Vancomycin

Vancomycin belongs to the glycopeptide family. To multiply, a bacterium must build its cell wall, a rigid envelope made of peptidoglycan that protects it and gives it its shape. Vancomycin binds to the D-alanyl-D-alanine end of the precursors of this peptidoglycan, just before they are assembled.

By occupying this target, it blocks glycosyltransferase, the enzyme that links the wall’s building blocks together. Construction stops, the wall weakens, the cell leaks its contents and eventually dies. This mechanism targets Gram-positive bacteria, whose thick wall is precisely the point of attack.

Vancomycin is used in two very different forms. Given intravenously, it treats serious infections caused by Gram-positive bacteria, first and foremost methicillin-resistant Staphylococcus aureus, MRSA, as well as endocarditis and sepsis. It then circulates throughout the body to reach the site of infection.

Taken by mouth, its behaviour changes completely. It is very poorly absorbed: its oral bioavailability remains below 10 %, so it stays in the intestine where it acts on the spot. This form is used to treat Clostridioides difficile diarrhoea and colitis, not general infections.

For Clostridioides difficile diarrhoea, the usual dose is 125 mg four times a day for 10 days. The doses are spread out at regular intervals throughout the day, generally over 7 to 10 days, to maintain a constant concentration in the intestine. Unless the doctor advises otherwise, you keep your usual diet.

The treatment is continued to the very end, even when symptoms improve before it is over. Its half-life is 4 to 6 hours in adults whose kidneys function normally, which explains the rhythm of four doses a day. Stopping too soon exposes you to relapse and gives the bacterium a chance to return.

The intravenous infusion can trigger a reaction linked to how fast it is administered, formerly called red man syndrome, with flushing and itching of the upper body. Its reported incidence varies widely, from 3.7 % to 47 %, and it depends on the speed of the infusion: slowing the flow rate limits it.

Other effects involve the ear and the blood. Ototoxicity, temporary or permanent, has been described with both the intravenous and oral routes: vertigo, hearing loss, tinnitus. A reversible neutropenia, meaning a drop in white blood cells, can occur with both forms; thrombocytopenia, a fall in platelets, remains rarer.

The kidney is the organ most exposed under intravenous vancomycin. The risk of toxicity, including acute kidney injury, rises when the trough level exceeds 15 mg/L and the area under the curve exceeds 650 mg·h/L. It also increases with age, after 65 years.

Certain combinations amplify this renal risk. Aminoglycosides, piperacillin-tazobactam, amphotericin B, ciclosporin, loop diuretics, non-steroidal anti-inflammatory drugs and iodinated contrast agents are all nephrotoxic. Their combination with vancomycin calls for particular vigilance and guides the doctor’s choice.

Given intravenously, vancomycin requires biological monitoring. Its serum concentrations are measured, with a target trough level of 10 to 20 µg/mL, drawn within the 30 minutes before the dose, and kidney function is watched. For severe infections, monitoring the area under the curve, the AUC, is preferred to fine-tune the dose.

The oral form behaves differently. Because it is barely absorbed into the bloodstream, it does not require serum level monitoring. Surveillance then focuses on how the digestive symptoms evolve rather than on blood levels.