Clinical pathology and hemostatic abnormalities in experimental African horsesickness.

Infection of naive North American horses with 10(4) cell culture infectious doses (CCID50) of virulence variants of African horsesickness virus (AHSV), designated AHSV/4SP, 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. Increased levels of serum creatine kinase, lactate dehydrogenase, aspartate aminotransferase, and alkaline phosphatase, 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.

Identification of Histoplasma capsulatum organisms in the pleural and peritoneal effusions of a dog.

Histoplasma capsulatum organisms were identified by cytologic evaluation in the thoracic and abdominal effusions of a 5-year-old sexually intact male Cocker Spaniel that was referred because of anorexia and lethargy. Treatment with amphotericin B and ketoconazole was instituted. The dog developed respiratory arrest, a complication of the disseminated disease, and died. Necropsy findings included pleural effusion, hepatomegaly, and enlarged tracheobronchial, hilar, mediastinal, and mesenteric lymph nodes. Granulomas containing periodic acid-Schiff (PAS)-positive yeast-like organisms identified as H capsulatum were seen in the lungs, liver, and lymph nodes. The lymphatic vessels were dilated, and fibrosis of the portal and periportal regions of the liver was noticed. Identification of Histoplasma organisms by cytologic examination of pleural and abdominal effusions is a rare laboratory finding and can provide a minimally invasive and inexpensive definitive diagnosis of histoplasmosis.

Clinical neosporosis in a 4-week-old Hereford calf.

Most reports of neosporosis associated with abortion in cattle are in dairy cattle and infected calves do not survive beyond 7 days of age. This paper reports neosporosis in a 4-week-old Hereford calf. The calf was full term and appeared clinically normal at birth. At 2 weeks of age, the calf had weakened and was unable to nurse unassisted. The calf was killed at 4 weeks because of paralysis. The primary lesions were in the brain and were associated with Neospora caninum tachyzoites. The diagnosis was confirmed by immunohistochemical staining with anti-Neospora rabbit serum.

Histologic and immunochemical study of the pathogenesis of heartwater (Cowdria ruminantium infection) in goats and mice.

Eleven adult goats and 32 adult outbred mice were inoculated IV with Cowdria ruminantium-infected blood (Kwanyanga isolate), monitored clinically, then serially euthanatized. Predominant clinical signs of disease in goats were depression, head tremors, seizures, and dyspnea. In mice, dyspnea and depression were the only clinical signs of disease noticed. Tissues were examined histologically and immunohistochemically for C ruminantium colonies or antigen. In goats, C ruminantium was detected only in endothelial cells of the brain, even though gross and microscopic lesions were confined to the thorax. In mice, C ruminantium was detected only in endothelial cells of the heart and lungs.