Division of Bacteriology, ICMR-National Institute of Cholera and Enteric Diseases, Kolkata, West Bengal, India.
Department of Zoology, University of Oxford, Oxford, United Kingdom.
J Antimicrob Chemother. 2022 May 29;77(6):1586-1591. doi: 10.1093/jac/dkac083.
Increased use of colistin in healthcare necessitates studies on the trend of colistin resistance and the underlying mechanisms.
To understand the susceptibility trend and molecular mechanisms of colistin resistance in neonatal isolates over a 12 year period.
Colistin susceptibility, mRNA expression, whole genome sequence and mutational analysis was performed. Phylogenomic comparison with a global collection of colistin-resistant Klebsiella pneumoniae strains (n = 70) was done.
Of 319 Enterobacterales (K. pneumoniae and Escherichia coli) studied, colistin resistance was found in 9 K. pneumoniae (2.8%). The transmissible colistin resistance gene, mcr, was absent. Colistin-resistant K. pneumoniae belonged to diverse sequence types (ST14/37/101/147/716) and exhibited multiple mechanisms of colistin resistance including overexpression of the two-component systems (TCS) (phoP/Q, pmrA/B), and AcrAB-TolC pump and its regulators. Mutations in TCS, mgrB, pumps, repressors, and lipopolysaccharide-modifying genes were detected. Phylogenomic comparison revealed that this global collection of colistin-resistant K. pneumoniae was diverse, with the presence of epidemic and international clones. Mutations in mgrB and TCS noted in global strains were comparable to the study strains. Co-occurrence of carbapenem resistance (n = 61, 87%) was observed in global strains. Co-existence of dual carbapenemases (blaNDM-5 with blaOXA-48/181) in multiple lineages within different replicons was found in neonatal colistin-resistant study isolates only.
Colistin resistance both in study and global strains is multifaceted and attributed to mutations in chromosomal genes leading to lipopolysaccharide modification or efflux of colistin through pumps. With no transmissible mcr, prevalence of colistin-resistant strains was low in this unit. Colistin-resistant strains with dual carbapenemases causing sepsis are alarming as they are practically untreatable.
在医疗保健中越来越多地使用粘菌素,这就需要研究粘菌素耐药的趋势和潜在机制。
了解 12 年来新生儿分离株中粘菌素耐药的敏感性趋势和分子机制。
进行粘菌素药敏试验、mRNA 表达、全基因组序列和突变分析。与全球 70 株耐粘菌素肺炎克雷伯菌(K. pneumoniae)菌株的基因组比较。
在 319 株肠杆菌科(肺炎克雷伯菌和大肠埃希菌)中,发现 9 株肺炎克雷伯菌(2.8%)对粘菌素耐药。不存在可传播的粘菌素耐药基因 mcr。耐粘菌素肺炎克雷伯菌属于多种序列型(ST14/37/101/147/716),表现出多种粘菌素耐药机制,包括两元系统(TCS)(phoP/Q、pmrA/B)过度表达,AcrAB-TolC 泵及其调节剂。检测到 TCS、mgrB、泵、抑制剂和脂多糖修饰基因的突变。基因组比较显示,全球耐粘菌素肺炎克雷伯菌具有多样性,存在流行和国际克隆。全球菌株中 noted 的 mgrB 和 TCS 突变与研究菌株相当。在全球菌株中观察到碳青霉烯耐药(n=61,87%)的共存。在不同复制子的多个谱系中发现了双重碳青霉烯酶(blaNDM-5 与 blaOXA-48/181)的共存,仅在新生儿耐粘菌素研究分离株中发现。
研究和全球菌株中的粘菌素耐药均具有多面性,这归因于导致脂多糖修饰或通过泵外排粘菌素的染色体基因突变。由于不存在可传播的 mcr,该单位耐粘菌素菌株的流行率较低。引起败血症的具有双重碳青霉烯酶的耐粘菌素菌株令人警惕,因为它们实际上无法治疗。