title: Necrotic enteritis-producing strains of Clostridium perfringens displace non-necrotic enteritis strains from the gut of chicks.
abstract: We inoculated broiler chicks with mixtures of Clostridium perfringens strains to investigate the single strain dominance observed in natural cases of necrotic enteritis (NE) [Nauerby, B., Pedersen, K., Madsen, M., 2003. Analysis by pulsed-field gel electrophoresis of the genetic diversity among Clostridium perfringens isolates from chickens. Vet. Microbiol. 94, 257-266]. Pre-inoculation bacteriologic culture of chick intestines yielded up to six pulsed-field gel electrophoresis (PFGE) types of C. perfringens. Birds developed typical NE lesions in response to administration (2x per day for 4 days) of a combined inoculum comprising one NE strain (JGS4143, PFGE pattern 8) and four non-NE strains (from piglet necrotizing enteritis, chicken normal flora, human gas gangrene, and bovine neonatal enteritis). After inoculation commenced, only the NE strain was recovered through the first post-inoculation day, in spite of intense efforts to recover pre-challenge flora strains and the other challenge strains. Thereafter, pre-inoculation and previously undetected PFGE types were found, and JGS4143 became undetectable. Birds inoculated simultaneously with five NE strains (from disease in chickens or turkeys, and including JGS4143) also developed lesions, but again only JGS4143 was recovered through the 1st day post-challenge. At that time, birds began to be repopulated with pre-challenge PFGE types. Two NE strains (JGS4143 and JGS4064) produced bacteriocins, which inhibited each other and normal flora strains (n=17), while normal flora strains inhibited neither NE strains nor each other. Thus, it appears that naturally occurring dominance of the gut by NE strains can be reproduced experimentally. Bacteriocins directed against normal flora could possibly provide the necessary advantage, although inhibition of one NE strain by another suggests that other factors may be partially or completely responsible for the dominance.
authors.affiliation: Department of Veterinary Science and Microbiology, The University of Arizona, Tucson, AZ 85721, USA.
authors.forename: Angelique J
authors.initials: AJ
authors.lastname: Barbara
authors.forename: Hien T
authors.initials: HT
authors.lastname: Trinh
authors.forename: Robert D
authors.initials: RD
authors.lastname: Glock
authors.forename: J
authors.initials: J
authors.lastname: Glenn Songer
mesh_terms: D000818:Animals; D015373:Bacterial Typing Techniques / Q000662:veterinary; D001430:Bacteriocins / Q000096:biosynthesis; D002645:Chickens; D003015:Clostridium Infections / Q000382:microbiology / Q000473:pathology / Q000662:veterinary*; D003016:Clostridium perfringens / Q000145:classification / Q000235:genetics / Q000302:isolation & purification / Q000472:pathogenicity*; D016521:Electrophoresis, Gel, Pulsed-Field / Q000662:veterinary; D004751:Enteritis / Q000382:microbiology / Q000473:pathology / Q000662:veterinary*; D005260:Female; D009336:Necrosis / Q000382:microbiology / Q000473:pathology / Q000662:veterinary; D011201:Poultry Diseases / Q000382:microbiology* / Q000473:pathology; D011897:Random Allocation
chemical_list: D001430:Bacteriocins