A 60-year-old woman with diabetic foot ulcer grows Pseudomonas aeruginosa and Enterococcus faecalis. Gentamicin is added for synergy with ampicillin against the enterococcus. High-level gentamicin resistance (HLAR) in enterocci is detected. The clinical implication of HLAR is that it:
- A Increases the MIC of gentamicin to >500 mcg/mL and abolishes cell wall agent synergy ✓
- B Causes cross-resistance to all aminoglycosides except streptomycin
- C Is mediated by altered 30S ribosomal subunit binding
- D Predicts resistance to vancomycin as well
Explanation
HLAR indicates gentamicin MIC >500 mcg/mL (or streptomycin >1000 mcg/mL), abolishing the synergistic bactericidal effect when combined with cell wall active agents. This eliminates the rationale for combination therapy in endocarditis. Option B is incorrect as HLAR does not predict streptomycin resistance. Option C describes a ribosomal mutation mechanism not typical of HLAR, which is usually due to modifying enzymes.
Reference: Katzung Basic and Clinical Pharmacology, 15th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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