No abstract

Coccidiosis is a protozoan disease of wild and domestic ruminant animals in every country of the world. This article provides basic information regarding the terminology, biology, epidemiology, pathology, diagnosis and control methods applicable to the causative agents and their interaction with host animals.

Tritrichomonas foetus causes bovine trichomoniasis in the reproductive tract of cattle and feline trichomoniasis in the large bowel of the domesticated cat. Bovine trichomoniasis is widespread in the USA especially in the Midwest and West and leads to significant economic losses. Although the disease has been endemic for over three decades in Wyoming, one of the largest beef cattle producing states in the USA little is known about its epidemiology and laboratory diagnosis. We statistically analyzed the data collected from the Wyoming State Veterinary Laboratory and the Wyoming Livestock Board. Individual prevalence in beef bull populations in Wyoming between 1997 and 2010 ranged from 0.21% to 2.69%. A steady decline in prevalence was linearly correlated with year since the enforcement of state laws on the disease began in 2000 (R=0.717, P=0.009). One exception was 2009 when a recurrence occurred. Between 2007 and 2010, average herd prevalence was 2.17%, with 15 of the 23 counties having at least one positive herd. In laboratory diagnosis advanced gel-PCR showed 99.9% agreement with traditional cell culture. This is the first epidemiological study on bovine trichomoniasis in Wyoming and demonstrates that T. foetus infection continues to be prevalent in beef cattle in the state where natural service is widely used.

Bluetongue virus (BTV) infection results in disparate clinical syndromes among ruminant species. An in vitro model system of BTV/target cell interaction was developed using umbilical vein endothelial cells (EC)from fetal lambs and calves. These cells had microscopic, ultrastructural, and immunocytochemical features typical of EC. BTV infection in these cells was examined using virus binding assays, plaque assays, a whole-cell enzyme-linked immunosorbent assay, flow cytometry, electron microscopy, and a bioassay for interferon activity. EC from both species supported cytopathic BTV infections. Ovine EC bound more BTV initially and produced more virus over time, whereas bovine EC underwent more rapid lysis subsequent to infection. An ultrastructural comparison of BTV-infected ovine and bovine EC, grown as differentiated capillary-like cords on a laminin-rich matrix or as monolayers, revealed no significant interspecies differences in viral morphogenesis between 1 minute and 24 hours after infection. The intracellular distribution of BTV nonstructural protein 1, which localized to virus inclusion bodies and tubules, was identical for ovine and bovine endothelial cells. Ovine and bovine EC produced a soluble mediator of interferon activity in response to BTV infection; however, ovine EC produced higher levels of interferon activity at lower levels of infection. These findings indicate differences in BTV-EC interaction that may contribute to the pathogenesis of the severe inflammatory disease that is characteristic of clinical bluetongue disease in sheep.

A recent outbreak of hemorrhagic fever in wild ruminants in the northwest United States was characterized by rapid onset of fever, followed shortly thereafter by hemorrhage and death. As a result, a confirmed 1,000 white-tailed deer and pronghorn antelope died over the course of 3 months. Lesions were multisystemic and included severe edema, congestion, acute vascular necrosis, and hemorrhage. Animals that died with clinical signs and/or lesions consistent with hemorrhagic fever had antibody to epizootic hemorrhagic disease virus serotype 2 (EHDV-2) by radioimmune precipitation but the antibody was limited exclusively to class immunoglobulin M. These findings, indicative of acute infection, were corroborated by the observation that numerous deer were found dead; however, clinically affected deer were rarely seen during the outbreak. Furthermore, only in animals with hemorrhagic lesions was EHDV-2 isolated and/or erythrocyte-associated EHDV-2 RNA detected by serotype-specific reverse transcription (RT)-PCR. By using a novel RT in situ PCR assay, viral nucleic acid was localized to the cytoplasm of large numbers of tissue leukocytes and vascular endothelium in tissues with hemorrhage and to vessels, demonstrating acute intimal and medial necrosis. Because PCR amplification prior to in situ hybridization was essential for detecting EHDV, the virus copy number within individual cells was low, <20 virus copies. These findings suggest that massive covert infection characterized by rapid dissemination of virus facilitates the severe and lethal nature of this disease.