Equine viral arteritis.

Abstract

Equine viral arteritis (EVA) can cause prominent economic losses for the equine industry. The purpose of this review is to provide the pathologist some familiarity with the clinical history, lesions, pathogenesis, and diagnosis of EVA. EVA is caused by an arterivirus (equine arteritis virus, EAV), and the vascular system is the principal but not unique viral target. EVA has variable presentations, including interstitial pneumonia, panvasculitis with edema, thrombosis and hemorrhage, lymphoid necrosis, renal tubular necrosis, abortion, and inflammation of male accessory genital glands. EAV antigen (EAVAg) can be demonstrated within the cytoplasm of epithelial cells such as alveolar pneumocytes, enterocytes, adrenal cortical cells, trophoblasts, thymus stroma, renal tubular cells, and male accessory genital gland cells. It can be also demonstrated within endothelia, in vascular, myometrial, and cardiac myocytes, macrophages, dendritelike cells of lymphoid organs, and chorionic mesenchymal stromal cells. In young and adult horses, following colonization of macrophages, the virus spreads systemically using circulating monocytes and enters the endothelium and tunica media of blood vessels, histiocytes, and dendritelike cells. Eventually, the virus multiplies within renal tubular cells. Lesions are uncommon in the aborted fetus; if present, they are mild, and EAVAg is frequently not detectable within fetal tissues and placenta. The clinical presentation and lesions of EVA may resemble those of other diseases. Complete pathologic examination associated with immunohistochemistry, virus isolation, and, especially in cases of abortion, serology will guarantee a directed and accurate diagnosis.