Novović Katarina, Jovčić Branko
Institute of Molecular Genetics and Genetic Engineering, University of Belgrade, Vojvode Stepe 444a, 11042 Belgrade, Serbia.
Faculty of Biology, University of Belgrade, Studentski Trg 16, 11000 Belgrade, Serbia.
Antibiotics (Basel). 2023 Mar 4;12(3):516. doi: 10.3390/antibiotics12030516.
is recognized as a clinically significant pathogen causing a wide spectrum of nosocomial infections. Colistin was considered a last-resort antibiotic for the treatment of infections caused by multidrug-resistant . Since the reintroduction of colistin, a number of mechanisms of colistin resistance in have been reported, including complete loss of LPS by inactivation of the biosynthetic pathway, modifications of target LPS driven by the addition of phosphoethanolamine (PEtN) moieties to lipid A mediated by the chromosomal operon and gene-encoded enzymes or plasmid-encoded genes and efflux of colistin from the cell. In addition to resistance to colistin, widespread heteroresistance is another feature of that leads to colistin treatment failure. This review aims to present a critical assessment of relevant published (>50 experimental papers) up-to-date knowledge on the molecular mechanisms of colistin resistance in with a detailed review of implicated mutations and the global distribution of colistin-resistant strains.
被认为是一种临床上具有重要意义的病原体,可引起广泛的医院感染。黏菌素曾被视为治疗多重耐药菌引起感染的最后一道抗生素防线。自黏菌素重新应用以来,已报道了多种细菌对黏菌素的耐药机制,包括通过生物合成途径失活导致脂多糖(LPS)完全缺失、由染色体上的pmr操纵子和pmr基因编码的酶或质粒编码的mcr基因介导的向脂质A添加磷酸乙醇胺(PEtN)基团驱动的靶标LPS修饰以及黏菌素从细胞内流出。除了对黏菌素耐药外,广泛存在的异质性耐药是细菌的另一个特征,这会导致黏菌素治疗失败。本综述旨在对已发表的(>50篇实验论文)有关细菌对黏菌素耐药分子机制的最新知识进行批判性评估,并详细综述相关突变以及耐黏菌素菌株的全球分布情况。