Fluoroquinolone resistance due to the plasmid-mediated qnr genes confers resistance through which mechanism?

• A Pentapeptide repeat proteins protect DNA gyrase and topoisomerase IV from quinolone binding ✓
• B Enzymatic acetylation of the fluoroquinolone piperazinyl group by acetyltransferase
• C Altered outer membrane porins reducing intracellular drug concentration
• D Point mutations in gyrA and parC genes altering the QRDR target site

Explanation

Qnr proteins are pentapeptide repeat proteins encoded on transferable plasmids. They bind to and protect the DNA gyrase-DNA complex and topoisomerase IV-DNA complex from fluoroquinolone interaction, reducing susceptibility by mimicking the DNA structure recognised by quinolones. This does not typically confer high-level resistance alone but combined with other mechanisms (efflux, mutations) produces clinical resistance. Chromosomal gyrA/parC mutations (option D) are the primary mechanism of high-level resistance but are NOT plasmid-mediated. Acetyltransferase and porin changes are separate resistance strategies.

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

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Written and medically reviewed by the StethoPrep medical team.