Antimicrobial resistance in Clostridium difficile ribotype 017

ABSTRACT

Introduction: Antimicrobial resistance (AMR) played an important role in the initial outbreaks of Clostridium difficile infection (CDI) in the 1970s. C. difficile ribotype (RT) 017 has emerged as the major strain of C. difficile in Asia, where antimicrobial use is poorly regulated. This strain has also caused CDI outbreaks around the world for almost 30 years. Many of these outbreaks were associated with clindamycin and fluoroquinolone resistance. AMR and selective pressure is likely to be responsible for the success of this RT and may drive future outbreaks.

Areas covered: This narrative review summarizes the prevalence and mechanisms of AMR in C. difficile RT 017 and transmission of these AMR mechanisms. To address these topics, reports of outbreaks due to C. difficile RT 017, epidemiologic studies with antimicrobial susceptibility results, studies on resistance mechanisms found in C. difficile and related publications available through Pubmed until September 2019 were collated and the findings discussed.

Expert opinion: Primary prevention is the key to control CDI. This should be achieved by developing antimicrobial stewardship in medical, veterinary and agricultural practices. AMR is the key factor that drives CDI outbreaks, and methods for the early detection of AMR can facilitate the control of outbreaks.

KEYWORDS:

• Antimicrobial resistance
• Clostridium difficile
• outbreak
• prevention
• ribotype 017

Article highlights

• Most outbreaks of C. difficile infection (CDI) in the past have been associated with antimicrobial resistance (AMR).

• C. difficile ribotype (RT) 017 displays a higher prevalence of AMR than other RTs.

• An increase in AMR prevalence in C. difficile RT 017 increases the risk of future outbreaks and may complicate treatment options for CDI.

Declaration of interest

T V Riley has received grants from Cepheid, Merck, Otsuka, Sanofi and Summit. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

K Imwattana is a recipient of Mahidol Scholarship from Mahidol University. D R Knight and D A Collins are recipients of the Early Career Fellowships from the National Health and Medical Research Council of Australia [APP1138257 and APP1156789]. B Kullin is a recipient of the Australia Awards Post-Doctoral Fellowship grant from Australia Africa University Network.