Role of the Intestinal Microbiota in Resistance to Colonization by Clostridium difficile
Open accessAbstract
Antibiotic-associated infection with the bacterial pathogen Clostridium difficile is a major cause of morbidity and increased health care costs. C difficile infection follows disruption of the indigenous gut microbiota by antibiotics. Antibiotics create an environment within the intestine that promotes C difficile spore germination, vegetative growth, and toxin production, leading to epithelial damage and colitis. Studies of patients with C difficile infection and animal models have shown that the indigenous microbiota can inhibit expansion and persistence of C difficile. Although the specific mechanisms of these processes are not known, they are likely to interfere with key aspects of the pathogen's physiology, including spore germination and competitive growth. Increasing our understanding of how the intestinal microbiota manage C difficile could lead to better means of controlling this important nosocomial pathogen.
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Susceptibility to CDI is predominantly driven by antibiotic-induced perturbations to the intestinal microbiota resulting in a loss of colonization resistance.
“Susceptibility to CDI is predominantly driven by antibiotic-induced perturbations to the intestinal microbiota resulting in a loss of colonization resistance”
From Bile salt hydrolases shape the bile acid landscape and restrict Clostridioides difficile growth in the murine gut (2023) · cites this paper as [24]
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“difficile infection are correlated with the findings of animal experimental studies [85].”
BackgroundAroutcheva, A., Auclair, J., Frappier, M., Millette, M., Lolans, K., de Montigny, D., Carrière, S., Sokalski, S., Trick, W. E., & Weinstein, R. A. (2016) · Probiotics and Antimicrobial Proteins · doi:10.1007/s12602-016-9209-y · Cited by 25 · see citing works
- Authors
- Britton, R. A., & Young, V. B.
- Affiliations
- Michigan State University (US)
- University of Michigan (US)
- Corresponding author
- Young, Vincent B.
- Venue
- Gastroenterology
- Publisher
- Elsevier BV
- Published
- 2014-05
- Volume
- 146
- Issue
- 6
- Pages
- 1547-1553
- ISSN
- 0016-5085 (ISSN-L)
- PMC
- PMC3995857
- OpenAlex
- W2025786976
- Cited by
- 446
- References
- 68
- Citations by year
- 2026: 13 · 2025: 27 · 2024: 34 · 2023: 38 · 2022: 30 · 2021: 40 · 2020: 44 · 2019: 39 · 2018: 37 · 2017: 35 · 2016: 44 · 2015: 46 · 2014: 19
- FWCI
- 6.66
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Gastroenterology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Public Health Service (U19090872)
- National Institute of Allergy and Infectious Diseases (U19AI090871, U19AI090872)
- National Institute of Diabetes and Digestive and Kidney Diseases (P30DK034933)
- Topics
- Health Sciences › Medicine › Infectious Diseases › Clostridium difficile and Clostridium perfringens research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
- Keywords
- Clostridium difficile, gut microbiota, antibiotic-associated diarrhea, Clostridium difficile infection, spore germination, toxin production, competitive exclusion, colitis, nosocomial infections, gut dysbiosis
- MeSH terms
- Animals, Anti-Bacterial Agents, Bile Acids and Salts, Biological Therapy, Disease Models, Animal, Enterocolitis, Pseudomembranous, Feces, Humans, Intestinal Mucosa, Intestines, Clostridioides difficile, Probiotics, Host-Pathogen Interactions, Microbiota, Dysbiosis
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