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Journal of Clinical Microbiology, March 2001, p. 883-888, Vol. 39, No. 3
0095-1137/01/$04.00+0   DOI: 10.1128/JCM.39.3.883-888.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Genotyping of Enterotoxigenic Clostridium perfringens Fecal Isolates Associated with Antibiotic-Associated Diarrhea and Food Poisoning in North America

Shauna G. Sparks,1 Robert J. Carman,2 Mahfuzur R. Sarker,1,dagger and Bruce A. McClane1,*

Department of Molecular Genetics and Biochemistry, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261,1 and TechLab, Inc., Corporate Research Center, Blacksburg, Virginia 240602

Received 29 September 2000/Returned for modification 28 November 2000/Accepted 8 December 2000

Clostridium perfringens type A isolates producing enterotoxin (CPE) are an important cause of food poisoning and non-food-borne human gastrointestinal (GI) diseases, including antibiotic-associated diarrhea (AAD). Recent studies suggest that C. perfringens type A food poisoning is caused by C. perfringens isolates carrying a chromosomal cpe gene, while CPE-associated non-food-borne GI diseases, such as AAD, are caused by plasmid cpe isolates. Those putative relationships, obtained predominantly with European isolates, were tested in the current study by examining 34 cpe-positive, C. perfringens fecal isolates from North American cases of food poisoning or AAD. These North American disease isolates were all classified as type A using a multiplex PCR assay. Furthermore, restriction fragment length polymorphism and pulsed-field gel electrophoresis genotyping analyses showed the North American AAD isolates included in this collection all have a plasmid cpe gene, but the North American food poisoning isolates all carry a chromosomal cpe gene. Western blotting demonstrated CPE expression by nearly all of these disease isolates, confirming their virulence potential. These findings with North American isolates provide important new evidence that, regardless of geographic origin or date of isolation, plasmid cpe isolates cause most CPE-associated AAD cases and chromosomal cpe isolates cause most C. perfringens type A food poisoning cases. These findings hold importance for the development of assays for distinguishing cases of CPE-associated food-borne and non-food-borne human GI illnesses and also identify potential epidemiologic tools for determining the reservoirs for these illnesses.

* Corresponding author. Mailing address: E1240 BST, Department of Molecular Genetics and Biochemistry, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261. Phone: (412) 648-9022. Fax: (412) 624-1401. E-mail: bamcc{at}pitt.edu.

dagger Present address: Department of Microbiology, Oregon State University, Corvallis, OR 97331.

Journal of Clinical Microbiology, March 2001, p. 883-888, Vol. 39, No. 3
0095-1137/01/$04.00+0   DOI: 10.1128/JCM.39.3.883-888.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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