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Journal of Clinical Microbiology, June 2005, p. 2685-2696, Vol. 43, No. 6
0095-1137/05/$08.00+0     doi:10.1128/JCM.43.6.2685-2696.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Molecular Epidemiology of Endemic Clostridium difficile Infection and the Significance of Subtypes of the United Kingdom Epidemic Strain (PCR Ribotype 1)

Warren N. Fawley, Peter Parnell, Paul Verity, Jane Freeman, and Mark H. Wilcox*

Department of Microbiology, Leeds Teaching Hospitals & University of Leeds, Leeds, United Kingdom

Received 24 September 2004/ Returned for modification 5 January 2005/ Accepted 1 February 2005

We previously identified two subtypes of the epidemic strain Clostridium difficile PCR ribotype 1, one clindamycin-sensitive strain (arbitrarily primed PCR [AP-PCR] type Ia) and a closely related clindamycin-resistant strain (AP-PCR type Ib) in our institution. We have now carried out prospective epidemiological surveillance for 4 years, immediately following the relocation of two acute medicine wards for elderly patients (wards A and B), to determine the clinical epidemiology of subtypes of the epidemic C. difficile PCR ribotype 1 group. To maximize the chance of strain discrimination, we used three DNA fingerprinting methods, AP-PCR, ribospacer PCR (RS-PCR), and pulsed-field gel electrophoresis (PFGE), to analyze C. difficile isolates recovered from symptomatic patients and from repeated environmental samplings. On ward B the incidence of C. difficile infection correlated significantly with the prevalence of environmental C. difficile both in ward areas closely associated with patients and health care personnel (r = 0.53; P < 0.05) and in high-reach sites (r = 0.85; P < 0.05). No such relationships were found on ward A. Seventeen distinct C. difficile genotypes were identified, 17 by AP-PCR, 12 by PFGE, and 11 by RS-PCR, but only 4 of 17 genotypes caused patient infection. Isolates recovered from the hospital ward environment were much more diverse (14 genotypes). AP-PCR type Ia represented >90% of the C. difficile isolates. In addition to this genotype, only two others were isolated from both patient feces and environmental surfaces. AP-PCR type Ib (clindamycin-resistant PCR ribotype 1 clone) was not associated with any cases of C. difficile infection and was isolated from the environment on only two occasions, after having been implicated in a cluster of six C. difficile infections 5 months before this study. The disappearance of this strain implies that differences in virulence and/or selective pressures may exist for this strain and the closely related, widespread C. difficile AP-PCR type Ia strain. Our findings emphasize the need to understand the epidemiology and virulence of clinically significant strains to determine successful control measures for C. difficile infections.

* Corresponding author. Mailing address: Clinical Director of Microbiology, Leeds General Infirmary & University of Leeds, Old Medical School, Leeds LS1 3EX, United Kingdom. Phone: 44 113 392 6818. Fax: 44 113 343 5649. E-mail: Mark.Wilcox{at}leedsth.nhs.uk.

Journal of Clinical Microbiology, June 2005, p. 2685-2696, Vol. 43, No. 6
0095-1137/05/$08.00+0     doi:10.1128/JCM.43.6.2685-2696.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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