Aminoglycoside antibiotics (e.g., gentamicin, amikacin): With which critical bacterial process do aminoglycosides primarily interfere?

Introduction / Context:
Aminoglycosides are potent bactericidal agents used for serious Gram-negative infections and synergistically for some Gram-positive infections. Their mechanism explains their spectrum, post-antibiotic effect, and toxicity.

Given Data / Assumptions:

• The drug class is aminoglycosides (e.g., gentamicin, tobramycin, amikacin).
• We seek the primary cellular process they disrupt.

Concept / Approach:
Aminoglycosides bind irreversibly to the 30S ribosomal subunit, causing misreading of mRNA and blocking initiation complexes. This leads to production of nonfunctional proteins and ultimately bacterial death. Entry is oxygen-dependent, explaining poor activity against strict anaerobes.

Step-by-Step Solution:
Locate target: 30S ribosomal subunit in bacteria. Define effect: misreading and inhibition of initiation → faulty proteins. Conclude primary interference: protein synthesis.

Verification / Alternative check:
Mutations in 30S components or methylation of 16S rRNA confer aminoglycoside resistance, confirming the mechanistic target.

Why Other Options Are Wrong:

• DNA function: inhibited by fluoroquinolones; not the main aminoglycoside action.
• Cell wall synthesis: target of beta-lactams and glycopeptides.
• Cell membrane function: polymyxins primarily disrupt membranes.

Common Pitfalls:
Assuming all bactericidal drugs disrupt membranes or DNA; many, like aminoglycosides, kill via aberrant protein synthesis.

Final Answer:
Protein synthesis