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. |
Lesions:
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. |
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