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Journal of Clinical Microbiology, January 1998, p. 30-36, Vol. 36, No. 1
Department of Molecular Genetics and
Biochemistry, School of Medicine, University of Pittsburgh,
Pittsburgh, Pennsylvania 15261
Received 5 May 1997/Returned for modification 1 August
1997/Accepted 1 October 1997
Clostridium perfringens enterotoxin (CPE) is
responsible for the diarrheal and cramping symptoms of human C. perfringens type A food poisoning. CPE-producing C. perfringens isolates have also recently been associated with
several non-food-borne human gastrointestinal (GI) illnesses, including
antibiotic-associated diarrhea and sporadic diarrhea. The current study
has used restriction fragment length polymorphism (RFLP) and
pulsed-field gel electrophoresis (PFGE) analyses to compare the
genotypes of 43 cpe-positive C. perfringens isolates obtained from diverse sources. All North American and European
food-poisoning isolates examined in this study were found to carry a
chromosomal cpe, while all non-food-borne human GI disease
isolates characterized in this study were determined to carry
their cpe on an episome. Collectively, these results
provide the first evidence that distinct subpopulations of
cpe-positive C. perfringens isolates may be
responsible for C. perfringens type
A food poisoning versus CPE-associated non-food-borne human GI
diseases. If these putative associations are confirmed in
additional surveys, cpe RFLP and PFGE genotyping assays may
facilitate the differential diagnosis of food-borne versus
non-food-borne CPE-associated human GI illnesses and may also be
useful epidemiologic tools for identifying reservoirs or
transmission mechanisms for the subpopulations of
cpe-positive isolates specifically responsible for
CPE-associated food-borne versus non-food-borne human GI diseases.
0095-1137/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Evidence That the Enterotoxin Gene Can Be
Episomal in Clostridium perfringens Isolates
Associated with Non-Food-Borne Human Gastrointestinal
Diseases
*
Corresponding author. Mailing address: E1240 Biomedical
Science Tower, School of Medicine, University of Pittsburgh,
Pittsburgh, PA 15261. Phone: (412) 648-9022. Fax: (412) 624-1401. E-mail: bamcc{at}pop.pitt.edu.
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