A mechanism of fluoroquinolone resistance in clinical bacteria involves plasmid-mediated protection of DNA gyrase via Qnr proteins. What is the PRIMARY mechanism by which Qnr proteins confer resistance?

• A Enzymatic acetylation and inactivation of the fluoroquinolone molecule
• B Efflux pump upregulation expelling the drug from the bacterial cell
• C Pentapeptide protein that physically protects DNA gyrase and topoisomerase IV from quinolone binding ✓
• D Mutation in the quinolone resistance-determining region (QRDR) of gyrA

Explanation

Qnr proteins belong to the pentapeptide repeat protein family and confer quinolone resistance by binding to DNA gyrase and topoisomerase IV, physically shielding the enzyme from fluoroquinolone interaction — a protection mechanism. This is distinct from enzymatic drug modification (e.g., AAC(6')-Ib-cr, which acetylates the drug's piperazinyl nitrogen), efflux pump upregulation (e.g., AcrAB-TolC), or chromosomal QRDR mutations in gyrA/gyrB/parC. Qnr-mediated resistance is plasmid-borne (horizontal gene transfer) and typically confers low-level resistance that facilitates selection of higher-level mutants.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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