Biology & Ecology
Biology
Gram Statusgram-positive
Oxygen Toleranceobligate anaerobe
Morphologybacillus (rod)
Key Traits
- biofilm-forming
- spore-forming
- toxin-producing
Ecology
Primary Nichesgut
Reservoiranimal, environment, human
Transmission
- fecal-oral
- healthcare-associated
Clinical Profile
Pathobiont
yes
no
context dependent
unknown
Clinical Rolesopportunistic pathogen; primary pathogen
Typical Specimencolon tissue; stool
Bloom Triggers
antibiotic exposure ·
broad-spectrum beta-lactams ·
D00277
clindamycin ·
dietary change ·
dysbiosis ·
fluoroquinolones ·
hospitalization ·
immunosuppression ·
inflammation
Risk Contextselderly; ICU / critical care; immunocompromised patients; inflammatory bowel disease (IBD); oncological disease; ongoing antibiotic treatment; post-antibiotic; prior CDI episode; renal insufficiency
AMR Highlights
3004305
multidrug-resistant (MDR)
Clinical Associations:
E3
E3 — Strong human clinical evidence
E2 — Moderate human evidence
E1 — Limited / preliminary
E3
E3 — Strong human clinical evidence
E2 — Moderate human evidence
E1 — Limited / preliminary
E3
E3 — Strong human clinical evidence
E2 — Moderate human evidence
E1 — Limited / preliminary
E3
E3 — Strong human clinical evidence
E2 — Moderate human evidence
E1 — Limited / preliminary
Antibiotic-induced disruption of the gut microbiome triggers germination of C. difficile spores into vegetative cells that produce enterotoxins, causing watery diarrhea and colonic inflammation.
PMID:
38584858
E1
E3 — Strong human clinical evidence
E2 — Moderate human evidence
E1 — Limited / preliminary
Clostridioides difficile was identified as the causative pathogen of diarrhea/colitis in one critically ill ICU patient (Patient 43) who had concurrent progressive fecal Enterobacteriaceae enrichment, representing an incidental CDI case within a 51-patient prospective cohort studying ICU-associated gut dysbiosis.
PMID:
36894652
E1
E3 — Strong human clinical evidence
E2 — Moderate human evidence
E1 — Limited / preliminary
In antibiotic-treated mice, cecal cholate levels become elevated while bacterial transformation to secondary bile acids (deoxycholate, lithocholate) is greatly suppressed; this antibiotic-induced shift in the bile acid pool promotes C. difficile spore germination by providing the cholate co-stimulant while removing the inhibitory secondary bile acids that are normally produced by commensal microbiota from primary bile acids.
PMID:
24503131
Last reviewed: 2026-04-03
Evidence Timeline
Related Taxa
Shared Niche = same body site
Shared Risk = same vulnerable population
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