Abstract
FosA, a glutathione S-transferase that inactivates fosfomycin, has been reported as the cause of enzymatic resistance to fosfomycin. We show that multiple lineages of FosA-producing extended spectrum β-lactamase Escherichia coli have circulated in France since 2012, potentially reducing the efficacy of fosfomycin in treating infections with antimicrobial drug–resistant gram-negative bacilli.
Highlights
Fosfomycin is a broad-spectrum bactericidal antibiotic commonly used in Europe as a first-line oral agent for uncomplicated urinary tract infection (1)
Conclusions the prevalence of plasmid-mediated fosA3 genes in human clinical E. coli isolates has remained low in France since 2012, these genes are observed across numerous clones, sequence types, and molecular determinants and are always associated with ESBL CTX-M enzymes, suggesting multiple propagation events
Medical records examination did not show a history of international travel in our patient population, and such a variety of fosfomycin-resistant E. coli lineages probably were not imported or transmitted
Summary
Fosfomycin is a broad-spectrum bactericidal antibiotic commonly used in Europe as a first-line oral agent for uncomplicated urinary tract infection (1). We report the prevalence and mechanisms of fosfomycin resistance among clinical human E. coli strains isolated in Paris, France. Among 1,354 E. coli isolates tested, 12 (0.9%) showed confirmed resistance (MIC >128 mg/L). Inhibition of FosA-mediated fosfomycin resistance by phosphonoformiate.
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