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Fecal bacteriotherapy in the treatment of recurrent Clostridium difficile infection

INTRODUCTION

Relapse of Clostridium difficile occurs in 10 to 25 percent of patients treated with metronidazole or vancomycin. Furthermore, multiple relapses in the same patient are common, and up to 10 or more bouts of relapsing colitis have occurred in some patients. Cumulative experience from case series and reports shows that fecal bacteriotherapy has been used successfully to treat relapsing C. difficile infection [1] and, more recently, for refractory inflammatory bowel disease [2].

This topic will review the use of fecal bacteriotherapy for the treatment of patients with recurrent C. difficile infection. Other issues related to C. difficile infection are discussed elsewhere. (See "Epidemiology, microbiology, and pathophysiology of Clostridium difficile infection in adults" and "Clinical manifestations and diagnosis of Clostridium difficile infection in adults" and "Treatment of Clostridium difficile infection in adults".)

GUT MICROBIOTA

Gut microbiota are probably the most important first-line host defense against pathogen colonization via mechanisms involving resistance to bacterial colonization and stimulation of the mucosal immune system. "Colonization resistance" involves the production of antimicrobial factors and competition for nutrients in the matrix and for binding sites on the epithelium by resident microbiota [3]. The gut microbiota also educates and primes the mucosal immune response to maintain homeostasis of commensal microbiota, while eliminating offending pathogens [4].

The complex host-microbe interactive system involves the effects of gut microbiota on the epithelium, the hosts' immune system, and intestinal factors including mucosal vascularity, lymphoid tissue mass, and peristalsis. Taken together, this system has been described as a "virtual organ" [4]. The integrity of each component is crucial to host defense and survival. For example, evidence suggests that gut microbiota positively influence immune and inflammatory responses by fermenting dietary fiber to produce short chain fatty acids that directly bind a chemoattractant receptor, GPR43, on immune cells [5].

Disruption of the normal gut microbiota, known as dysbiosis, is caused by infectious agents and antibiotic use (eg, in patients with C. difficile infection). Studies have shown that patients with initial or recurrent C. difficile infection are deficient in Bacteroides and Firmicutes [6,7]. (See "Epidemiology, microbiology, and pathophysiology of Clostridium difficile infection in adults".)

              

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Literature review current through: 20.6: May 2012
This topic last updated: Aug 4, 2011
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