Related Experiment Video
Updated: Apr 11, 2026
11:13
Culturing and Maintaining Clostridium difficile in an Anaerobic Environment
Published on: September 14, 2013
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Acidification-dependent suppression of C. difficile by pathogenic and commensal enterococci
Holly R Neubauer1, Ibukun M Ogunyemi1, Alicia K Wood1
1Binghamton Biofilm Research Center, Department of Biological Sciences, Binghamton University, SUNY, Binghamton NY 13902 USA.
Biorxiv : the Preprint Server for Biology
|April 10, 2026
Summary
Vancomycin-resistant Enterococcus faecium (VRE) suppresses Clostridioides difficile growth by producing acid from specific sugars in vitro. However, dietary sugar supplementation did not prevent C. difficile colonization in mice.
Area of Science:
- Microbiology
- Pathogen Interactions
- Gut Microbiome Research
Background:
- Clostridioides difficile and Vancomycin-resistant Enterococcus faecium (VRE) are frequently co-isolated in hospital settings.
- VRE often dominates the gut after antibiotic treatment, increasing susceptibility to C. difficile infection.
Purpose of the Study:
- To develop a co-culture model to study interactions between C. difficile and VRE.
- To investigate the potential of dietary sugar supplementation to suppress C. difficile growth in the presence of VRE.
Main Methods:
- Co-culturing C. difficile and VRE in biofilm-promoting media with various carbon sources (glucose, fructose, trehalose).
- Measuring pH changes and pathogen growth inhibition.
- Testing dietary fructose supplementation in VRE-colonized mice challenged with C. difficile.
Main Results:
- VRE produced acid from specific sugars, lowering pH and inhibiting C. difficile growth in vitro.
- Acidification by VRE was essential and sufficient for C. difficile suppression in liquid and cecal content models.
- Dietary fructose supplementation in mice did not lower gut pH or prevent C. difficile colonization.
Conclusions:
- VRE suppresses C. difficile growth via carbon source-dependent organic acid production in vitro.
- Therapeutic pH modulation in the mammalian gut may require more complex strategies than simple dietary sugar supplementation.
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