Genotyping of enterotoxigenic Clostridium perfringens fecal isolates associated with antibiotic-associated diarrhea and food poisoning in North America

Citation
Sg. Sparks et al., Genotyping of enterotoxigenic Clostridium perfringens fecal isolates associated with antibiotic-associated diarrhea and food poisoning in North America, J CLIN MICR, 39(3), 2001, pp. 883-888
Citations number
26
Categorie Soggetti
Clinical Immunolgy & Infectious Disease",Microbiology
Journal title
JOURNAL OF CLINICAL MICROBIOLOGY
ISSN journal
00951137 → ACNP
Volume
39
Issue
3
Year of publication
2001
Pages
883 - 888
Database
ISI
SICI code
0095-1137(200103)39:3<883:GOECPF>2.0.ZU;2-2
Abstract
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 stud ies suggest that C. perfringens type A food poisoning is caused by C. perfr ingens isolates carrying a chromosomal cpe gene, while CPE-associated non-f ood-borne GI diseases, such as AAD, are caused by plasmid cpe isolates. Tho se putative relationships, obtained predominantly with European isolates, w ere tested in the current study by examining 34 cpe-positive, C. perfringen s fecal isolates from North American cases of food poisoning or AAD. These North American disease isolates were all classified as type A using a multi plex PCR assay. Furthermore, restriction fragment length polymorphism and p ulsed-field gel electrophoresis genotyping analyses showed the North Americ an AAD isolates included in this collection all have a plasmid cpe gene, bu t the North American food poisoning isolates all carry a chromosomal cpe ge ne. Western blotting demonstrated CPE expression by nearly all of these dis ease isolates, confirming their virulence potential. These findings with No rth American isolates provide important new evidence that, regardless of ge ographic origin or date of isolation, plasmid cpe isolates cause most CPE-a ssociated AAD cases and chromosomal cpe isolates cause most C. perfringens type A food poisoning cases. These findings hold importance for the develop ment of assays for distinguishing cases of CPE-associated food-borne and no n-food-borne human GI illnesses and also identify potential epidemiologic t ools for determining the reservoirs for these illnesses.