Side by side

1. 1.Binds the lipid A portion of lipopolysaccharide in the outer membrane.
2. 2.Displaces magnesium and calcium ions, destabilising the membrane.
3. 3.Increases membrane permeability, which kills the bacterium and releases endotoxin.
4. 4.The prodrug colistimethate must be hydrolysed in the body to become active.
5. 5.Intrinsic resistance occurs in some species, including Proteus and Serratia.

• Multidrug-resistant Acinetobacter, Pseudomonas and carbapenemase-producing Enterobacterales infections
• Nebulised therapy in resistant respiratory infection
• Combination therapy with other antibiotics for resistant Gram-negatives

• Microbiological activity against many carbapenem-resistant organisms
• Nephrotoxicity in a substantial minority of treated patients
• Neurotoxicity, including paraesthesia and neuromuscular weakness
• Debate continues over whether combination therapy improves survival

• Acute kidney injury
• Neurotoxicity, paraesthesia and dizziness
• Neuromuscular blockade, rarely apnoea
• Bronchospasm with nebulised use
• Rash
• Nausea

Research context only - a hospital antibiotic of last resort. Colistimethate is dosed in international units, commonly a loading dose around 9 million IU followed by maintenance doses adjusted for kidney function, with nebulised regimens used in some centres; modern trials have compared colistin combinations against other agents in resistant infection, with mortality as the endpoint.

Research context only