Abstract. Late in 1991, an enveloped RNA virus (now called porcine reproductive and respiratory syndrome [PRRS] virus) was identified as the etiologic agent for mystery swine disease. In 1992, laboratory procedures for the diagnosis of this disease evolved rapidly, and veterinary diagnosticians started applying these tests to field cases. This report is written from the perspective of veterinary laboratory diagnosticians and utilizes 3 case studies to define the advantages and disadvantages of the various available diagnostic laboratory PRRS test procedures in different clinical situations. The diagnostic procedures currently used in our laboratory for investigating PRRS are pathologic examination, serologic testing, fluorescent antibody (FA) testing, and virus isolation. Interstitial pneumonia, characterized by mononuclear cell infiltration of alveolar walls with normal airway epithelium, is a hallmark lesion for the disease, especially in neonatal pigs with respiratory distress. Interstitial pneumonia is not a specific lesion and must be coupled with other tests to verify PRRS virus infection. Demonstration of seroconversion is helpful, especially in sows that have experienced reproductive failure. The indirect FA test detects antibody sooner than the serum neutralization test and will likely become the serologic test of choice. The direct FA test on fresh tissue utilizes monoclonal antibody and is useful for investigating PRRS virus-associated pneumonia. Virus isolation utilizing swine alveolar macrophages has also been a useful diagnostic procedure. All of the above tests have been universally unrewarding when applied to aborted, mummified, or stillborn piglets.
Abstract. Out of 45 cases of fatal chronic pneumonia in calves examined for Mycoplasma bovis infection from February to July 1994, 11 cases with pulmonary abscesses that were culture positive for M. bovis were encountered. The cases were studied in detail using a recently developed monoclonal antibody-based immunoperoxidase technique. Mycoplasma bovis organisms were detected in specific locations at all stages of abscessation observed. In bronchioles or terminal airways within which abscesses developed, M. bovis was located at the epithelial surface and in close association with infiltrating neutrophils and macrophages. Abscessed airways that had lost the epithelium were encapsulated and were seen as coagulative necrotic foci that stained intensely for M. bovis, especially at the periphery. Some foci stained weakly and such might have been resolving lesions. Mycoplasma bovis was also demonstrated at sites of mild mononuclear cell infiltration in the livers and kidneys of 2 calves. The mycoplasma was detected within bile ducts in the liver and in the tubular epithelium of the kidney. Abscesses not staining for M. bovis, presumably caused by other pathogens, were seen concurrently with M. bovis-associated abscesses in some lungs. Thirteen other M. bovis-positive cases showed no abscesses, possibly indicating heterogeneity among M. bovis strains. Three other cases with abscesses were negative for M. bovis by culture and immunoperoxidase staining. The monoclonal antibody-based immunohistochemical technique is efficient for specific detection of M. bovis in cases of enzootic pneumonia of calves with or without abscessation. Mycoplasma bovis is implicated in the pathogenesis of lung abscesses in some calves.Naturally occurring infectious pneumonias of clinical significance usually have complex causes, often requiring the interaction of two or more organisms and predisposing environmental factors.2 Calf pneumonia resistant to antibiotic therapy is frequently encountered in the United States of America and Canada. 10 In areas where calves dying of chronic pneumonia would normally have been treated for bacterial agents, diagnostic effort is necessarily geared towards elucidating the role of viruses and mycoplasmas. Viral agents often cause acute pneumonia in calves, with a histological picture of bronchointerstitial pneumonia. 2Among bovine mycoplasmas recognized in the USA, Canada, and Europe, Mycoplasma bovis stands out as the most invasive and destructive. This mycoplasma can cause pneumonia and arthritis in calves and mastitis in adult cattle .2,7 Mycoplasma bovis has also been cultured from blood.11 There are studies in which M. Received for publication October 7, 1994. bovis was inoculated into calves concurrently with Pasteurella hemolytica, 3 respiratory syncytial virus, 11 and bovine viral diarrhea virus and P. hemolytica. 8 Lesions produced by M. bovis alone were described as focal areas of coagulative necrosis surrounded by mononuclear cells and suppurative bronchiolitis with varying degrees of lympho...
The susceptibility of wild ruminants, especially cervids, to bovine viral diarrhea virus (BVDV) has remained an enigma. Two white-tailed deer (Odocoileus virginianus) were submitted to the Animal Disease Research and Diagnostic Laboratory (ADRDL) in the fall of 2003 by the South Dakota Game Fish and Parks for chronic wasting disease (CWD) testing. Both animals were CWD negative. The animals were necropsied and histopathology, viral antigen detection, and virus isolation were performed. A noncytopathic (NCP) BVDV was isolated from the lungs and several other tissues of both animals. Formalin-fixed ear notches from both animals were positive for BVDV antigen by immunohistochemistry. The BVDV isolates were typed with the use of polymerase chain reaction in 5' untranslated region (UTR) and one isolate was typed a Type 2a and the other a Type 1b. Future field surveys to determine the incidence of BVDV along with experimental studies to determine if white-tailed deer fawns can be persistently infected with BVDV are needed.
Infections by Clostridium perfringens type A are perhaps the most common causes of clostridial hemorrhagic enteritis in neonatal ruminants. Affected calves exhibit tympany, hemorrhagic abomasitis, and abomasal ulceration. Gram-positive bacilli are often found on affected mucosa and in submucosa. Aspects of etiology beyond the infecting organism are little understood, but probably include dietary issues, perhaps relating to overfeeding, feeding of barely thawed or contaminated colostrum, or conditions which effect decreased gut motility. Fatal hemorrhagic enteritis in a cloned gaur calf is illustrative of the syndrome. The calf developed pasty yellow and bloody diarrhea, and the abdomen became distended and painful. In spite of intensive therapy, the calf died approximately 48 h after birth. At necropsy, the distended abomasum contained clotted milk and bloody fluid, and the abomasal and omasal walls were thickened and hemorrhagic. The proximal duodenum was hemorrhagic and emphysematous, and microscopic examination revealed Gram-positive rods in association with acute, necrotizing, hemorrhagic mucosal inflammation. Isolates of C. perfringens from this calf were PCR positive for cpb2, the gene encoding beta2 toxin. This finding is of unknown significance; only 14.3% (8/56) of isolates from other calves with the syndrome have been cpb2 positive, and only 50% of cpb2 positive bovine isolates express CPB2. The most prominent needs to further our understanding of this problem are consistent experimental reproduction of the disease, elucidation of virulence attributes, and development and application of prevention and control strategies.
Abstract.A ranch in central South Dakota had a number of dead calves because of arsenic poisoning. The clinical picture included diarrhea, central nervous system signs, and death. Gross necropsy findings included adequate body fat, stomachs full of normal-appearing ingesta, and large amounts of greenish brown watery fluid in the intestine and colon. Microscopically there was severe lymphoid tissue necrosis in the mesenteric lymph nodes and gut-associated lymphoid tissue. Chemical analysis of kidneys showed no significant amounts of lead; however, kidney arsenic concentrations were 25 to 44 ppm. The source was a small pile of Paris Green (common name for cupric acetoarsenite) found in an old dump site in the pasture.
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