Clostridium difficile infection (CDI) is the leading health care–associated illness. Both human and animal models have demonstrated the importance of the gut microbiota’s capability of providing colonization resistance against C. difficile. Risk factors for disease development include antibiotic use, which disrupts the gut microbiota, leading to the loss of colonization resistance and subsequent CDI. Identification of the specific microbes capable of restoring this function remains elusive. Future studies directed at how microbial communities influence the metabolic environment may help elucidate the role of the microbiota in disease development. These findings will improve current biotherapeutics for patients with CDI, particularly those with recurrent disease.
Development of disease is dependent on different stages of the C. difficile life cycle. Initial spore exposure from various sources does not necessarily result in disease, particularly in a healthy individual. A healthy, diverse microbiota is capable of interfering with C. difficile spore germination and vegetative growth. However, if the metabolic and microbial environment of the gut has been perturbed, spore germination, vegetative outgrowth, and toxin production will occur. Epithelial damage, inflammation, and clinically overt disease will result from toxin production. Sporulation of C. difficile, release of spores into the environment, and transmission to new hosts perpetuates the infectious cycle.
