaccinated horses were seropositive for antibodies against EAV.

Notwithstanding the widespread global distribution of EAV and the prevalence of infection in certain breeds, laboratory-confirmed outbreaks of EVA have been relatively infrequent, being recorded only in Europe and North America. There are indications that this situation is changing, however, with an increase in the frequency of disease outbreaks reported in the past 15 to 20 years. Whereas this upward trend may reflect in part a greater industry awareness of EVA and improved diagnostic capability, it is considered to be primarily a result of continued increase in the volume of international trade in horses and semen that has taken place during this period.


The natural and experimental host range of EAV appears to be restricted primarily to equids. Despite the extensive distribution of the virus in the world, outbreaks of EVA are relatively uncommon and are most frequently associated with movement of horses or use of shipped semen. Although widespread transmission can occur at racetracks or on breeding farms, such occurrences are not always characterized by clinical disease. It must be reiterated that most horses with natural infections with EAV are asymptomatic.

A range of virus-, host-, and environment-related factors is known to be involved in the epidemiology of EVA, including variation in pathogenicity and other phenotypic characteristics among naturally occurring strains of EAV, modes of transmission during acute and chronic phases of infection, occurrence of the carrier state, nature of acquired immunity to infection, and economic trends in the horse industry.


Transmission of EAV may occur by respiratory, venereal, congenital, or indirect means. Although shed in various secretions and excretions of acutely infected horses, EAV is found in the greatest quantity in respiratory tract secretions. Infectious virus has been detected for 7 to 16 days in nasopharyngeal swabs collected during the acute phase of the infection. Not surprisingly, therefore, respiratory transmission is the primary means of spread of EAV at performance events, horse sales, equine hospitals, on farms, and wherever horses are congregated. Evidence indicates that close, direct contact with an acutely infected horse is necessary for virus transmission by this route. Compared with the other important viral respiratory pathogens of the horse, EAV is not as contagious as equine influenza virus or equine herpesviruses 1 or 4, perhaps because aerosol transmission does not play as significant a role in spread of the virus as it does in the other two diseases. EAV can also be transmitted venereally by an acutely infected stallion or mare.

Except for certain stallions and postpubertal colts in which the virus can persist in the reproductive tract, specifically the accessory sex glands, EAV is no longer detectable in most body fluids or tissues beyond 28 days after infection. Disappearance of the virus from serum coincides with the appearance of homologous serum neutralizing antibodies.

Although not frequently regarded as epidemiologically significant, EAV can be spread on breeding farms, racetracks, or other equine establishments by indirect means through shared use of tack or breeding shed equipment. Virus can also be transferred on the hands of personnel or through contact with infective material on the apparel of individuals not observing appropriate sanitary safeguards when handling infected horses.

Carrier State

Field and experimental studies conducted since 1984 have confirmed a carrier state in sexually mature intact males, including postpubertal colts and stallions, but not in fillies, mares, or geldings. Establishment and persistence of EAV in the reproductive tract of stallions is testosterone dependent. Frequency of the carrier state can vary among breeds, ranging from less than 10% to greater than 70%. EAV localizes primarily in the accessory sex glands of the reproductive tract, especially the ampullae of the vasa differentia, where it can persist for weeks, months, or years. Carrier stallions shed the virus constantly in the sperm-rich fraction of the semen, but not in any other secretions or excretions, and can therefore only transmit infection by the venereal route. Virus is readily transmitted to susceptible mares during live cover or artificial insemination with infective fresh-cooled or cryopreserved semen. Transmission rates as high as 85% to 100% have been reported. Persistence of virus in the stallion has no adverse effect on clinical condition or, apparently, fertility. A variable percentage of long-term carrier stallions spontaneously eliminate EAV from the reproductive tract, with no indication of reversion to a shedding state at a later date. Genetic modulation occurs over the course of persistent infection in the reproductive tract of carrier stallions, resulting in the emergence of novel viral variants. Carrier stallions play an important role in the epidemiology of EVA, not only in serving as the reservoir of EAV but also as the principal means whereby genetic diversification of the virus can occur.

May 28, 2016 | Posted by in EQUINE MEDICINE | Comments Off on Equine Viral Arteritis

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