Equine viral arteritis

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Equine viral arteritis, scrotal edema. Courtesy of Dr. Peter J. Timoney
Equine viral arteritis, lacrimation. Courtesy of Dr. Peter J. Timoney
Equine viral arteritis, ocular edema. Courtesy of Dr. Peter J. Timoney
Equine viral arteritis, urticarial-type skin reaction. Courtesy of Dr. Peter J. Timoney

Equine viral arteritis (EVA) is an acute, contagious, viral disease of equids caused by equine arteritis virus. It is characterized by fever, depression, dependent edema (especially of the limbs, scrotum, and prepuce in the stallion), conjunctivitis, nasal discharge, abortion, and infrequently, death in young foals[1].

Cause

Equine arteritis virus is a small, enveloped RNA virus and the prototype virus of the genus Arterivirus, family Arteriviridae, order Nidovirales. While only one serotype of the virus has been identified—the prototype Bucyrus strain—there is ample evidence of genomic and antigenic variation among temporally and geographically disparate isolates. Furthermore, strains of the virus vary in their ability to produce disease, including abortion, with some causing only a mild to moderate fever.

After aerosol exposure, the virus multiplies in the bronchial and alveolar macrophages and, within 48 hr of infection, can be found in the regional lymph nodes. This is followed by a leukocyte-associated viremia, during which the virus becomes widely disseminated in various tissues and fluids throughout the body. The virus localizes in the vascular endothelium of the smaller blood vessels, especially the arterioles, and in the epithelium of certain tissues, particularly the adrenals, seminiferous tubules, thyroid, and liver. Characteristic vascular lesions include endothelial swelling and degeneration, neutrophil infiltration, and necrosis of the tunica media of affected vessels. The vascular lesions give rise to edema and hemorrhage in many tissues and organs.

The pathogenesis of abortion caused by equine arteritis virus is still open to speculation. It may result from myometritis in the pregnant mare, leading to impairment of placental circulation and eventually death of the fetus.

Except for certain stallions, infectious virus is no longer detectable in most tissues or body fluids beyond day 28 after infection. A variable percentage of stallions can remain infected for extended periods. The virus is localized primarily in certain accessory sex glands (especially the ampulla of the vas deferens) in the carrier stallion.

The natural and experimental host range of equine arteritis virus appears to be restricted to equids. Based on the findings of serologic surveys and reported outbreaks of EVA, the virus is present in horse populations in many countries throughout the world; Japan and Iceland are notable exceptions. However, outbreaks of EVA are uncommon and usually associated with the movement of horses or shipment of semen. While the virus is known to infect many breeds of horses, the prevalence of infection varies widely, usually being highest in Standardbreds and Warmbloods. There is little evidence of infection in populations of wild equids.

The epidemiology of EVA involves virus-, host-, and environment-related factors, including variability in pathogenicity among naturally occurring strains of the virus, routes of transmission, existence of the carrier state in the stallion, and the nature of acquired immunity to infection. Outbreaks of EVA are usually linked to the movement of animals or the shipment of semen. Viral transmission can be widespread at racetracks or on breeding farms; such occurrences are not always associated with the appearance of clinical illness characteristic of EVA. In fact, the vast majority of cases of natural infection with the virus are asymptomatic.

Transmission of EAV infection can occur by respiratory, venereal, congenital, or indirect means. Aerosol transmission is the principal mode of spread by horses acutely infected with the virus. It is primarily responsible for dissemination of infection among horses at racetracks, shows, sales, veterinary clinics, and on breeding farms. The virus can also be transmitted venereally by the acutely infected mare and by the acutely or chronically infected (carrier) stallion. Mares can be infected by the venereal route either following natural service or artificial insemination with infective semen. The virus can also be transmitted indirectly through the use of virus-contaminated fomites (eg, shanks, twitches, head collars, and breeding shed equipment) and on the hands or clothing of animal handlers.

