Alfa Institute of Biomedical Sciences (AIBS), Athens, Greece.
Drug Resist Updat. 2010 Aug-Oct;13(4-5):132-8. doi: 10.1016/j.drup.2010.05.002. Epub 2010 Jun 17.
Polymyxins act by binding to lipid A moiety of the bacterial lipopolysaccharide and subsequently disintegrating the bacterial membranes. The most important mechanism of resistance includes modifications of the bacterial outer membrane structure, including lipopolysaccharide. Lipopolysaccharide modification is mostly mediated by PmrA/PmrB and PhoP/PhoQ two-component regulatory systems. These mechanisms exist with some differences in many gram-negative bacterial species. Resistance to polymyxins is generally less than 10%. In specific regions, such as the Mediterranean basin, Korea and Singapore, they tend to be higher. Heteroresistance to polymyxins is associated with exposure to polymyxins and especially suboptimal therapeutic dosage. Polymyxin combination regimens, tigecycline and fosfomycin may be useful options for the treatment of polymyxin-resistant gram-negative infections.
多黏菌素通过与细菌脂多糖的脂质 A 部分结合，随后破坏细菌膜而起作用。最重要的耐药机制包括改变细菌外膜结构，包括脂多糖。脂多糖的修饰主要由 PmrA/PmrB 和 PhoP/PhoQ 两种成分调控系统介导。这些机制在许多革兰氏阴性菌物种中存在一些差异。对多黏菌素的耐药性一般小于 10%。在特定地区，如地中海盆地、韩国和新加坡，耐药性往往更高。多黏菌素异质性耐药与接触多黏菌素和特别是治疗剂量不足有关。多黏菌素联合治疗方案、替加环素和磷霉素可能是治疗多黏菌素耐药性革兰氏阴性感染的有用选择。
