Theoretical Basis
The hypothesis behind fecal bacteriotherapy rests on the concept of bacterial interference, i.e. using harmless bacteria to displace pathogenic organisms. This approach to combating bacterial infections is not new and has long been used in animals, for example, to prevent salmonellosis in chickens. In the case of CDI, the C.difficile pathogen is identifiable. However in the case of pseudomembranous colitis, whilst C. difficile is the most common cause, there are other C. difficile-negative pseudomembranous colitis cases. In patients with relapsing CDI, the mechanism of action may be the restoration of missing components of the flora including Bacteroidetes and Firmicutes. The introduction of normal flora results in durable implantation of these components. Another theoretical mechanism entails the production of antimicrobial agents (Bacteriocins) by the introduced colonic flora to eradicate C.difficile. This may be a similar mechanism to that of Vancomycin which originated from soil bacteria, and bacillus thuringiensis which has been proven to produce bacteriocins specific for C. difficile. The potential combination of replacement of missing components and production of antimicrobial products manufactured by the incoming flora are likely to be the mechanisms curing CDI. In the case of ulcerative colitis, no single 'culprit' pathogen has been identified in humans. However since C.difficile colitis responds so well to FMT, it is conceivable that ulcerative colitis may respond in a similar fashion, where the offending infective agent/s are still unknown. It is also possible that an infection persists but cannot be identified as was the case with pseudomembranous colitis when it was first treated in 1958.
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