Discrepancies in fluoroquinolone clinical categories between the European Committee on Antimicrobial Susceptibility Testing (EUCAST) and CLSI for Escherichia coli harbouring qnr genes and mutations in gyrA and parC

Sir, Fluoroquinolones are broad-spectrum antibacterial agents commonly used in clinical practice. When quinolones became widely used, bacterial resistance to them emerged rapidly and, over the past three decades, resistance has continued to increase. In Gram-negative bacteria, quinolone resistance is due primarily to mutations in chromosomal genes encoding quinolone targets DNA gyrase and topoisomerase IV.1 More recently, plasmid-mediated mechanisms have been reported, such as those mediated by qnr genes encoding pentapeptide repeat proteins, aac(6′)-Ib-cr, encoding an acetyltransferase, and qepA or oqxAB, encoding active efflux pumps.2 The CLSI and European Committee on Antimicrobial Susceptibility Testing (EUCAST) criteria to define clinical breakpoints for fluoroquinolones in Enterobacteriaceae3,4 are indicated in Table 1. The EUCAST/European Medicines Agency has set somewhat lower breakpoints and those values have been accepted by the BSAC Resistance Surveillance Project.5 Although the epidemiological cut-off of ciprofloxacin for Escherichia coli has been established at 0.032 mg/L (www.eucast.org), the definition of wild-type strains is difficult due to the possible expression of unknown low-level quinolone resistance mechanisms.6