Vancomycin
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Direct answer
Vancomycin is a glycopeptide antibiotic that binds the terminal D-alanyl-D-alanine of peptidoglycan precursors, blocking both polymerisation and cross-linking of the bacterial cell wall. It is the classical drug for MRSA and, given orally with negligible absorption, for Clostridioides difficile colitis. Infusion must be slow to avoid the histamine-mediated red man syndrome, and therapy is guided by trough concentration monitoring.
What you must remember
- Mechanism: complexes with the D-alanyl-D-alanine terminus of the pentapeptide chain, sterically preventing transglycosylation and transpeptidation; bactericidal against staphylococci but only bacteriostatic against enterococci.
- Spectrum: gram-positive organisms only — MRSA, methicillin-resistant coagulase-negative staphylococci, penicillin-resistant pneumococci, enterococci and Corynebacterium jeikeium; gram-negatives are intrinsically protected by their outer membrane.
- Key indications: MRSA bacteraemia, endocarditis, pneumonia, osteomyelitis and dialysis-line infection; empirical cover in severe beta-lactam allergy; oral therapy for Clostridioides difficile colitis, exploiting its negligible gastrointestinal absorption.
- Dosing and monitoring: intermittent infusion over at least one hour with trough-guided adjustment — typical targets around ten to twenty micrograms per millilitre for serious infection, with area-under-curve-guided monitoring increasingly preferred per current guidance.
- Red man syndrome: vancomycin-induced histamine release during rapid infusion producing flushing, pruritus and hypotension — not allergy; managed by slowing or pausing the infusion, premedication with antihistamines, and longer infusion times.
- Nephrotoxicity, heightened with concurrent aminoglycosides or loop diuretics and with prolonged high troughs, plus rare ototoxicity at extreme levels, complete the toxicity profile.
- Resistance: VanA enterococci acquire D-alanine-D-lactate termini that vancomycin cannot bind, creating VRE — treated with linezolid or daptomycin; teicoplanin is a related glycopeptide available in India.
Common confusion
Red man syndrome is repeatedly mislabelled vancomycin allergy, leading to unnecessary drug avoidance; it is rate-dependent histamine release, fully preventable by slower infusion. The second confusion concerns route: intravenous vancomycin never treats colitis because it achieves no luminal levels, while oral vancomycin never treats bacteraemia because it is not absorbed.
Exam-focused takeaway
Theory answers should explain D-alanyl-D-alanine binding, enumerate MRSA and Clostridioides difficile indications, describe trough monitoring, and contrast red man syndrome with true allergy. Viva examiners ask why oral vancomycin suits colitis and what creates VRE. MCQs test the mechanism, red man syndrome, enterococcal bacteriostasis, nephrotoxic potentiation by aminoglycosides and oral-versus-intravenous route logic.
Frequently asked questions
What is the mechanism of action of vancomycin?
It binds the terminal D-alanyl-D-alanine of peptidoglycan precursors, sterically blocking cell-wall polymerisation and cross-linking in gram-positive bacteria.
What is red man syndrome and how is it managed?
Histamine-mediated flushing, itching and hypotension during rapid vancomycin infusion — managed by stopping or slowing the infusion and infusing over at least one hour subsequently; it is not a true allergy.
Why is oral vancomycin used for Clostridioides difficile colitis?
Oral vancomycin is not absorbed, so it reaches high colonic luminal concentrations precisely where the organism resides, with no systemic exposure.
How is vancomycin therapy monitored?
Through trough concentrations sampled before steady-state doses, aiming for levels appropriate to infection severity, with serial creatinine; area-under-curve-guided dosing is now preferred in many centres.
How do enterococci become vancomycin-resistant?
By acquiring genes that substitute D-alanine-D-lactate for D-alanyl-D-alanine, eliminating the vancomycin binding target — the basis of VRE.