The effect of interpreting an ELISA at a lower cut-off on detection of clinical cases of bovine Johne's disease.
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OBJECTIVE: The objective of this study was to determine the sensitivity of abattoir surveillance of intestinal tract lesions for detecting ovine Johne's disease (OJD) under normal meatwork conditions. DESIGN: The design of this study was a diagnostic test validation. The three OJD inspectors were the diagnostic test and follow-up histopathological examination was used for test validation. PROCEDURE: Approximately 1200 sheep were procured from known high prevalence OJD infected farms. The sheep viscera were tagged (numbered) and then examined as they were processed on the abattoir line by three experienced meat inspectors. Their observations were independently recorded on a cassette tape. Specified sections of viscera were prepared and subjected to histopathological examination and these results were compared with the inspector diagnoses. RESULTS: The sensitivity of abattoir inspection for OJD varied between inspectors from 53 percent to 87 percent. The specificity varied from 97 to 100 percent. It appeared that the level of sensitivity for detecting disease was higher in lines of sheep where the disease was more prevalent. It also appeared that formal training was an important aspect in ensuring a high level CONCLUSION: Abattoir surveillance is a very economical and rapid method of assessing the OJD status of sheep. On the basis of these results it is reasonable to suggest that abattoir surveillance has a sensitivity of approximately 70 percent. This technique is useful as an ancillary to other testing regimes for negative assurance programs where a sheep identification system is used.
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An outbreak of Johne's disease in a herd of farmed red deer was studied for four years. Serological, histopathological and cultural techniques were used to monitor the progress of the disease, and delayed type hypersensitivity skin tests were also applied. The results of the serological tests showed that they were poor predictors of future clinical cases and did not consistently identify animals harbouring mycobacteria. The histopathological methods provided a sensitive and specific means of confirming the infection. The skin tests had a low sensitivity and the results were poorly correlated with the serological results in seropositive animals. A vaccination policy was instituted which was accompanied by a change in the pattern of disease. Although the histopathological evidence suggested that the infection was still occurring, there was a marked reduction in the incidence of clinical disease. Vaccinated animals showed a good response to the skin test.
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Inducible nitric oxide synthase (iNOS) is important in the control of a number of intracellular pathogens, including mycobacteria, and is a marker of classic macrophage activation. In human granulomatous diseases such as leprosy, a spectrum of granulomatous lesions is described, ranging from the tuberculoid to lepromatous types. Tuberculoid granulomas are associated with enhanced iNOS production and improved clinical outcomes over the lepromatous types. The aim of this study is to determine whether an association exists between morphology of bovine Johne's disease granulomas and lesion macrophage effector functions. To accomplish this, we retrospectively evaluated 24 cases of bovine Johne's disease. In each case, we recorded the predominant granuloma morphology and evaluated iNOS immunoreactivity and bacterial burden by acid-fast stains and mycobacterial immunolabeling. The results of this study demonstrate that all cases had granulomas with features most similar to the lepromatous type. This morphology correlated with heavy bacterial burdens demonstrated by acid-fast staining and mycobacterial immunoreactivity. None of the cases had high expression of iNOS in mycobacterial-positive granulomas. When iNOS immunoreactivity was identified, it was usually located near the crypts and was distinct from the granulomatous foci.
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At the present time, there is no convincing indication that Crohn's disease is a bacterial disease, although an association with mycobacteria has been hypothesised for many years. The hypothesis that bacteria could be the cause, or at least an important concause of Crohn's disease is supported by several experimental and clinical observations: animals kept in a germ-free environment fail to develop intestinal inflammation; bacteria are the cause of human and animal intestinal diseases similar to Crohn's disease; luminal content is necessary for causing gut lesions; and, moreover, antibiotics are successfully used in the treatment of Crohn's disease. Bradford Hill criteria recently used to assess a causal relationship for Helicobacter pylori and peptic ulcer can be applied for establishing or excluding a causality between mycobacteria and Crohn's disease. Of these criteria, only biological plausibility, coherence and analogy are satisfied. However, failure to identify a specific pathogen does not exclude a possible role for bacteria in causing Crohn's disease lesions and symptoms. Pathogenic or commensal enteric bacteria could overinfect the primary lesions, leading to chronic intestinal inflammation in genetically susceptible hosts. Another possibility is that components of the normal intestinal flora could acquire pathogenic characteristics.
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