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J Glob Antimicrob Resist. 2018 Sep 25. pii: S2213-7165(18)30182-6. doi: 10.1016/j.jgar.2018.09.009. [Epub ahead of print]

Antimicrobial susceptibility and mechanisms of resistance of Greek Clostridium difficile clinical isolates.

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Department of Microbiology, University Hospital of Larissa, Larissa, Greece.
​First Department of Microbiology, Aristotle University of Thessaloniki, Medical School, Thessaloniki, Greece.
Biomedical Center, Faculty of Medicine, Charles University, Pilsen, Czech Republic.
Department of Microbiology, University Hospital of Larissa, Larissa, Greece. Electronic address:



In the present study, we examined the antimicrobial susceptibility and resistance mechanisms of Clostridium difficile recovered in Greek hospitals, during 2012-2015.


C. difficile isolates were collected from clinically-confirmed CDI from symptomatic patients in 10 Greek hospitals. MICs of various antimicrobial agents were determined by Etest. The isolates were typed by MLST. Toxin and resistance genes were detected by PCR. Chromosomal mutations in the gyrA, gyrB and rpoB genes were identified by PCR and sequencing. The genetic environment of resistance genes was characterized by Illumina sequencing.


A total of 88C. difficile were studied. The C. difficile isolates comprised 26 STs, with ST37 (n=26) and ST11 (n=21) being the most prevalent. All isolates were susceptible to vancomycin and metronidazole, while the rates of resistance to other antimicrobials varied. 45.5% of the isolates were MDR, and the majority of them belonged to ST11 and ST37. The presence of chromosomal mutations in the gyrA, gyrB and rpoB genes was mainly observed in high risk clones, like ST11 and ST37. The resistance genes ermB, mefA, msrA and tetM were identified in different prevalence and combinations. Additionally, the cfrB and cfrC were identified for the first time in Greece, and were carried by the Tn6218 transposon and a novel plasmid, respectively.


To our knowledge, this is the first study examining the resistant profiles and the respective mechanisms of C. difficile recovered in Greek hospitals. Gut commensals, like C. difficile, may serve as hubs for the further transfer of resistance genes.


ST11; ST37; Tn6218; cfrC; ermB


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