Antimicrobials 1 dk okuma

Glycopeptide and Lipopeptide Antibiotics

Vancomycin and daptomycin target gram-positive bacteria by disrupting cell wall synthesis and membrane integrity, respectively, serving as critical agents against MRSA and VRE.

Overview

Glycopeptides (vancomycin, teicoplanin, oritavancin) and lipopeptides (daptomycin) are critical agents against multidrug-resistant gram-positive bacteria including MRSA and VRE. They have distinct mechanisms that bypass the beta-lactam resistance of MRSA (PBP2a alteration) and have complex pharmacokinetic/pharmacodynamic characteristics requiring monitoring.

Vancomycin: Mechanism

Vancomycin is a glycopeptide that forms hydrogen bonds with the D-Ala-D-Ala terminus of peptidoglycan precursors (lipid II), physically blocking transglycosylation (polymerization) and transpeptidation. This prevents cell wall assembly, causing osmotic lysis. Acts exclusively on gram-positive organisms (cannot penetrate the outer membrane of gram-negatives). Bactericidal against staphylococci; bacteriostatic against enterococci.

Vancomycin Dosing: AUC/MIC Target

ASHP/IDSA/SIDP 2020 guidelines recommend AUC/MIC (24h AUC: 400-600 mg·h/L for MIC ≤1 mg/L) as the pharmacodynamic target for MRSA infections, replacing trough-only monitoring. AUC-guided dosing is associated with similar efficacy but reduced nephrotoxicity compared to trough-guided dosing. Bayesian software is used to calculate AUC from 1-2 pharmacokinetic samples.

Vancomycin Resistance

VRE (vancomycin-resistant enterococci): VanA/VanB operons reprogram cell wall synthesis to produce D-Ala-D-Lac terminus, which vancomycin binds with 1000x lower affinity. VanA: resistance to both vancomycin and teicoplanin. VanB: resistant to vancomycin only. VISA/VRSA: Rare staphylococcal resistance; VISA has thickened cell wall trapping vancomycin before it reaches PBPs.

Novel Glycopeptides

Oritavancin and dalbavancin: Long half-lives (245h and 346h respectively) allowing single-dose therapy for ABSSSI. Oritavancin also disrupts bacterial membrane integrity.

Daptomycin: Mechanism

Daptomycin is a lipopeptide that inserts its lipid tail into the bacterial cytoplasmic membrane in a calcium-dependent manner, causing membrane depolarization, potassium efflux, and rapid cell death. Rapid concentration-dependent bactericidal activity. Active against gram-positives including MRSA, VISA, VRE.

Key limitation: Inactivated by pulmonary surfactant — NOT used for pneumonia. Use for bacteremia, right-sided endocarditis, and skin infections.

Resistance: Membrane phospholipid rearrangements reduce daptomycin binding. Cross-resistance with vancomycin can occur.

Key Takeaways

  • Vancomycin blocks D-Ala-D-Ala-mediated cell wall synthesis; AUC/MIC 400-600 is the current dosing target
  • VRE carries VanA/VanB genes that reprogram cell wall precursors to D-Ala-D-Lac, reducing vancomycin binding 1000-fold
  • Daptomycin is inactivated by lung surfactant and must NOT be used for pneumonia
  • Oritavancin and dalbavancin enable once-weekly or single-dose treatment of skin infections

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