Side by side

1. 1.Binds the D-Ala-D-Ala terminus of cell-wall precursors, blocking the transglycosylation and cross-linking steps.
2. 2.Prevents peptidoglycan assembly, so the bacterium cannot build a stable wall.
3. 3.Bactericidal against dividing Gram-positive organisms.
4. 4.The oral route is not absorbed, so the drug stays in the gut lumen.
5. 5.Gram-negative bacteria are intrinsically resistant because of their outer membrane.

• MRSA bacteraemia and complicated skin infection
• Clostridioides difficile infection (oral)
• Endocarditis and bone and joint infection caused by Gram-positive organisms
• Surgical prophylaxis in hospitals with high MRSA rates
• Meningitis with Gram-positive cover (intravenous, sometimes intraventricular)

• Clinical cure rates of roughly 70 to 85% in MRSA bacteraemia trials
• Bacteriological clearance in C. difficile with oral therapy
• Nephrotoxicity risk that rises with higher exposure and concurrent kidney-toxic drugs
• Infusion-related flushing known as red man syndrome

• Nephrotoxicity, especially with other kidney-toxic drugs
• Red man syndrome from rapid infusion
• Ototoxicity with high exposure
• Neutropenia with prolonged use
• Phlebitis at the infusion site
• Rare thrombocytopenia

Research context only - a hospital antibiotic. Standard intravenous dosing is 15 to 20 mg per kilogram every 8 to 12 hours with the interval adjusted to kidney function, monitored through an AUC/MIC target of about 400 to 600 or trough levels; oral C. difficile dosing is typically 125 mg four times daily for 10 days. Trials follow clinical and microbiological cure at test-of-cure visits.

Research context only