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Canadian Journal of Infectious Diseases and Medical Microbiology
Volume 19, Issue 6, Pages 409-412
Original Article

Genotypic Investigation of Clostridium difficile in Prince Edward Island

H Martin,1 LP Abbott,2 DE Low,3 B Willey,3 M Mulvey,4 and J Scott Weese5

1Department of Clinical Studies, University of Guelph, Guelph, Ontario, Canada
2Queen Elizabeth Hospital, Charlottetown, Prince Edward Island, Canada
3Department of Microbiology, Mount Sinai Hospital, Toronto, Ontario, Canada
4National Microbiology Laboratory, Public Health Agency of Canada, Winnipeg, Manitoba, Canada
5Department of Pathobiology, University of Guelph, Guelph, Ontario, Canada

Received 25 June 2008; Accepted 4 September 2008

Copyright © 2008 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Clostridium difficile is an important cause of disease in Canada; however, little information is available about the disease in the Maritime provinces. The objective of the present study was to characterize C difficile isolates obtained from people hospitalized with C difficile infection in Prince Edward Island. One hundred twenty-six C difficile ELISA toxin-positive stool samples were obtained and cultured using an enrichment protocol. C difficile was isolated from 105 of 126 (83%) samples. Twenty-two different ribotypes were identified. The most common ribotype, ribotype W, was a North American pulsotype 2 (NAP2), toxinotype 0 strain, which represented 18% of isolates. The next most common ribotype was a NAP1, toxinotype III strain, which accounted for 11% of isolates. Ribotype 027/NAP1 only accounted for five (4.7%) isolates. Forty-five per cent of isolates possessed genes encoding production of binary toxin. Three different ribotypes, all NAP1, toxinotype III strains, had a frameshift mutation in the tcdC gene (Δ117), while one isolate (ribotype 078, NAP4, toxinotype V) had a truncating mutation (C184T) in the tcdC gene.