Is plasmid-mediated quinolone resistance a clinically significant problem?
Although resistance to quinolones is commonly chromosomally-encoded in Enterobacteriaceae, the emergence of plasmid-mediated quinolone resistance (PMQR) has also been reported, with at least three known resistance mechanisms to date, i.e., Qnr, aminoglycoside acetyltransferase AAC(6')-Ib-cr and QepA. Qnr proteins protect target enzymes (DNA gyrase and type IV topoisomerase) from quinolone inhibition, the AAC(6')-Ib-cr enzyme acetylates norfloxacin and ciprofloxacin, and the QepA efflux pump extrudes hydrophilic fluoroquinolones. Although these PMQR determinants confer only low-level resistance to quinolones and/or fluoroquinolones, they may provide a favourable background in which the selection of additional chromosomally-encoded quinolone resistance mechanisms can occur.
Poirel
L
L
Cattoir
V
V
Nordmann
P
P
D000123:Acetyltransferases / Q000235:genetics*; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D001426:Bacterial Proteins / Q000235:genetics; D024881:Drug Resistance, Bacterial; D004755:Enterobacteriaceae / Q000187:drug effects* / Q000235:genetics; D006801:Humans; D010957:Plasmids / Q000235:genetics*; D015363:Quinolones / Q000494:pharmacology*
D000900:Anti-Bacterial Agents; D001426:Bacterial Proteins; D015363:Quinolones; D000123:Acetyltransferases; C019681:aminoglycoside acetyltransferase