Pharmacology · Antimicrobials (Cell Wall Inhibitors, Protein Synthesis Inhibitors, Fluoroquinolones)

Fluoroquinolone resistance in Gram-negative bacteria most commonly arises due to:

  • A Enzymatic inactivation of the fluoroquinolone by acetyltransferases
  • B Plasmid-mediated tetracycline efflux pumps that also transport fluoroquinolones
  • C Point mutations in gyrA (DNA gyrase subunit A) reducing drug-enzyme binding affinity ✓
  • D Altered 30S ribosomal subunit preventing fluoroquinolone binding
Correct answer: C. Point mutations in gyrA (DNA gyrase subunit A) reducing drug-enzyme binding affinity

Explanation

The primary mechanism of acquired fluoroquinolone resistance is chromosomal mutation in the quinolone resistance-determining regions (QRDR) of gyrA (encoding DNA gyrase subunit A) and/or parC (topoisomerase IV subunit C). These mutations alter the amino acids at positions 83 and 87 (for GyrA) reducing drug binding while retaining enzymatic function. Plasmid-mediated resistance (via qnr genes, AAC(6')-Ib-cr enzyme, or efflux plasmids) is the second mechanism. Fluoroquinolones are not acetylated by conventional acetyltransferases, and they act on DNA gyrase/topoisomerase, not ribosomes.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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