FosA3 overexpression with transporter mutations mediates high-level of fosfomycin resistance and silence of fosA3 in fosfomycin-susceptible Klebsiella pneumoniae producing carbapenemase clinical isolates.

ABSTRACT: The effective treatment of carbapenemase-producing Klebsiella pneumoniae infection has been limited and required novel potential agents. Due to the novel drug development crisis, using old antimicrobial agents and combination therapy have been highlighted. This study focused on fosfomycin which inhibits cell wall synthesis and has potential activity on Enterobacteriaceae. We evaluated fosfomycin activity against carbapenemase-producing K. pneumoniae and characterized fosfomycin resistance mechanisms. Fosfomycin revealed effective activity against only 31.8% of carbapenemase-producing K. pneumoniae isolates. The major resistance mechanism was FosA3 production. The co-occurrence of FosA3 overexpression with the mutation of glpT (or loss of glpT) and/or uhpT was mediated high-level resistance

SUBMITTER: Singkham-In U 

PROVIDER: S-EPMC7454978 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature