I am becoming increasingly interested in colistin resistance in CPE, not least because of this work that we will be presenting on colistin resistance in CPE at ECCMID in a few months time. I have been brushing up on how colistin resistance occurs in CPE, and why it is important, so thought I’d share my findings. I started with a pubmed search for “colistin resistance mechanism” on 12/02/16 and this is what I found (85 hits from the initial search):
Colisin
Colistin is an old class (discovered during WWII) of cationic antibiotic. Colistin (polymyxin E) is a polypeptide bactericidal agent and is one of the two clinically available forms of polymyxin agents (polymyxin B and polymyxin E). Colistin interacts with lipopolysaccharide in the outer membrane, resulting in a leaky and ultimately dead bacterial cell.1 Issues with presumed nephrotoxicity have kept colistin very much on the top shelf, but the emergence of CPE has brought colistin down a shelf or two – and we are learning that the nephrotoxicity tradionally associated with colisin may not be so bad afterall.1
