Aminoglycoside uptake into bacteria is enhanced by agents that dissipate the transmembrane proton gradient. This explains why aminoglycosides have poor activity against:
- A Gram-positive cocci, because they lack the outer membrane porin required for aminoglycoside entry
- B Pseudomonas aeruginosa, because it produces MexAB-OprM efflux pump exclusively for aminoglycosides
- C Obligate anaerobes, which lack the electron transport chain-driven proton motive force needed for energy-dependent aminoglycoside uptake ✓
- D Acid-fast mycobacteria, because their mycolic acid layer prevents aminoglycoside binding to 30S ribosomes
Explanation
Aminoglycoside uptake across the bacterial cytoplasmic membrane (EDAC phase 2) is an energy-dependent process driven by the electrochemical proton gradient (proton motive force) generated by aerobic electron transport. Obligate anaerobes lack functional oxidative phosphorylation and therefore cannot maintain the membrane potential required for aminoglycoside translocation into the cytoplasm. This is why aminoglycosides are ineffective against anaerobes, and synergy with beta-lactams exploits the enhanced membrane permeability caused by cell wall disruption.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.