Which statement about the mechanism of resistance to fluoroquinolones mediated by plasmid-encoded Qnr proteins is CORRECT?
- A Qnr proteins enzymatically acetylate the quinolone ring, inactivating the drug
- B Qnr proteins protect DNA gyrase and topoisomerase IV from quinolone binding ✓
- C Qnr proteins act as efflux pump enhancers, increasing quinolone extrusion
- D Qnr proteins alter the outer membrane porin channel, reducing quinolone entry
Explanation
Plasmid-mediated quinolone resistance (PMQR) via Qnr proteins works by a pentapeptide repeat mechanism: Qnr proteins bind to and physically shield DNA gyrase and topoisomerase IV from quinolone molecules, reducing drug-target interaction. This confers low-level resistance that can facilitate selection of higher-level chromosomal resistance. Enzymatic inactivation of quinolones is mediated by a separate PMQR gene product—AAC(6')-Ib-cr—which acetylates the piperazinyl nitrogen. Efflux pumps (OqxAB, QepA) and porin changes are separate resistance mechanisms.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.