The dominant biochemical mechanism by which gram-negative bacilli acquire high-level resistance to gentamicin and amikacin is:
- A Beta-galactosidase cleavage of the aminocyclitol ring
- B Mutation of the 30S ribosomal protein S12
- C Enzymatic modification of the antibiotic by aminoglycoside acetyltransferases, adenyltransferases and phosphotransferases ✓
- D Substitution of D-Ala-D-Lac in peptidoglycan precursors
Explanation
Clinically important aminoglycoside resistance in gram-negatives rests overwhelmingly on plasmid-mediated modifying enzymes: N-acetyltransferases, O-adenyltransferases and O-phosphotransferases that alter the drug so it binds the ribosome poorly. Ribosomal protein S12 mutation causes streptomycin resistance but is uncommon clinically. Peptidoglycan precursor substitution is the vancomycin resistance strategy, and no cleaving galactosidase exists for these drugs.
Reference: Ananthanarayan and Paniker's Textbook of Microbiology, 11th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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