Aminoglycosides such as gentamicin are uniformly inactive against obligate anaerobes like Bacteroides fragilis. The pharmacological basis of this gap in the antibacterial spectrum is:
- A Uptake of aminoglycosides across the bacterial inner membrane is an oxygen-dependent, energy-requiring process ✓
- B Anaerobes possess an impermeable LPS layer that blocks aminoglycoside entry
- C Anaerobes carry ribosomal methylase genes that block the 30S binding site
- D Anaerobic metabolism degrades aminoglycosides before they reach the ribosome
Explanation
Aminoglycoside entry into bacteria occurs in two phases: initial energy-independent binding followed by energy-dependent active transport across the inner membrane that requires oxidative metabolism. Obligate anaerobes cannot generate the membrane potential needed for this transport, so the drug never reaches its 30S target. This is why gentamicin must be paired with metronidazole or clindamycin when anaerobic cover is needed. Ribosomal methylases and modifying enzymes confer resistance in aerobic organisms but do not explain the intrinsic anaerobic gap.
Reference: Katzung Basic and Clinical Pharmacology, 15th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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