Solid feed provision reduces fecal clostridial excretion in veal calves

Enterotoxemia is characterized by a highly fatal hemorrhagic enteritis in cattle, caused by Clostridium perfringens. Production systems with intensive feeding, such as the veal industry, are predisposed. The primary objective of this study was to determine the effect of solid feed provision on fecal C. perfringens excretion in veal calves. Ten Holstein Friesian bull veal calves were randomly assigned to one of two test diets. Group I received solemnly milk replacer twice daily, while group 2 received milk replacer and a maximum of 300g solid feed/day, consisting of a mixture of 30% barley, 30% corn, 30% hulled wheat and 10% chopped straw. The number of C. perfringens per g feces or fecal clostridia! counts (FCC) were determined for all calves. Mean FCC were significantly lower in the calves fed milk replacer and solid feed, than in the calves fed solemnly milk replacer. Although the correlation between FCC and enterotoxemia risk remains to be determined, the provision of solid feed to veal calves reduced clostridial excretion, which might contribute to the prevention of this disease

Synergistic Effects of Clostridium perfringens Enterotoxin and Beta Toxin in Rabbit Small Intestinal Loops

The ability of Clostridium perfringens type C to cause human enteritis necroticans (EN) is attributed to beta toxin (CPB). However, many EN strains also express C. perfringens enterotoxin (CPE), suggesting that CPE could be another contributor to EN. Supporting this possibility, lysate supernatants from modified Duncan-Strong sporulation (MDS) medium cultures of three CPE-positive type C EN strains caused enteropathogenic effects in rabbit small intestinal loops, which is significant since CPE is produced only during sporulation and since C. perfringens can sporulate in the intestines. Consequently, CPE and CPB contributions to the enteropathogenic effects of MDS lysate supernatants of CPE-positive type C EN strain CN3758 were evaluated using isogenic cpb and cpe null mutants. While supernatants of wild-type CN3758 MDS lysates induced significant hemorrhagic lesions and luminal fluid accumulation, MDS lysate supernatants of the cpb and cpe mutants caused neither significant damage nor fluid accumulation. This attenuation was attributable to inactivating these toxin genes since complementing the cpe mutant or reversing the cpb mutation restored the enteropathogenic effects of MDS lysate supernatants. Confirming that both CPB and CPE are needed for the enteropathogenic effects of CN3758 MDS lysate supernatants, purified CPB and CPE at the same concentrations found in CN3758 MDS lysates also acted together synergistically in rabbit small intestinal loops; however, only higher doses of either purified toxin independently caused enteropathogenic effects. These findings provide the first evidence for potential synergistic toxin interactions during C. perfringens intestinal infections and support a possible role for CPE, as well as CPB, in some EN cases