An equine plague

For four decades, equine viral arteritis (EVA) has exerted a devastating impact on breeding and racingEquine viral arteritis (EVA) was the most talked about equine infectious disease of 1993. A major outbreak at Arlington International Racecourse in Illinois that spread to surrounding states and racetracks generated new interest in the economic and disease potential of this virus. Multiple smaller outbreaks continue to be diagnosed as veterinarians and owners deal with this previously ignored pathogen. This discussion will review the history, clinical signs, epidemiology, transmission, diagnosis, and treatment of EVA. Emphasis will be placed on management of the carrier stallion and the economic hardships that EVA can create.

Epidemiology
Equine viral arteritis was first identified in this country as a specific disease entity in an outbreak on a farm near Bucyrus, Ohio, in 1953. During the past 40 years, there have been 56 documented outbreaks in the United States and Europe. Major outbreaks have occurred in Kentucky (1977 and 1984), Colorado (1984), Illinois (1993), and England (1993). Cases of EVA have been diagnosed on all major continents. Although the Bucyrus strain is the only prototype strain as yet identified, there have been antigenic and pathogenic differences between the different outbreaks to suggest possible strain variations.
The best example of variations in the pathogenic potential of this virus may be the occurrence of EVA-
abortion. In 22 of the 56 outbreaks, EVA-abortion has occurred, suggesting that certain strains may be more abortigenic. In addition, certain strains appear to affect the circulatory system, while others affect the respiratory system.

Clinical signs
Clinical signs associated with EVA primarily involve the respiratory, circulatory, and reproductive systems. Initial signs are fever (102-to-106 F), anorexia, and depression. As the disease progresses, ventral edema of the legs, scrotum, prepuce, and abdomen may be observed. Conjunctivitis and rhinitis can be observed as a pus-type discharge. Increased tearing is also commonly associated with this conjunctivitis. The old veterinary literature refers to this as epizootic pinkeye. Coughing, colic, and diarrhea also may be seen. Skin rashes may occur and are most commonly seen on the side of the neck.
The incubation period for EVA ranges from 3-to-14 days, and clinical signs can last for 2-to-14 days. At the recent outbreak at Arlington International, the average time for an infected horse to return to racing was 37 days. Morbidity has been reported to be from 15%-to-70%. Like most infectious diseases, EVA is more severe in younger and older animals. Mortality rarely occurs following natural exposure to EVA.
Abortion is observed between the fifth and tenth months of pregnancy. The aborted foal is partially decomposed, and there are no specific lesions found upon necropsy in which to make a diagnosis of EVA. Viral isolation from the infected fetal tissues is required to establish a definite diagnosis. Incidence rates for abortion can range from 0%-to-60%. EVA will not produce abnormalities in the foals of non-aborting exposed mares. No long-term effects on mare fertility have been associated following EVA infection.
Stallions may experience reproductive failure for a short period of time following initial infection with EVA. This temporary infertility or subfertility is due to the decreased motility and poor concentrations of semen being produced by the affected stallion. These temporary effects on sperm quality appear to be linked with fever, scrotal edema, and the subsequent thermal insult to the testicles. There appear to be no long-term effects on stallion fertility, even in the persistently infected carrier stallion.

Pathogenesis
EVA is initially taken up by the white blood cells in the respiratory tract and carried to the regional lymph nodes. Within 72 hours, dissemination of the virus to the smaller blood vessels occurs. A strong affinity for the lining of the smaller arteries results in inflammation and a focal necrosis (death) of these vessels. This resulting vasculitis and serum leakage is the primary lesion responsible for all the clinical signs associated with this disease, with the possible exception of abortion. The exact pathogenesis of EVA-abortion has not been determined. However, theories that have been proposed include:

