Abstract
BackgroundClostridium 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.AimTo analyze baiCD gene abundance in C. difficile positive and negative fecal samples.Material & methodsA 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.ResultsThe 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.ConclusionFecal 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.
Highlights
Clostridium difficile infection (CDI) is the major cause of hospital-acquired diarrhea and is associated with significant morbidity and mortality [1,2,3]
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
No differences in baiCD gene cluster prevalence were seen between NC and non-toxigenic C. difficile colonization (NTCD) or NC and toxigenic C. difficile colonization (TCD) samples
Summary
Clostridium difficile infection (CDI) is the major cause of hospital-acquired diarrhea and is associated with significant morbidity and mortality [1,2,3]. Direct mechanisms include the competition for nutrients, the conversion of nutrients (e.g. small chain fatty acids, SCFA) or host metabolites to other compounds (e.g. secondary bile acids), as well as the inhibition of C. difficile by the production of primary microbial products (e.g. thuricin CD produced by Bacillus thuringiensis) [4, 7,8,9,10]. Indirect inhibition relates to microbiota-induced host immune reaction to control C. difficile colonization and proliferation. 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
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