Comparison of the Johne''s absorbed EIA and the complement-fixation test for the diagnosis of Johne''s disease in cattle

A commercially available absorbed ELISA for the diagnosis of Johne's disease (JD) (paratuberculosis) in cattle, the Johne's Absorbed EIA, was compared with the conventional complement-fixation test (CFT) used in Australia. Stored plasma from 3 Victorian dairy herds with a history of JD, sera from specimens submitted from animals showing clinical signs of JD and sera from the US National Repository for Paratuberculosis Specimens were used to determine the sensitivity of each test. The EIA detected 48.8% of 43 Australian animals with subclinical JD, while the CFT detected only 12 (21.4%) of 56 subclinically affected cattle. Of 150 subclinically infected US cattle, the EIA detected 47.3% and the CFT detected 52.0%. The EIA detected 59.7% of animals which at the time of sampling were shedding Mycobacterium paratuberculosis in their faeces, but showed no clinical signs of JD, while the CFT detected 57.3%. The EIA correctly identified 88.2% of 136 histologically confirmed clinical cases, and the CFT detected 83.4%. The specificity of each test was determined by testing sera collected at slaughter from animals residing in a known JD-free area of Australia, and from samples from the US National Repository of Paratuberculosis Specimens collected from certified-free herds in Wisconsin. The EIA was found to have a specificity of 99.8% when 998 Australian animals were used as the test population, and 99.0% when 196 US animals were used. The specificity of the CFT using Australian samples was 96.9% and 95.2% using American samples.     

The pathology and pathogenesis of pleural adhesions in sheep

Pleural adhesions in 155 young (3 to 15 months old) and 474 older sheep were examined macroscopically and by light microscopy. The pulmonary tissue under the adhesions was also examined. Two major types of adhesions were encountered, and were called type I and type II adhesions. Stages in the development and resolution of the type I adhesions were called fibrinous, early dense, dense and thin. Except for abnormalities of the blood circulatory system, the type I adhesions were similar to those in experimental models. Type II adhesions were proliferative lesions with villous projections, strands and nodules. Abnormality of the blood circulatory system also occurred in these adhesions. Most type I adhesions appeared to have developed in association-with pulmonary abscessation and pneumonia. No relationship between type II adhesions and lesions in the underlying lung was obvious.     

The pathology of peracute experimental Clostridium perfringens type D enterotoxemia in sheep.

The pathological findings in sheep with peracute experimental Clostridium perfringens type D enterotoxemia are described. Of 16 animals inoculated intraduodenally with a whole culture of this microorganism and a starch solution in the abomasum, 12 developed clinical signs including increased respiratory efforts, recumbency, paddling, bleating, convulsions, blindness, and opisthotonus. Diarrhea was not observed in any of the animals. The time lapse between the beginning of intraduodenal infusion and onset of clinical signs varied between 30 minutes and 26 hours, and the clinical course varied between 1 and 9 hours. Gross postmortem changes were observed in these 12 animals and included pulmonary edema; excess pericardial, peritoneal, or pleural fluid with or without strands of fibrin; liquid small intestinal contents; leptomeningeal edema; cerebellar coning; and subcapsular petechiae on kidneys. Histological changes consisted of severe edema of pleura and interlobular septa and around blood vessels and airways and acidophilic, homogeneous, proteinaceous perivascular edema in the brain. Five of 12 animals (42%) with clinical signs consistent with enterotoxemia lacked specific histological lesions in the brain. None of the intoxicated or control animals developed nephrosis. Glucose was detected in the urine of 3 of 6 animals that were tested for this analyte. These results stress the importance of the use of histological examination of the brain, coupled with epsilon toxin detection, for a definitive diagnosis of C. perfringens type D enterotoxemia in sheep.     

The comparative pathology of Clostridium difficile-associated disease

Clostridium difficile is a confirmed pathogen in a wide variety of mammals, but the incidence of disease varies greatly in relation to host species, age, environmental density of spores, administration of antibiotics, and possibly, other factors. Lesions vary as well, in severity and distribution within individuals, and in some instances, age groups, of a given species. The cecum and colon are principally affected in most species, but foals and rabbits develop severe jejunal lesions. Explanations for variable susceptibility of species, and age groups within a species, are largely speculative. Differences in colonization rates and toxin-receptor densities have been proposed. Clostridium difficile-associated disease is most commonly diagnosed in Syrian hamsters, horses, and neonatal pigs, but it is reported sporadically in many other species. The essential virulence factors of C. difficile are large exotoxins, toxin A (TcdA) and toxin B (TcdB). Receptor-mediated endocytosis of the toxins is followed by endosomal acidification, a necessary step for conversion of the toxin to its active form in the cytosol. Cell-surface receptors have been characterized for TcdA, but remain to be identified for TcdB. Both TcdA and TcdB disrupt the actin cytoskeleton by disrupting Rho-subtype, intracellular signaling molecules. Disruption of the actin cytoskeleton is catastrophic for cellular function, but inflammation and neurogenic stimuli are also involved in the pathogenesis of the disease.     

