Clinical Pathology and Hemostatic Abnormalities in Experimental African Horsesickness

Infection of naive North American horses with lo4 cell culture infectious doses (CCID,,) of virulence variants of African horsesickness virus (AHSV), designated AHSVMSP, AHSV/9PI, and AHSV/4PI, reproduced three classical forms of African horsesickness: acute (pulmonary), subacute (cardiac), and febrile, respectively. Distinct clinicopathologic and hemostatic abnormalities were associated with each form of disease. Hemostatic abnormalities included increased concentration of fibrin degradation products and prolongation of prothrombin, activated partial thromboplastin, and thrombin clotting times. Hemostatic findings indicated activation of the coagulation and fibrinolytic systems with clotting factor consumption in acute and subacute cases of African horsesickness. Hematologic abnormalities in acute and subacute cases of African horsesickness included leukopenia, decreased platelet counts, elevated hematocrit, and increased erythrocyte counts and hemoglobin concentration. Leukopenia was characterized by lymphopenia, neutropenia, and a left shift. In- creased levels of serum creatine kinase, lactate dehydrogenase, aspartate aminotransferase, and alkaline phos- phatase, hypocalcemia, hypoalbuminemia, hypoproteinemia, and elevated creatinine, phosphorus, and total bilirubin levels were present in some but not all horses. Metabolic acidosis, indicated by decreased total bicarbonate and increased lactate and anion gap, was present in horses with the acute form of disease. Mild thrombocytopenia and leukopenia were occasionally associated with the febrile form of disease. These results suggest a role for intravascular coagulation in the pathogenesis of African horsesickness. African horsesickness (AHS) is an arthropod-borne, noncontagious disease of horses. The causative agent, African horsesickness virus (AHSV), is classified as an orbivirus within the family Reoviridae and is closely related to bluetongue virus (BTV) and epizootic hem- orrhagic disease virus (EHDV).'O Infection of suscep- tible horses with AHSV can result in high morbidity and mortality. In 192 1, Theiler33 described four clin- icopathologic forms of AHS: the acute (pulmonary), subacute (cardiac), mixed, and febrile forms of the dis- ease. The disease in its acute form is characterized by rapid onset of high fever, signs of respiratory distress, pulmonary edema, pleural effusion, hemorrhage, and death. The subacute form is characterized by hydro- pericardium, endocardia1 hemorrhage, marked accu- mulation of edema fluid in the head and neck, partic- ularly in the supraorbital fossae, ligamentum nuchae, and fascia1 planes of the cervical musculature. The mixed form consists of clinical signs and lesions typical of both acute and subacute AHS. The febrile form is characterized by mild, remittent fever that is some- times associated with vague clinical signs, which may escape clinical recognition. Recent evidence indicates that in naive horses, the major determinant of the clin- icopathologic form of disease is the viral virulence phenotype.19