An isolate of Klebsiella pneumoniae shows high-level gentamicin resistance despite an intact outer membrane permeability profile. The most common mechanism of aminoglycoside resistance in such clinical isolates is:
- A Plasmid-mediated enzymes that acetylate, adenylate or phosphorylate the drug ✓
- B Methylation of the 16S rRNA target by erm-type enzymes
- C Substitution of D-Ala-D-Lac in the cell wall precursor
- D Efflux pumps belonging to the Tet family
Explanation
The dominant mechanism of aminoglycoside resistance worldwide is plasmid-mediated modifying enzymes: N-acetyltransferases, O-adenyltransferases and O-phosphotransferases that chemically alter the antibiotic so it binds poorly to the ribosome. Methylation of 16S rRNA does occur but is less common. The D-Ala-D-Lac substitution causes glycopeptide resistance, and erm-mediated 23S methylation causes macrolide resistance, making both distractors category mismatches.
Reference: Katzung Basic and Clinical Pharmacology, 15th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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