The current status of sheep pox disease

Sheep are the moving banks of shepherds and their economic contribution in terms of meat, wool and skin/hide is immense. Various infectious diseases jeopardize the optimum productivity; among which sheep pox is more important as the disease restricts the export of sheep and their products besides other economic losses. Although, clinical signs are indicative of the disease but a laboratory confirmation is necessary for unequivocal diagnosis and studying epidemiology. The causative agent, sheep pox virus (SPV), is antigenically and genetically closely related to goat pox virus (GPV) and lumpy skin disease virus (LSDV), the other members of the genus capripox virus. In some countries, SPV and GPV are cross infective to small ruminants posing problem in diagnosis and epidemiology. However, recent studies have showed that the viruses are phylogenetically distinct and can be differentiated by molecular tools. Prophylaxis using attenuated vaccines is the choice of control measure as the immunity is long lasting. Detailed information on isolation, identification, pathology, epidemiology, diagnosis and prophylaxis would not only help in updating the knowledge of scientific fraternity but will be useful to the policy makers in order to formulate appropriate measures for control and eradication of the disease. This synthesis is to present an up-to-date review of the disease and its control to provide the reader with an overview of the problem.     

The laboratory diagnosis of nairobi sheep disease

Summary The laboratory methods available for the isolation and identification of Nairobi sheep disease virus have been compared. The results show that inoculation of tissue culture (BHK 21 C 13) with suspensions of infected organs or plasma followed by fluorescent antibody tests on coverslip preparations gave the quickest means of identification. This test did not depend on the production of a cytopathic effect. Primary isolation of the virus in infant mouse brain and identification either by fluorescent antibody methods or by complement fixation with antigen prepared from the mouse brain offers a slightly more sensitive isolation system and would be recommended where no tissue culture facility exists.

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Diagnóstico De Laboratorio De La Enfermedad Nairobi De Las Ovejas

Resumen Se compararon los métodos de laboratorio disponibles para el aislamiento e identificación del virus de la enfermedad Nairobi de las ovejas. Los resultados demostraron, que la inoculación de cultivos de tejidos (BHK 21C13) con suspensiones de órganos afectados o plasma, con pruebas de anticuerpos fluorescentes en preparaciones sobre cubreobjetos fué el sistema más rápido para la identificación del agente etiológico. Esta prueba no dependió de la producción de efecto citopático. El aislamiento primario del virus en cerebro de ratón lactante, y su identificación posterior utilizando anticuerpos fluorescentes o fijación del complemento con antígenos preparados de cerebro de ratón, ofrece un sistema de aislamiento un poco más sensitivo. Este último método se recomienda en donde no existan facilidades para cultivo de células.

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Diagnostic De Laboratoire De La Maladie De Nairobi Du Mouton

Résumé Les méthodes de laboratoire utilisées pour isoler et identifier le virus de la maladie de Nairobi du mouton sont comparées. Les résultats montrent que l'inoculation de cultures de cellules (BHK 21, C 13) avec des suspensions d'organes ou de plasma infectés, avec examen consécutif de cultures surlamelle et immunofluorescence constituent les moyens les plus rapides d'identification. Ce dernier test ne dépend pas de la production d'effet cytopathique.L'isolement initial du virus sur cerveau de souriceau et son identification soit par la méthode des anticorps fluorescents ou par la fixation du complément avec l'antigène préparé à partir du cerveau de souris constituent des méthodes légèrement moins sensibles qui pouvent être recommandées là où n'existe aucune facilité de pratiquer la culture des cellules.

     

Johne's disease in sheep

Extract

Inoculation of susceptible laboratory animals with a suspension of kidney tissue is a widely used method of diagnosing leptospirosis in livestock and of isolating leptospiral serotypes. A recent experience has indicated a potential cause of failure which may not be generally realized in laboratories using this technique.     

Akabane disease in sheep

Perinatal lamb mortality, associated with malformations of the CNS due to Akabane viral infection, occurred in 4 of 9 flocks of ewes lambing on 3 farms between 26 May and 14 November, 1976. Cases were restricted to ewes conceiving prior to the second week of March and lambing between 26 May and 19 July. As judged by seroconversion in sentinel flocks on 2 of the farms, field infection with Akabane virus occurred mainly between mid-February and mid-April. Malformations of the CNS occurred in 42.5%, 51.2%, 100% and 31.0% of the dead lambs examined in the affected flocks respectively. Prevalence in the 4 affected flocks, expressed as the proportion of ewes lambing which delivered at least one malformed foetus, was 6.1%, 8.4%, 88.9% and 5.7% respectively. Lamb mortality due to malformations of the CNS was 7.1%, 5.5%, 92.3% and 5.7% of lambs born. Age-specific prevalence was calculated for 3 of the 4 flocks and 2-year-old ewes accounted for 71.4% and 76.9% of total cases respectively in 2 flocks, whereas in one flock malformations occurred at equivalent frequencies throughout several older age groups. Birthweights of affected lambs were usually significantly lighter than those of unaffected lambs of similar sex and birth-type, and their mean duration of gestation was slightly, and significantly, prolonged. Micrencephaly (88.1% of cases) and hydrocephalus (68.7% of cases) were the outstanding pathological features of the malformations with hydranencephaly, microgyria, porencephaly and attenuation of the spinal cord occurring at much lower frequencies.(ABSTRACT TRUNCATED AT 250 WORDS)