M. H. Wilcox

This study identifies a mutation in C. difficile that causes metronidazole resistance and links it to fluoroquinolone resistance, contributing to the spread of drug-resistant strains.

The paper identifies amino acid substitutions in penicillin binding proteins (PBPs) PBP1 and PBP3 as a mechanism of cephalosporin resistance in C. difficile, which co-occurs with fluoroquinolone resistance in epidemic lineages.

This study shows that trehalose supplementation remodels the human gut microbiota, preventing simulated Clostridioides difficile infection in an in vitro model.

This study evaluates three rifaximin formulations on the human colonic microbiota using chemostat models, finding that formulation {kappa} caused the least disruption.

This paper introduces hash-cgMLST, a method for rapid genome comparison in Clostridium difficile, showing it matches standard cgMLST performance but with faster processing.

This study evaluates the predictive value of quantitative nucleic acid amplification test (NAAT) cycle threshold (CT) values for C. difficile toxin gene in faecal samples to assess toxin status and patient outcomes.

The paper simulates enteric colonization by Carbapenemase Producing Enterobacteriaceae (CPE) using an in-vitro human gut model and screens for CPE.

The paper investigates the evolutionary history of Clostridium difficile RT078, finding that tetracycline resistance genes, particularly tetM, were acquired independently in multiple clonal expansions, contributing to its increased prevalence.