Summary Clostridium perfringens type C, which produces α‐ and β‐toxin, causes severe haemorrhagic and necrotic enteritis in animals and humans. A polymerase‐chain‐reaction (PCR) assay was developed for the specific detection of the genes encoding α‐, β‐, ε‐ and enterotoxin of C. perfringens for rapid typing of C. perfringens strains, and especially for the identification of type C strains. Both the α‐ and β‐toxin genes were detected directly in porcine C. perfringens type C cultures and also in type B and type C collection strains to a sensitivity of 103 cells without purification of the DNA. The α‐toxin gene was detected in all types of C. perfringens. The ε‐toxin gene was found in type B and type D, and the enterotoxin gene in some type A strains. Nine other species of Clostridium and a variety of intestinal pathogenic bacteria showed no signal for these toxin genes in this PCR assay. The α‐ and β‐toxin genes PCR assay were used to identify C. perfringens strains isolated from intestinal contents of 36 necropsied piglets that had suddenly died or died after premonitory signs of diarrhoea. At necropsy, 20 piglets showed necrotizing enteritis (15 acute and 5 chronic cases) and were suspected to have suffered from a C. perfringens type C infection. All of them had C. perfringens which gave a positive PCR signal for α‐ and β‐toxin genes, and, hence, were identified as type C strains. From the 16 other piglets with lesions other than necrotizing enteritis, C. perfringens strains with the α‐toxin gene, but no β‐toxin gene, were isolated. The necropsy findings and the anamnesis showed a very good correlation with the PCR identification of toxin genes. It was therefore concluded that the PCR‐based toxin gene examination is a good alternative to the time‐consuming, less specific, and more expensive mouse neutralization test in the routine diagnostic laboratory.

Summary A total of 70 puppies and their dams, distributed in 14 litters, were submitted to weekly fecal examinations for C. difficile during the first 10 weeks after birth. During the study, 94.3% of the puppies and 42.9% of the dams harboured C. difficile at least once in their feces. We calculated that 58% of the puppies carried toxigenic C. difficile at least once during the survey. In the puppies, C. difficile carriage rates ranging from 3.1% to 67.1% were observed at different moments of the observation period. In comparison, C. difficile carriage rate was 1.4% in a control group of healthy dogs more than 3 months old. Discrepancies in the toxigenic phenotype of the C. difficile strains isolated in the same litter showed that the neonate dogs were transiently infected with different strains, and that the dam is often not the source of infection with C. difficile. We could not demonstrate any pathogenicity of C. difficile for neonate dogs.