Antimicrobial susceptibility and mechanisms of resistance of Greek Clostridium difficile clinical isolates
Language English Country Netherlands Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
30266640
DOI
10.1016/j.jgar.2018.09.009
PII: S2213-7165(18)30182-6
Knihovny.cz E-resources
- Keywords
- ST11, ST37, Tn6218, cfrC, ermB,
- MeSH
- Anti-Bacterial Agents pharmacology MeSH
- Bacterial Proteins genetics MeSH
- Clostridioides difficile classification drug effects genetics MeSH
- Clostridium Infections microbiology MeSH
- Humans MeSH
- Microbial Sensitivity Tests MeSH
- Drug Resistance, Multiple, Bacterial genetics MeSH
- Multilocus Sequence Typing MeSH
- Mutation MeSH
- Hospitals MeSH
- Bacterial Typing Techniques MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Geographicals
- Greece MeSH
- Names of Substances
- Anti-Bacterial Agents MeSH
- Bacterial Proteins MeSH
OBJECTIVES: This study examined the antimicrobial susceptibility and resistance mechanisms of Clostridium difficile recovered in Greek hospitals during 2012-2015. METHODS: C. difficile isolates (n=88) were collected from clinically-confirmed C. difficile infection from symptomatic patients in 10 Greek hospitals. Minimum inhibitory concentrations (MICs) of various antimicrobial agents were determined by Etest. Isolates were typed by multilocus sequence typing (MLST). Toxin and resistance genes were detected by PCR. Chromosomal mutations in gyrA, gyrB and rpoB were identified by PCR and sequencing. The genetic environment of resistance genes was characterised by Illumina sequencing. RESULTS: The 88 C. difficile isolates comprised 27 sequence types (STs), with ST37 (n=26) and ST11 (n=21) being the most prevalent. All isolates were susceptible to vancomycin and metronidazole, with variable resistance rates to other antimicrobials. Of the 88 isolates, 45.5% were multidrug-resistant and the majority belonged to ST11 and ST37. The presence of chromosomal mutations in gyrA, gyrB and rpoB was mainly observed in high-risk clones such as ST11 and ST37. The antimicrobial resistance genes ermB, mefA, msrA and tetM were identified at different prevalences and combinations. Additionally, cfrB and cfrC were identified for the first time in Greece and were carried by a Tn6218 transposon and a novel plasmid, respectively. CONCLUSIONS: To our knowledge, this is the first study examining the resistance profiles and respective mechanisms of C. difficile recovered in Greek hospitals. Gut commensals such as C. difficile may serve as hubs for further transfer of antimicrobial resistance genes.
Biomedical Center Faculty of Medicine Charles University Pilsen Czech Republic
Department of Microbiology University Hospital of Larissa Larissa Greece
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