INTRODUCTION

Relapse of Clostridium difficile (C. 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 inflammatory bowel disease [2,3]. The term fecal microbiota transplantation (FMT) is preferable to fecal bacteriotherapy as it is unknown whether its efficacy is due to one or more bacteria or other gut microorganisms or agents acting alone or in combination.

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

RATIONALE FOR FECAL MICROBIOTA TRANSPLANTATION

The gastrointestinal tract harbors a stable, highly complex community of microorganisms which exists in symbiosis with the host. The human gut microbiota is estimated to consist of as many as 1000 to 1200 bacterial species and at least 10¹⁴ bacteria, most of which are in the colon [4]. The beneficial roles mediated by the microbiota for the host include the synthesis of vitamins, the fermentation of dietary carbohydrates, the metabolism of bile and host hormones and competitive exclusion ("colonization resistance") of pathogens taking residence in the gut community [5]. The microbiota also influences the development and maturation of the immune system through interactions with the gut epithelium [6,7].

The composition of the microbiota is significantly affected by the extensive use of antibiotics which could lead to a selective removal of a group of bacteria species that serve as a barrier to colonization and/or persistence of pathogens [8,9]. Antibiotic-mediated changes in the composition of the gut microbiota may also lead to homeostatic imbalance through alterations in the gut barrier functions and result in mucosal immune defects, which would predispose the host to enteric infections such as C. difficile by allowing environmentally acquired spores to germinate and successfully colonize the gut [10].

Although specific antimicrobial therapy is effective against C. difficile infection, recurrence of C. difficile infection is an increasing problem following therapy. Recurrent C. difficile is associated with a decrease in fecal microbial diversity deficient in Bacteroides and Firmicutes, both of which generally dominate within the gut microbiota [11,12]. Transplantation of stool from healthy individuals to patients with recurrent C. difficile restores these strains and breaks the cycle of recurrence [13-16].