UNASSIGNED: A total of 2301 bacterial isolates collected at six hospitals were assessed. Their response to polymyxin was evaluated by minimum inhibitory concentration (MIC) analysis, and the mobilized colistin resistance (mcr) and carbapenemase gene were explored. Mutations on mgrB, phoPQ, pmrAB, and crrAB in polymyxin-resistant K. pneumoniae were detected by PCR. phoP, phoQ, pmrK, pmrA, pmrB, and pmrC transcriptional levels were quantified by RT-qPCR. Pulsed-field gel electrophoresis (PFGE) and multi-locus sequence typing were performed to determine the phylogenetic relationship between the polymyxin-resistant isolates.
UNASSIGNED: Of the E. coli and K. pneumoniae isolates identified, 0.3% and 1.4% were polymyxin-resistant, respectively, with MICs of 4-64 μg/mL. All polymyxin-resistant isolates were susceptible to tigecycline. Four E. coli isolates were mcr-1-positive and one was carbapenem-resistant, carrying bla NDM-5 and mcr-1. One K. pneumoniae isolate was mcr-1-positive and nine were carbapenem-resistant (PRCRKP), carrying bla KPC-2 but not mcr-1. The five E. coli isolates belonged to four sequence types (ST2, ST132, ST632, and ST983). All PRCRKP isolates belonged to ST11. However, all 16 isolates belonged to different PFGE types with <95% genetic similarity. Insertion sequences in mgrB were detected in nine (81.8%) polymyxin-resistant K. pneumoniae samples. Colistin resistance was linked with pmrHFIJKLM operon upregulation, with phoP, phoQ, and pmrK being overexpressed in all but one of the polymyxin-resistant K. pneumoniae samples. Furthermore, 33.3% of patients carrying polymyxin-resistant isolates had previously used polymyxin, and 66.7% patients displayed good clinical outcomes.
UNASSIGNED: The K. pneumoniae polymyxin resistance rate was slightly higher than that of E. coli and mcr-1 was more common in E. coli than in K. pneumoniae. Moreover, the insertion of ISkpn14 into mgrB may be the main contributor to polymyxin-resistance in K. pneumoniae in Henan.
■评估了在六家医院收集的总共2301种细菌分离株。他们对多粘菌素的反应通过最小抑制浓度(MIC)分析来评估,并对动员粘菌素抗性(mcr)和碳青霉烯酶基因进行了探索。mgrB突变,phoPQ,pmrAB,PCR检测多粘菌素耐药肺炎克雷伯菌中的crrAB。phoP,phoQ,pmrK,pmrA,pmrB,和pmrC转录水平通过RT-qPCR定量。进行了脉冲场凝胶电泳(PFGE)和多位点序列分型,以确定多粘菌素抗性分离株之间的系统发育关系。
■在鉴定的大肠杆菌和肺炎克雷伯菌分离株中,0.3%和1.4%为多粘菌素耐药,分别,MIC为4-64μg/mL。所有多粘菌素耐药菌株均对替加环素敏感。4株大肠杆菌mcr-1阳性,1株碳青霉烯类耐药,携带BLANDM-5和MCR-1。一株肺炎克雷伯菌mcr-1阳性,九株耐碳青霉烯(PRCRKP),携带BLAKPC-2但不携带MCR-1。五种大肠杆菌分离物属于四种序列类型(ST2、ST132、ST632和ST983)。所有PRCRKP分离株都属于ST11。然而,所有16个分离株都属于不同的PFGE类型,遗传相似性<95%。在9个(81.8%)多粘菌素抗性肺炎克雷伯菌样品中检测到mgrB中的插入序列。粘菌素抗性与pmrHFIJKLM操纵子上调有关,用phoP,phoQ,pmrK在所有多粘菌素耐药肺炎克雷伯菌样品中过表达。此外,携带多粘菌素耐药菌株的患者中,33.3%以前使用过多粘菌素,66.7%的患者表现出良好的临床结局。
■肺炎克雷伯菌多粘菌素耐药率略高于大肠杆菌,mcr-1在大肠杆菌中比在肺炎克雷伯菌中更常见。此外,将ISkpn14插入mgrB可能是河南肺炎克雷伯菌多粘菌素耐药的主要原因。