期刊
GASTROENTEROLOGY
卷 160, 期 3, 页码 941-U492出版社
W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1053/j.gastro.2020.10.046
关键词
Antimicrobial Resistance; Amidase; Cell Wall Peptidoglycan; Gram Positive
资金
- NIH [DK114007]
- Center for Individualized Medicine, Mayo Clinic, Rochester, Minnesota
The study identified a potential plasmid-mediated mechanism leading to decreased sensitivity of C difficile to vancomycin, which may contribute to treatment failure, and further experimental results supported this hypothesis.
The increasing incidence of primary and recurring Clostridioides difficile infections (CDI), which evade current treatment strategies, reflects the changing biology of C difficile. Here, we describe a putative plasmid-mediated mechanism potentially driving decreased sensitivity of C difficile to vancomycin treatment. We identified a broad host range transferable plasmid in a C difficile strain associated with lack of adequate response to vancomycin treatment. The transfer of this plasmid to a vancomycinsusceptible C difficile isolate decreased its susceptibility to vancomycin in vitro and resulted in more severe disease in a humanized mouse model. Our findings suggest plasmid acquisition in the gastrointestinal tract to be a possible mechanism underlying vancomycin treatment failure in patients with CDI, but further work is needed to characterize the mechanism by which plasmid genes determine vancomycin susceptibility in C difficile.
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