Step 1: Define the pharmacodynamic patterns. Antibacterial killing follows two broad patterns. In concentration-dependent killing, the rate and extent of bacterial kill rise as drug concentration increases well above the MIC; the predictive parameters are peak/MIC (Cmax/MIC) and AUC/MIC. In time-dependent killing, kill plateaus once concentration exceeds about 4 x MIC, and efficacy depends on the time above MIC (T>MIC).
Step 2: Classify aminoglycosides. Aminoglycosides (gentamicin, amikacin, tobramycin) are the prototype concentration-dependent bactericidal drugs and also have a prolonged post-antibiotic effect. This is the rationale for once-daily (extended-interval) dosing - a high peak maximises killing while the trough falls low enough to limit nephro- and ototoxicity.
Step 3: Why the others are wrong. Beta-lactams and glycopeptides (vancomycin) are time-dependent; their efficacy depends on T>MIC (vancomycin is best tracked by AUC/MIC but is not concentration-dependent in the aminoglycoside sense). Macrolides are largely time-dependent/bacteriostatic.
Key fact: Aminoglycosides (with fluoroquinolones, metronidazole and daptomycin) are classic concentration-dependent killers, justifying once-daily dosing.