1. Myometrial edema resulting from the local vasculitis causes placental separation and fetal death.
   
2. The virus crossing the placental barrier and directly infecting the fetus, causing death.
   
3. The effect of stress and severe systemic disease on pregnant mares.
   

Transmission
EVA is spread by respiratory and venereal transmission. Shedding of the virus in aerosolized droplets from the respiratory tract is the most common route of infection in acute outbreak situations. This is especially evident during outbreaks at racetracks, where venereal transmission is limited. The shedding of these aerosolized viral droplets from the respiratory tract can continue for 2-to-16 days. The virus can also be shed in the urine for up to 21 days, and indirect transmission can occur via contaminated objects.
Venereal transmission is the more significant route of infection, in that clinically normal, persistently infected stallions ensure the maintenance of EVA in the equine population. EVA can be transmitted at breeding in semen or via vaginal secretions for variable lengths of time. Acutely infected mares shed the virus in vaginal secretions for 2-to-9 days. Of exposed stallions, 30%-to-60% can become persistent viral shedders and yet remain clinically normal. The EVA persists in the ampulla of the vas deferens, and carrier stallions shed the virus in the sperm-rich fraction of 90%-to-100% of their ejaculates. Unprotected mares can be infected with EVA when bred to carrier stallions, and they can then act as vectors, laterally transmitting the virus to in-contact horses and causing clinical disease. Therefore, bred mares acting as vectors can expose horses distant from the stallion.
With the increased use of shipped cool semen and frozen semen in most breeds, the potential for rapid dissemination of EVA is troubling. With the EVA status of many stallions unknown and the lack of rules and regulations regarding the interstate shipment of semen, the potential for exposure to EVA is unlimited.
No treatment exists for the clearing of the carrier stallion. However, some stallions have cleared the infection spontaneously after being infected for up to ten years. Mares and geldings do not become persistent long-term carriers of EVA, as the carrier state appears to be testosterone dependent.
To the individual horse owner, EVA-abortions and the establishment of the carrier stallion present the severest threats. The financial loss from EVA-abortion is more obvious than those incurred by the carrier stallion. Many mare owners find it unattractive to expose their mare to carrier stallions. The demand for cool and frozen semen also may decrease when reports of persistently infected stallions become known. Finally, international markets are lost, as importation of carrier stallions and infected semen is not allowed by other countries.

Management
EVA prevention begins with good management. For breeding farms, it is critical to know the EVA status of all stallions owned by the farm and of all the mares they are breeding. Isolation of horses returning to the farm for 30 days at a distance of at least 100 feet from other horses should be a standard protocol. Segregation of pregnant mares from other horses should be strictly enforced during EVA outbreaks.
Persistently infected stallions can continue to be bred under strict guidelines. The stallion should be isolated to avoid contact with susceptible horses. Breeding is only allowed to mares who have been vaccinated for at least three weeks. Following breeding, mares should be isolated, since EVA shedding may occur for short periods following natural exposure. Mare owners should be advised that the stallion in question is a viral shedder prior to natural breeding or receiving his shipped semen for artificial insemination.
Vaccination prevents clinical disease and abortions and limits virus transmission and the establishment of carrier stallions. Arvac (Fort Dodge Laboratories) is a modified live virus vaccine that is administered as a one-shot protocol. Annual boosters are recommended to maintain adequate protection.
Mares and stallions should be vaccinated at least three weeks prior to breeding. No stallion should be vaccinated without serologic screening. If he is seropositive, a semen culture should be performed to see if he is persistently infected. Open mares and non-breeding males can be vaccinated at any time. Pregnant mares and foals younger than six weeks of age should not be vaccinated unless the risk of known natural exposure is great. Vaccination in the face of an EVA outbreak is recommended and was used successfully during the Arlington outbreak to minimize further disease and viral shedding. Vaccination of immature colts is strongly recommended between six and 12 months of age to prevent the future establishment of persistent infections.
A word of warning: The antibody levels stimulated by vaccination cannot be distinguished from natural infection and may prevent international export. South American countries are currently the only ones which refuse importation of all seropositive horses. As of January 1, 1993, seropositive horses could be exported into the European Economic Community (EEC). Mares and geldings with stable titers are readily admitted. Stallions that are seropositive on pre-export screening must undergo semen culturing for the virus. Stallions seronegative prior to vaccination and negative on semen culturing are readily admitted into the EEC countries.

Summary
Equine viral arteritis is a significant disease of the equine species, resulting in respiratory infections, abortions, and the creation of carrier stallions. Although the number of reported cases of EVA has increased significantly since 1984, many people are unaware of the disease and its potential. Recent outbreaks have demonstrated the ability of the virus to infect a large number of horses and cause considerable financial loss. These outbreaks also demonstrated the lack of immunity in many segments of our equine population. Vaccination is the most effective means of preventing and controlling EVA in the U. S. Through increased prevention and heightened awareness of this disease, the impact of EVA on the equine industry can be limited.

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Douglass B. Hutchins, MS, DVM, is a veterinarian in the Professional Services Department of Fort Dodge Laboratories.