Studies of lesions produced in the brains of colostrum deprived lambs by Clostridium welchii (Cl. perfringens) Type D toxin

Buxton, D.; Morgan, K.T.

doi:10.1016/0021-9975(76)90012-8

Cited by 60 publications

(56 citation statements)

References 7 publications

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“…This pathogenesis is consistent with the main histologic alteration observed in our study, perivascular proteinaceous edema, which suggests damage to the vascular endothelium. FSE similar to what was observed in one of our experimental animals was previously described in cattle and speculatively attributed to ETX of C. perfringens type D. 1,9,11,19,20 Our results lend support to that speculation. Two animals inoculated with SUPNT recovered after developing transient mild CNS clinical alterations, which is notable because no such spontaneous recovery has been reported in ruminants with type D enterotoxemia.…”

Section: Discussionsupporting

confidence: 91%

Clinicopathologic Features of ExperimentalClostridium perfringensType D Enterotoxemia in Cattle

et al. 2009

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Abstract. This study was designed to experimentally reproduce enterotoxemia by Clostridium perfringens type D in cattle and to characterize the clinicopathologic findings of this disease. Fourteen 9-month-old calves were inoculated intraduodenally according to the following schedule: group 1 (n 5 4), C. perfringens type D whole culture; group 2 (n 5 3), C. perfringens type D washed cells; group 3 (n 5 5), C. perfringens type D filtered and concentrated supernatant; group 4 (n 5 2), sterile, nontoxic culture medium. In addition, all animals received a 20% starch solution in the abomasum. Ten animals from groups 1 (4/4), 2 (3/3), and 3 (3/5) showed severe respiratory and neurologic signs. Gross findings were observed in these 10 animals and consisted of acute pulmonary edema, excessive protein-rich pericardial fluid, watery contents in the small intestine, and multifocal petechial hemorrhages on the jejunal mucosa. The brain of one animal of group 2 that survived for 8 days showed multifocal, bilateral, and symmetric encephalomalacia in the corpus striatum. The most striking histologic changes consisted of perivascular high protein edema in the brain, and alveolar and interstitial proteinaceous pulmonary edema. The animal that survived for 8 days and that had gross lesions in the corpus striatum showed histologically severe, focal necrosis of this area, cerebellar peduncles, and thalamus. Koch's postulates have been met and these results show that experimental enterotoxemia by C. perfringens type D in cattle has similar clinical and pathologic characteristics to the natural and experimental disease in sheep.

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Section: Discussionsupporting

confidence: 91%

Clinicopathologic Features of ExperimentalClostridium perfringensType D Enterotoxemia in Cattle

et al. 2009

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“…3,5,8,10,11,17 Most of these models were based on intravenous inoculation of C. perfringens type D epsilon toxin in mice, 6,10,11 rats, 12 and sheep. 8,13,14 Characterization of the pathology of enterotoxemia in sheep has therefore largely depended on animals inoculated intravenously with epsilon toxin. 8,10,11,13 However, the gross and microscopic pathology of animals inoculated intravenously with epsilon toxin does not always reflect the changes of the natural disease.…”

Section: Introductionmentioning

confidence: 99%

The Pathology of Peracute Experimental Clostridium Perfringens Type D Enterotoxemia in Sheep

et al. 2004

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Abstract. 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.

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“…It has also been suggested that ETX acts directly on neurons (15). Many clinical signs and postmortem changes of natural type D enterotoxemia in sheep and goats may be reproduced by intravenous injection of purified ETX (7,16). However, while current evidence suggests that ETX is an important virulence factor for type D disease, there is no rigorous proof that, at natural disease production levels, ETX is an important virulence factor for type D disease.…”

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confidence: 99%

Epsilon Toxin Is Essential for the Virulence of Clostridium perfringens Type D Infection in Sheep, Goats, and Mice

et al. 2013

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dClostridium perfringens type D causes disease in sheep, goats, and other ruminants. Type D isolates produce, at minimum, alpha and epsilon (ETX) toxins, but some express up to five different toxins, raising questions about which toxins are necessary for the virulence of these bacteria. We evaluated the contribution of ETX to C. perfringens type D pathogenicity in an intraduodenal challenge model in sheep, goats, and mice using a virulent C. perfringens type D wild-type strain (WT), an isogenic ETX null mutant (etx mutant), and a strain where the etx mutation has been reversed (etx complemented). All sheep and goats, and most mice, challenged with the WT isolate developed acute clinical disease followed by death in most cases. Sheep developed various gross and/or histological changes that included edema of brain, lungs, and heart as well as hydropericardium. Goats developed various effects, including necrotizing colitis, pulmonary edema, and hydropericardium. No significant gross or histological abnormalities were observed in any mice infected with the WT strain. All sheep, goats, and mice challenged with the isogenic etx mutant remained clinically healthy for >24 h, and no gross or histological abnormalities were observed in those animals. Complementation of etx knockout restored virulence; most goats, sheep, and mice receiving this complemented mutant developed clinical and pathological changes similar to those observed in WT-infected animals. These results indicate that ETX is necessary for type D isolates to induce disease, supporting a key role for this toxin in type D disease pathogenesis.

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Studies of lesions produced in the brains of colostrum deprived lambs by Clostridium welchii (Cl. perfringens) Type D toxin

Cited by 60 publications

References 7 publications

Clinicopathologic Features of ExperimentalClostridium perfringensType D Enterotoxemia in Cattle

Clinicopathologic Features of ExperimentalClostridium perfringensType D Enterotoxemia in Cattle

The Pathology of Peracute Experimental Clostridium Perfringens Type D Enterotoxemia in Sheep

Epsilon Toxin Is Essential for the Virulence of Clostridium perfringens Type D Infection in Sheep, Goats, and Mice

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