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Polymerase Chain Reaction Test for Clostridium difficile Toxin B Gene Reveals Similar Prevalence Rates in Children With and Without Inflammatory Bowel Disease

Lamousé-Smith, Esi S.N.*; Weber, Sarah*; Rossi, Richard F.; Neinstedt, Liliane J.*; Mosammaparast, Nima; Sandora, Thomas J.§; McAdam, Alexander J.; Bousvaros, Athos*

Journal of Pediatric Gastroenterology and Nutrition: September 2013 - Volume 57 - Issue 3 - p 293–297
doi: 10.1097/MPG.0b013e3182999990
Original Articles: Gastroenterology

Objective: Clinicians often evaluate for Clostridium difficile infection (CDI) in patients with inflammatory bowel disease (IBD) presenting with exacerbations. A highly sensitive polymerase chain reaction (PCR) test for the toxin B gene of C difficile is increasingly used to diagnose CDI. The aim of this study was to determine the prevalence of positive C difficile PCR results in children and young adults with and without active IBD compared with patients with non-IBD gastrointestinal disease.

Methods: Fecal samples were obtained from patients with ulcerative colitis (UC, n = 76) or Crohn disease (CD, n = 69) and 51 controls followed in our gastroenterology program. Samples were analyzed for C difficile using a PCR test for the C difficile toxin B gene (BD GeneOhm Cdiff assay). Proportions of positive tests in each group were compared using the Pearson χ 2 test.

Results: The prevalence of positive PCR results was 11.6% in patients with CD, 18.4% in patients with UC, and 11.8% in controls (P = 0.25). There were no significant differences in the prevalence of positive C difficile results among patients with IBD with and without active disease or among patients with and without diarrhea.

Conclusions: Positive C difficile PCR results occur with similar frequency in patients with IBD with and without active disease and in patients with other gastrointestinal diseases. A positive result in a highly sensitive PCR assay that detects low copy numbers of a toxin gene in C difficile may reflect colonization in a subset of patients with IBD, confounding clinical decision making in managing disease exacerbations.

*Division of Pediatric Gastroenterology and Nutrition

Department of Laboratory Medicine, Boston Children's Hospital, Boston, MA

Department of Pathology and Immunology, Washington University in St Louis, St Louis, MO

§Division of Infectious Diseases, Boston Children's Hospital, Boston, MA.

Address correspondence and reprint requests to Esi S.N. Lamousé-Smith, Division of Pediatric Gastroenterology and Nutrition, Hunnewell Ground HU-002, 300 Longwood Ave, Boston, MA 02115 (e-mail:

Received 12 January, 2013

Accepted 24 April, 2013

Drs Bousvaros and McAdam contributed equally to the conception and design, acquisition, analysis, and interpretation of data, and manuscript preparation.

This study was supported in part by the Rasmussen Family Fund, the MacInnes Friends and Family Fund, and the Wolfman Family Fund.

A.B. has received honoraria from Merck, consulting fees from Cubist and Dyax, and research support from Prometheus Inc and UCB. E.S.N.L.-S. receives research support from the Robert Wood Johnson Foundation. A.J.M has received consulting fees from BioMerieux. The other authors report no conflicts of interest.

© 2013 by European Society for Pediatric Gastroenterology, Hepatology, and Nutrition and North American Society for Pediatric Gastroenterology,