difficile was grown at 37☌ in an anaerobic chamber (Coy Laboratories, USA). difficile colonies was confirmed by amplifying by PCR the triose phosphate isomerase gene ( tpi) of C. The institutional review board of the CHUS had approved our study protocol and informed consent was obtained from all patients. Feces were obtained from patients recruited during a non-outbreak period at the Centre Hospitalier Universitaire de Sherbrooke in the province of Quebec, Canada. difficile reference strains ATCC 9689, ATCC 43255 (VPI 10463) and 630 were used along with 7 other clinical isolates that were purified from feces after alcohol shock and growth on CDMN selective agar ( Clostridium difficile agar base supplemented with moxalactam and norfloxacin) (Oxoid, Canada). For this, we used a microscopic method to count vegetative cells and spores present within colonies growing on agar, as well as a classical spore recovery assay after growth and sporulation in broth cultures.Ĭ. The objective of this study was to determine the impact of sub-MIC concentrations of 5 antibiotics on sporulation of 10 different isolates of C. This suggests that antibiotics can potentially influence the number of spores that are formed during CDI and as such, directly impact the treatment outcome and the risk of recurrence. More recently, sub-MIC concentrations of fidaxomicin were shown to inhibit spore formation and toxin production in C. Previous reports suggested that sub-inhibitory (sub-MIC) concentrations of certain antibiotics can trigger C. However, the factors that affect this process are not well known. difficile is capable of forming spores, as suggested by the induction of sporulation-associated gene transcription as soon as 8 h post-infection. difficile sporulate more efficiently and to higher levels than non epidemic strains, which might explain why epidemic strains disseminate easily in hospitals, but this hypothesis is a matter of debate. Some studies suggested that epidemic strains of C. In addition, they are resistant to all known antibiotics including metronidazole (MTZ) and vancomycin (VAN).

difficile are highly resistant to harsh environments and household disinfectants and are likely responsible for efficient dissemination of C. difficile spores in the intestinal tract of the patient is possibly a prerequisite to this condition. The same strain has been isolated in 50-90% of recurrence cases, which indicates that persistence of C. difficile in the intestinal tract, or re-infection by the same or a different strain. Recurrence can be caused by the persistence of C. Prolonged disruption of the intestinal microbiota by antibiotic treatment may also increase patients’ susceptibility to recurrent CDI. Disruption of the normal intestinal microbiota is associated with a higher risk of CDI and antibiotics are generally the triggering factor. This rate ranges from 8-50% and the likelihood of recurrence increases with the number of CDI episodes, which makes the management of recurrence challenging.

difficile, NAP1/027, was associated with more severe disease, and a higher recurrence rate. The emergence of an epidemic strain of C. Several outbreaks caused by Clostridium difficile have been reported worldwide over the last decade.

C diff spore forming