Resistance to fluoroquinolones in Gram-negative bacteria most commonly occurs via which mechanism?
- A Enzymatic acetylation of the fluoroquinolone hydroxyl group by acetyltransferases
- B Overexpression of efflux pumps (e.g., MexAB-OprM) combined with target mutations in gyrA ✓
- C Plasmid-mediated beta-lactamase inactivating the quinolone ring
- D Decreased production of lipopolysaccharide reducing drug entry
Explanation
Fluoroquinolone resistance in Gram-negatives typically involves multiple co-existing mechanisms: point mutations in gyrA (DNA gyrase subunit) and/or parC (topoisomerase IV) that reduce drug binding, combined with upregulated efflux pumps like MexAB-OprM in Pseudomonas, which actively extrude drug. Acetylation (option A) is a mechanism for aminoglycosides, not quinolones. There are no beta-lactamases for quinolones; reduced LPS production is not the primary resistance mechanism.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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