Antimicrobial susceptibility and resistance mechanisms of clinical Clostridium difficile from a Chinese tertiary hospital.

Clostridium difficile is a predominant cause of antibiotic-associated diarrhoea. It is increasingly difficult to treat C. difficile infection efficiently owing to its multidrug resistance. In the present study, 60 clinical C. difficile isolates were collected and analysed for their genotype, antimicrobial susceptibility and resistance mechanisms. Tandem repeat sequence typing (TRST) generated 21 types, including the epidemic clone tr017. Antimicrobial susceptibility testing of eight antibiotics was performed by the agar dilution method. Rifampicin, metronidazole and vancomycin remained the most potent agents in vitro, whilst the resistance rates of other agents such as ciprofloxacin, cefoxitin, clindamycin, tetracycline and moxifloxacin varied from 30% to 100%. 73.33% of the strains were multiresistant to at least three classes of antibiotics, and tr017 strains made up the greatest proportion of multidrug resistance. By further investigating the resistance mechanisms, amino acid substitutions in target enzymes encoded by gyrA/gyrB and rpoB were observed in fluoroquinolone- and rifampicin-resistant strains, respectively. The erm(B) gene was the most prevalent in macrolide-lincosamide-streptogramin B (MLS(B))-resistant strains, and the ErmB determinant 'Erj2', a novel genetic organisation identified in this study, plays a central role in conferring resistance, especially in epidemic strains. Moreover, transposon Tn916 carrying the tet(M) gene is more common than Tn5397 in tetracycline resistance.