Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro

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C. Difficile and Fecal Microbiota Therapy
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Nat. Rev. Gastroenterol. Hepatol. doi:10.1038/nrgastro.2015.220 Figure 2 Underlying mechanisms for emerging treatment approaches for CDI Figure 2 | Underlying mechanisms for emerging treatment approaches for CDI. After antibiotic exposure, depletion of the gut microbiota permits intestinal colonization by C. difficile; production of C. difficile toxin B leads to cytotoxicity of the mucosal epithelial barrier, resulting in acute diarrhoeal illness (1). Although standard CDI antibiotic therapies suppress C. difficile, they also further suppress the gut microbiota, increasing the risk of CDI recurrence (2). Emerging narrow-spectrum antibiotics suppress C. difficile whilst sparing the gut microbiota, potentially reducing the risk of CDI recurrence (3). FMT restores a more normal gut microbiota diversity, which promotes resistance to C. difficile colonization and reduces the risk of CDI recurrence (4). Anti-toxin antibodies, produced as a result of either passive immunization with monoclonal antibodies or vaccination, are released from the systemic circulation into the gut lumen, neutralize C. difficile toxins and prevent CDI (5). Spores of NTCD strain germinate in the gut; the vegetative NTCD microorganisms colonize the gut, outcompete toxigenic C. difficile and prevent CDI recurrence (6). CDI, Clostridium difficile infection; FMT, faecal microbiota transplantation; NTCD, nontoxigenic Clostridium difficile. Kociolek, L. K. & Gerding, D. N. (2016) Breakthroughs in the treatment and prevention of Clostridium difficile infection Nat. Rev. Gastroenterol. Hepatol. doi:10.1038/nrgastro.2015.220