Encephalomalacia associated with vitamin E deficiency in commercially raised emus.

Thirteen of 64 emus on a commercial emu farm in Ohio exhibited neurological signs that included backward staggering, incoordination, generalized weakness, and sitting on their hocks with head retracted backward. Eight of the birds showing such signs were found dead. Two of these emus were necropsied, and no significant gross lesions were observed. Major histopathological lesions were found in the cerebellum and included multiple malacic foci in association with neuropil rarefaction and astrogliosis within the white matter of folia. In addition, the hepatic vitamin E level of one emu was determined at the Michigan State University Animal Health Diagnostic Laboratory (MSU-AHDL) to be 14.61 micrograms/g dry weight. This vitamin E level was in the lower percentile (35%) of 30 emu liver samples examined at MSU-AHDL. A diagnosis of vitamin E-associated encephalomalacia was made based on clinical signs, gross and histological lesions, and liver vitamin E levels.

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.

Detection of African horse sickness virus by reverse transcription-PCR.

Reverse transcription-PCR (RT-PCR) was used to detect African horse sickness virus (AHSV). A single primer pair which amplified a 423-bp fragment of the S8 gene which encodes the NS2 protein of AHSV was identified. Amplification of this fragment from all nine serotypes of AHSV was achieved with these primers. Between 10(1) and 10(2) copies of AHSV genomic double-stranded RNA could be detected by RT-PCR followed by agarose gel electrophoresis and ethidium bromide staining. Application of RT-PCR to blood samples from AHSV-infected horses resulted in earlier detection of viremia than virus isolation did. Furthermore, viremia was detected by RT-PCR in blood samples from horses infected with an avirulent isolate of AHSV which were negative by virus isolation. AHSV was also detected by RT-PCR in spleen and lung samples from horses which died of AHSV infection. These results indicate that RT-PCR is a rapid and sensitive method for the identification of horses infected with AHSV.

Characterization of virulence variants of African horsesickness virus.

There are three clinicopathologic syndromes associated with African horsesickness (AHS) virus infection in horses. These different forms of AHS (pulmonary, cardiac, and fever forms) vary in the organs affected, the severity of lesions, time of onset of clinical signs and mortality rates. We have studied the effects of infection with three cell culture passaged variants of AHS virus in naive North American horses. One of these viruses, AHS/4SP, consistently caused the pulmonary form of AHS with rapid onset of severe pulmonary edema and 100% mortality. A second variant, AHS/9PI, resulted in signs and lesions typical of the cardiac form of AHS: pericardial effusion, subendocardial hemorrhage and widespread subcutaneous edema. Mortality was approximately 70%. The third variant, AHS/4PI, produced mild to subclinical disease in horses, usually expressed only as transient mild fever. No mortality occurred in horses due to infection with AHS/4PI. All surviving infected animals did, however, seroconvert with both neutralizing and ELISA-reactive antibodies. The results of these studies indicate clearly that in naive horses the form of disease expressed is a property of the AHS virus inoculum.

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.