Emergence of Plasmid-Mediated Fosfomycin-Resistance Genes among Escherichia coli Isolates, France

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.

Keywords: ESBL; Escherichia coli; France; acquired resistance; antimicrobial resistance; bacteria; enteric infectious; extended spectrum β-lactamase; food safety; foodborne infections; fosA; fosfomycin; phosphonoformiate.

Figure

Inhibition of FosA-mediated fosfomycin resistance by phosphonoformiate. A modified Kirby-Bauer disk diffusion susceptibility assay was performed. In brief, a Mueller-Hinton agar plate was streaked with a 0.5 McFarland suspension of the isolate assayed. Three disks were placed on the agar: 200-µg fosfomycin disk (upper left), a 100-µg phosphonoformiate disk (lower center), and a disk with both a 200-µg fosfomycin and 100-µg phosphonoformiate (upper right). The diameter of the growth inhibition zone around each disk was measured after 18–24 h incubation at 35°C (+2°C). FosA-mediated fosfomycin resistance is inhibited by phosphonoformiate and is demonstrated by an increase in the diameter of the growth inhibition zone by >4 mm.