Table 1.

General mechanisms of pathogenesis of Clostridioides difficile infection that represent targets of microbiota restoration therapy.

Pathogenesis of rCDI
Antibiotic classes differ in their potential to deplete the gut microbiome, predisposing patients to CDI and recurrences of CDI11,12 and producing immune and inflammatory events. 13	Primary bile acids (e.g. cholic acid) produced in the liver lead to the germination of C. difficile spores 14 with enhanced toxigenicity, 15 with reduced levels of secondary bile acids 16 caused by antibiotic-induced alterations of the microbiome (dysbiosis), all contributing to the pathogenesis of rCDI.
Microbiome changes in microbiota replacement therapy of C. difficile recurrence by FMT or LBP
Reestablishment of a diverse microbiome depleted by antibiotics as measured by α- and β-diversity 17 leads to resistance to CDI and a healthy gut. 18	Intestinal colonization resistance improves enhancing the immune system and a healthy epithelial barrier. 19	Diverse colonic microbiota modify primary bile aids producing secondary bile acids (related to lithocholic acid), preventing C. difficile spore germination and growth of vegetative cells. 20

CDI, Clostridium difficile infection; α-diversity, mean species diversity; β-diversity, species diversity between two microbial communities; LBP, live biotherapeutic product; rCDI, recurrent CDI.