BaiCD gene cluster abundance is negatively correlated with Clostridium difficile infection

PLoS One. 2018 May 8;13(5):e0196977. doi: 10.1371/journal.pone.0196977. eCollection 2018.

Abstract

Background: Clostridium difficile infection (CDI) is a major cause of hospital-acquired diarrhea. Secondary bile acids were shown to confer resistance to colonization by C. difficile. 7α-dehydroxylation is a key step in transformation of primary to secondary bile acids and required genes have been located in a single bile acid-inducible (bai) operon in C. scindens as well as in C. hiranonis, two Clostridium sp. recently reported to protect against C. difficile colonization.

Aim: To analyze baiCD gene abundance in C. difficile positive and negative fecal samples.

Material & methods: A species-specific qPCR for detecting baiCD genes was established. Fecal samples of patients with CDI, asymptomatic toxigenic C. difficile colonization (TCD), non-toxigenic C. difficile colonization (NTCD), of C. difficile negative (NC) patients, and of two patients before and after fecal microbiota transplantation (FMT) for recurrent CDI (rCDI) were tested for the presence of the baiCD genes.

Results: The prevalence of the baiCD gene cluster was significantly higher in C. difficile negative fecal samples than in samples of patients diagnosed with CDI (72.5% (100/138) vs. 35.9% (23/64; p<0.0001). No differences in baiCD gene cluster prevalence were seen between NC and NTCD or NC and TCD samples. Both rCDI patients were baiCD-negative at baseline, but one of the two patients turned positive after successful FMT from a baiCD-positive donor.

Conclusion: Fecal samples of CDI patients are less frequently baiCD-positive than samples from asymptomatic carriers or C. difficile-negative individuals. Furthermore, we present a case of baiCD positivity observed after successful FMT for rCDI.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Anti-Bacterial Agents / therapeutic use
  • Bacterial Proteins / genetics*
  • Bacterial Toxins
  • Bile / microbiology
  • Bile Acids and Salts / biosynthesis
  • Bile Acids and Salts / genetics*
  • Clostridioides difficile / genetics*
  • Clostridioides difficile / pathogenicity
  • Clostridium Infections / genetics*
  • Clostridium Infections / microbiology
  • Clostridium Infections / transmission
  • Diarrhea / genetics*
  • Diarrhea / microbiology
  • Fecal Microbiota Transplantation
  • Feces / microbiology
  • Female
  • Humans
  • Male
  • Microbiota / genetics

Substances

  • Anti-Bacterial Agents
  • Bacterial Proteins
  • Bacterial Toxins
  • Bile Acids and Salts

Grants and funding

This project was supported by grants from the German Center for Infection Research (DZIF). Work in the laboratory of Sebastian Suerbaum was funded by DZIF and by a grant from the State of Lower Saxony in the framework of the consortium “CDiff: Epidemiology and systems biology of the bacterial pathogen Clostridium difficile” (VW NZ 2889). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.