W. R. Miller

This study identifies the MadRS system and its operon madEFG as mediators of resistance to antimicrobial peptides and antibiotics in Enterococcus faecalis, linking membrane lipid changes to stress response and virulence.

This study identifies LiaX as a surrogate marker for cell-envelope stress and daptomycin non-susceptibility in Enterococcus faecium and validates its use through ELISA and genomic analysis of clinical isolates.

This study identifies the role of cardiolipin synthase and the LiaFSR system in daptomycin resistance by redistributing anionic phospholipids in Enterococcus faecalis.

This study investigates how Enterococcus faecium develops resistance to a combination of daptomycin and fosfomycin, finding that resistance mechanisms are largely independent and that fosfomycin resistance involves changes in phosphoenolpyruvate flux.

This study shows that disrupting the LiaFSR pathway in Enterococcus faecium delays daptomycin resistance development, suggesting potential for combinatorial therapy with a LiaFSR inhibitor.

This study shows how different environments shape daptomycin resistance mechanisms in Enterococcus faecium through distinct evolutionary pathways.

The paper identifies two U.S. clinical isolates of Pseudomonas aeruginosa ST309 resistant to carbapenems and beta-lactam/beta-lactamase inhibitor combinations, harboring tandem GES 19 and 26 enzymes, and reports successful treatment with ceftazidime/avibactam plus aztreonam.