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Clostridioides difficile colonization and expansion is a complex biological process rather than a single molecular target. It describes the stage of infection where C. difficile spores germinate and the resulting vegetative bacteria proliferate within the human colon, typically following the disruption of the protective gut microbiota by broad-spectrum antibiotics (Seekatz & Young, 2014). This expansion is a prerequisite for the production of Toxin A and Toxin B, which are the primary virulence factors responsible for the mucosal inflammation and damage seen in Clostridioides difficile infection (CDI) (Guery et al., 2018). While traditional therapies like vancomycin and fidaxomicin target the bacteria directly to stop expansion, newer live biotherapeutic products such as SER-109 and Rebyota aim to suppress this process by restoring the ecological balance and 'colonization resistance' of the microbiome (FDA, 2023). Because this term encompasses a multi-step pathological event involving bacterial adherence, nutrient competition, and metabolic interactions with bile acids, it is classified as a disease process or phenotype rather than a discrete therapeutic target like a receptor or enzyme (Czepiel et al., 2019).
Inhibition of bacterial cell wall synthesis or RNA polymerase, neutralization of bacterial toxins, or restoration of gut microbiota to provide colonization resistance.
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