Unlike mares, geldings, or sexually immature colts, carrier stallions are viral reservoirs and are primarily responsible for persistence of the virus in different horse populations throughout the world. The virus is shed constantly in the semen. Such animals transmit infection to >85% of susceptible mares to which they are bred. While the duration of the carrier state varies between individuals, the virus may persist in some clinically healthy stallions for years. Such stallions do not suffer any apparent decrease in fertility. Spontaneous resolution of the carrier state has been observed in a variable percentage of persistently infected stallions.

Clinical signs

Exposure to equine arteritis virus may result in clinical or inapparent infection, depending on the virus strain involved, viral dose, age, and physical condition of the animal(s), and various environmental factors. Studies have shown that most cases of natural infection are subclinical. The onset of clinical signs is preceded by an incubation period of 3-14 days, which varies mainly with the route of exposure. Signs vary widely in range and severity between outbreaks of EVA and among affected individuals in the same outbreak. Typically, any combination of the following may be seen: fever of 2-9 days duration, leukopenia, depression, anorexia, limb edema (especially of the hindlimbs), and edema of the prepuce and scrotum. Less consistent signs include conjunctivitis, lacrimation and photophobia, periorbital or supraorbital edema, rhinitis and nasal discharge, edema of the ventral body wall (including the mammary glands of mares), an urticarial-type skin reaction that is frequently localized to the sides of the neck or head (although it can sometimes be generalized), stiffness of gait, dyspnea, diarrhea, icterus, and ataxia.

Abortion may occur late in the acute phase or early in the convalescent phase of the disease. It may also supervene in subclinically infected mares. Mares may abort any time from 3 mo to over 10 mo of gestation. In natural outbreaks, abortion rates can vary from <10% to as high as 50%. Abortion does not result from a mare being bred to a carrier stallion or inseminated with infective semen. Mares that abort are already pregnant at time of exposure, which principally occurs by the respiratory route from an acutely infected in-contact animal. Mares infected late in gestation may not abort, but give birth to a congenitally infected foal.

Stallions affected with EVA may undergo a period of short-term subfertility. This is believed to result from increased intratesticular temperature caused by the high fever and severe scrotal edema that can be experienced by acutely infected stallions.

Clinical signs are more severe in young, old, and debilitated animals. Mortality is rare in natural outbreaks; it has been reported infrequently in young foals from a few days to several months of age that succumb from a fulminating pneumonia or pneumoenteritis.

The gross and microscopic lesions reflect the extensive and considerable vascular damage caused by the virus. The most prominent gross findings include edema, congestion, and hemorrhages, especially in the subcutis of the limbs and abdomen; excess peritoneal, pleural, and pericardial fluid; and edema and hemorrhage of the intra-abdominal and thoracic lymph nodes and of the small and large intestine, especially the cecum and colon. Pulmonary edema, emphysema and interstitial pneumonia, enteritis, and infarcts in the spleen have been described in fatal cases of the disease in foals. Aborted fetuses are usually partly autolyzed, and gross lesions, if present, may be limited to an excess of fluid in body cavities and a variable degree of interlobular pulmonary edema. The characteristic vascular lesions and immune-mediated changes seen in mature animals are not always a significant feature in fetuses infected with the virus.

The characteristic microscopic lesion is a vasculitis, involving primarily small arteries but also small veins. Histologically, the changes can range from vascular and perivascular edema, with occasional lymphocytic infiltration and endothelial cell hypertrophy in mild cases, to fibrinoid necrosis of the tunica media, extensive lymphocytic infiltration, necrosis and loss of endothelium, and thrombus formation in severe cases. Microscopic lesions are not a constant feature in abortions. Vasculitis, if present, has been observed in placenta, brain, liver, spleen, and lungs of the fetus. Fatal cases of infection in young foals are characterized by interlobular edema, congestion and mononuclear cell infiltration in the lungs, lymphoid depletion and hemorrhage in lymphoreticular tissues, and when there is an associated enteritis, focal hemorrhages and necrosis of the mucosa of the small intestine.

