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JAC Advance Access published online on April 28, 2005
Journal of Antimicrobial Chemotherapy, doi:10.1093/jac/dki120
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© The Author 2005. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For Permissions, please e-mail: journals.permissions@oupjournals.org
Received September 3, 2004
Revised March 9, 2005
Accepted March 14, 2005

Original article

Effects of piperacillin/tazobactam on Clostridium difficile growth and toxin production in a human gut model

Simon D. Baines 1, Jane Freeman 1, and Mark H. Wilcox 1*

1 Department of Microbiology, University of Leeds and The General Infirmary, Old Medical School, Leeds LS1 3EX, UK

* To whom correspondence should be addressed.
Mark H. Wilcox, E-mail: mark.wilcox{at}leedsth.nhs.uk


  Abstract

Objectives: Clostridium difficile infection (CDI) is a major cause of morbidity in the nosocomial environment. Antimicrobial agents such as the third-generation cephalosporins, lincosamides and aminopenicillins are well known for their propensity to induce CDI, but the definitive reasons why remain to be elucidated. Despite their broad spectrum of activity against both aerobic and anaerobic bacteria, the ureidopenicillins remain a class of antimicrobials infrequently associated with the development of CDI.

Methods: We used a triple-stage chemostat model that simulates the human gut to study the effects of the ureidopenicillin/{beta}-lactamase inhibitor combination piperacillin/tazobactam on gut bacterial populations and C. difficile.

Results: Piperacillin/tazobactam rapidly reduced all enumerated gut bacterial populations (including bacteroides, bifidobacteria and lactobacilli) below the limits of detection by the end of the piperacillin/tazobactam instillation period. Despite such widespread disruption of gut bacterial populations, C. difficile populations remained principally as spores, with no sustained proliferation or high-level cytotoxin production observed.

Conclusions: Factors other than reduced colonization resistance must be responsible for determining whether CDI develops following antimicrobial administration. We believe the gut model is a promising approach for the study of C. difficile pathogenesis reflecting in vivo events likely to occur in CDI.

Keywords: colonization resistance; pathogenesis; germination; spores.
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