Inactivation of the gene (cpe) encoding Clostridium perfringens enterotoxin eliminates the ability of two cpe‐positive C. perfringens type A human gastrointestinal disease isolates to affect rabbit ileal loops

Abstract

The authors of this article, which was published in Mol Microbiol (1999) 33 (5): 946-958, would like to apologize for the omission of the following in the Acknowledgements section: 'The authors also wish to thank Dr Stephen Melville, University of Tennessee School of Medicine, Memphis, TN, USA, for the generous gift of C. perfringens strain SM101. ' In addition, in recognition of this gift, they would like to add the following amendments to their text. On page 947, the first sentence of the first paragraph in column two should read: 'In order to evaluate the contribution of CPE to the GI pathogenesis of cpe-positive C. perfringens isolates better, our current study prepared an isogenic cpe knock-out mutant of SM101, which is an electroporatable derivative of C. perfringens type A food poisoning isolate NCTC 8798 (Zhao and Melville, 1998) On page 954, sentence eight of the full paragraph in column two should read: 'Consequently, we (for F4969) and others (for SM101; Zhao and Melville, 1998) expended considerable effort identifying wild-type cpe-positive isolates susceptible, at any frequency, to electroporation; we then faced the challenge of introducing our suicidal plasmid into these isolates, which was made more difficult by the low frequency of electroporation of this suicidal plasmid into SM101 and F4969.' Reference Zhao, Y., and Melville, S.B. (1998) Identification and characterization of sporulation-dependent promoters upstream of the enterotoxin gene (cpe) of Clostridium perfringens.

The enteric toxins of Clostridium perfringens

“…Some earlier in vivo studies using CPE-treated rabbit ileal loops observed inflammatory cell (mostly PMNs) infiltration (McDonel et al 1978), while other studies using the same in vivo model failed to detect any CPE-induced inflammation (Sarker et al 1999;Sherman et al 1994). The presence or absence of inflammatory cell infiltration in those rabbit ileal loop experiments appeared to be CPE dose-dependent, with inflammation more prominent in the ileal loops treated with high CPE doses (McDonel and Duncan 1975).…”

“…More recently, molecular Koch's postulates analyses using an isogenic cpe mutant of SM101 (a transformable derivative of food poisoning isolate NCTC 8798) confirmed that CPE expression is required for CPE-positive, type A food poisoning isolates to cause GI effects in animal models (Sarker et al 1999). Additionally, CPE-positive type A isolates became implicated during the mid-1980s as the cause of up to 5-15% of all human nonfood-borne GI disease cases, e.g., antibiotic-associated diarrhea (AAD; Borriello et al 1984).…”

“…Additionally, CPE-positive type A isolates became implicated during the mid-1980s as the cause of up to 5-15% of all human nonfood-borne GI disease cases, e.g., antibiotic-associated diarrhea (AAD; Borriello et al 1984). Molecular Koch's postulate analyses have also supported the importance of CPE expression for the enteric virulence of the nonfood-borne human GI disease type A isolate F4969 (Sarker et al 1999). Finally, CPE-positive type A isolates have recently been linked to some veterinary diarrheas (Songer 1996).…”

“…The reasons for these specific cpe genotype:GI disease relationships are just now emerging. Chromosomal cpe isolates appear to be strongly associated with food poisoning because (1) these are the predominant cpe-positive isolates present in foods (Wen 2004), and (2) the higher heat resistance of spores/vegetative cells of these isolates (versus the spores/cells of plasmid cpe isolates; Sarker et al 1999) favors their survival in temperature-abused foods. The strong linkage between plasmid cpe isolates and AAD/SD could be explained, at least in part, by recent studies demonstrating the transfer of the cpe plasmid between C. perfringens isolates (Brynestad et al 2001).…”

Clostridium perfringens enterotoxin

“…For example, this toxin is detectable in the feces of virtually all people suffering from C. perfringens type A food poisoning and human volunteer feeding studies showed that ingestion of purified CPE is sufficient to reproduce the diarrhea and cramping symptoms of the natural food poisoning [1]. Most importantly, Molecular Koch's postulate analyses showed that CPE expression is required for the enteric virulence of food poisoning isolates in rabbit ileal loops [8].…”