Diagnosis

Because of the clinical similarity of EVA to other respiratory and certain nonrespiratory diseases of horses, a clinical diagnosis cannot be made without corroborative virologic, serologic, or histopathologic findings. Equine influenza; infection with equine herpesvirus 1 and 4, equine rhinitis A and B viruses, or equine adenoviruses; and streptococcal infections, with particular reference to purpura hemorrhagica, are among the more common diseases that clinically resemble EVA. The latter must also be differentiated from sporadic cases of equine infectious anemia and toxicosis caused by hoary alyssum (Berteroa incana). Among the exotic equine diseases that clinically mimic EVA are Getah virus infection and African horse sickness.

Abortion caused by equine arteritis virus can be differentiated from abortion caused by equine herpesvirus 1 (and rarely 4) in that the mare seldom displays any premonitory signs in herpesviral abortion. Furthermore, fetuses aborted due to herpesvirus infection are invariably fresh at expulsion and often have characteristic gross and microscopic lesions. In contrast, fetuses aborted due to equine arteritis virus are usually partly autolyzed and frequently devoid of any diagnostic lesions.

Appropriate specimens for confirmation of a diagnosis include nasopharyngeal and conjunctival swabs and unclotted blood samples (preferably citrated or EDTA samples) for virus isolation or detection by PCR. These should be obtained as early as possible following the onset of clinical signs. Acute and convalescent sera taken 3-4 wk apart should also be collected for serologic examination using the microneutralization or a validated ELISA test. Placental and fetal fluids, together with placenta, lung, lymphoreticular, and other fetal tissues, can be productive sources of virus from suspect cases of equine arteritis virus abortion. The carrier state can be readily confirmed in seropositive stallions by demonstration of the virus in semen that includes the sperm-rich fraction of the ejaculate either by virus isolation or PCR. When death has occurred and infection with equine arteritis virus is suspected, specimens of body cavity fluids, lung, and reticuloendothelial tissues, especially the lymph nodes associated with the GI and respiratory tracts, should be taken for virus isolation or PCR. These tissues should also be submitted for histopathologic and immunohistochemical examination for the characteristic vascular lesions. It is advisable to consult with a qualified laboratory before collecting specimens for virologic or serologic testing.

Swabs for attempted virus isolation should be transferred to a suitable viral transport medium and shipped (together with any fluids or tissues collected for either virus isolation or PCR) refrigerated or frozen in an insulated container via an overnight delivery service. Unclotted blood samples must be transported refrigerated but not frozen.

Treatment

There is no known specific antiviral treatment for EVA. Because virtually all acutely affected horses recover completely, symptomatic treatment (eg, antipyretic, anti-inflammatory, and diuretic agents) is indicated only in severe cases, especially in stallions in which prolonged fever and extensive scrotal edema can result in short-term subfertility. Good nursing care and rest with a gradual return to normal activity are desirable. As yet, there is no proven therapeutic means of successfully eliminating the carrier state in stallions.

EVA is a preventable disease that can be controlled by sound management practices and selective use of a commercial, modified live virus vaccine. While the vaccine is both safe and immunogenic for stallions and nonpregnant mares, it is not recommended for use in pregnant mares, especially in the last 2 mo of gestation, or in foals <6 wk old, unless there is a high risk of exposure to natural infection.

Most prevention and control programs are focused on preventing or curtailing dissemination of equine arteritis virus in breeding populations, to minimize the risk of virus-related abortion or death in young foals and establishment of the carrier state in stallions. Such programs are based on good breeding management practices, identification of any carrier stallions, and immunization of the noncarrier breeding stallion population. Carrier stallions should be managed separately to avoid the risk of inadvertent viral spread to previously uninfected or unvaccinated horses on the premises. They should be bred only to naturally seropositive mares or mares adequately immunized against EVA. The natural reservoir of the virus may be reduced by vaccinating all colts against the disease at 6-12 mo of age, while they are still prepubertal and before there is any significant likelihood of natural exposure to infection.

Infective fresh-cooled or frozen semen also constitutes an important source of infection. Semen used for artificial insemination, especially if imported, should be tested for virus. Provided that precautions equivalent to those recommended when breeding a mare to a carrier stallion are observed, infective semen can be used with minimal risk of spread of the virus to other horses on the premises.

References