Prevalence of Clostridium perfringens type A isolates in commercial broiler chickens and parent broiler breeder hens in Egypt.

نویسندگان

  • K M Osman
  • Y A Soliman
  • Z M S Amin
  • M A K Aly
چکیده

The aim of this study was to determine the presence of genes coding for alpha (cpalpha), beta (cpbeta), epsilon (epsilontx), iota (iotaA), enterotoxin (cpepsilon) and beta2 (cpbeta2) toxins in Clostridium perfringens isolates from broiler chickens and parent broiler breeder hens, using multiplex polymerase chain reaction (PCR) assay. The prevalence of C. perfringens in the intestinal segments and the effects of age were also investigated. The highest isolation rate was from the duodenum, at 41.7% in broiler chickens and 58.4% in parent broiler breeder hens; the lowest isolation rates came from the ileum, at 15.6% and 27.1%, respectively. Chickens harboured C. perfringens in the intestine and this increased with age. Clostridium perfringens was detected in 35.4% (17/48) of asymptomatic broiler chickens and 22.1% (17/77) of asymptomatic parent broiler breeder hens. The bacterium was detected in 100% of the broiler chickens and parent broiler breeder hens with clinical signs (31/31 and 60/60, respectively). The multiplex PCR assay indicated that in 99 (79.2%) of the 125 samples that tested positive for C. perfringens the strains isolated were type A and were shown to carry the cpalpha gene (99/99, or 100%). The gene encoding cpbeta2-toxin was present in 62.6% (62/99) of the isolates. A significant association was found between C. perfringens possessing the beta2-toxin gene and necrotic enteritis in broiler chickens and parent broiler breeder hens, suggesting that this gene might play a key role in the pathogenesis of the disease in Egypt. The authors suggest that the presence of the cpbeta2-toxin gene in C. perfringens isolates found in broiler chickens and parent broiler breeder hens during this study poses a risk of transmission to humans through the food chain.

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عنوان ژورنال:
  • Revue scientifique et technique

دوره 31 3  شماره 

صفحات  -

تاریخ انتشار 2012