Glycopeptides
One-Sentence Definition
Glycopeptides (vancomycin, teicoplanin) bind D-Ala-D-Ala peptidoglycan precursors, blocking cell wall polymerization — essential for serious Gram-positive infections including MRSA, with vancomycin-intermediate/resistant (VISA/VRSA) and VRE as major resistance concerns.
Simple Explanation
They grab the bacterial wall building block before it joins the chain — key for MRSA and serious Gram-positives when β-lactams fail.
Detailed Scientific Explanation
| Drug | Notes |
|---|---|
| Vancomycin | IV mainstay MRSA bacteremia/endocarditis (with dosing/TDM) |
| Teicoplanin | Long half-life; not interchangeable MIC rules with vancomycin in all contexts |
| Oral vancomycin | C. difficile colitis (luminal, not systemic) |
Spectrum: Gram-positive aerobes/anaerobes (many); no Gram-negative envelope penetration.
Resistance: VRE (van → D-Ala-D-Lac); VISA/VRSA (thick wall / vanA transfer rare); not for β-lactam-susceptible bugs if equally effective β-lactam exists (stewardship).
Monitoring: trough-guided AUC/MIC strategies for serious infections; nephrotoxicity with concomitant nephrotoxins.
Mechanism
Bind terminal D-Ala-D-Ala → prevent transglycosylation/transpeptidation (Bacterial Cell Wall).
Clinical Importance
- MRSA bacteremia — treat with appropriate doses + source control; consider daptomycin/others if intolerance or resistance
- Not first choice for MSSA if β-lactam tolerated (Antimicrobial Stewardship)
AMR Relevance
- MRSA vs VRE mechanisms differ — know mecA vs van
- Drives linezolid/daptomycin use when vancomycin fails
Related MOCs
Active Recall Questions
- VanA VRE — binding site change?
- Oral vs IV vancomycin — different syndrome?
- Why avoid vancomycin for MSSA if possible?