He Xiujuan, Li Henan, Wang Qi, Zhao Chunjiang, Li Shuguang, Wang Xiaojuan, Zhang Yawei, Wang Ruobing, Yin Yuyao, Jin Longyang, Zhang Feifei, Wang Hui
Department of Clinical Laboratory, Peking University People's Hospital, Beijing 100044, China.
Sheng Wu Gong Cheng Xue Bao. 2018 Aug 25;34(8):1218-1225. doi: 10.13345/j.cjb.180196.
To investigate the resistance mechanisms of tigecycline-non-susceptible Acinetobacter baumannii and for providing the evidence of the control of nosocomial infection and rational use of antibiotics. The minimum inhibitory concentrations (MICs) of 94 non repetitive tigecycline-non-susceptible A. baumannii from 20 hospitals in 12 cities of China were determined by agar dilution method and broth microdilution method. The molecular epidemiology was studied by Multilocus sequence typing (MLST) and eBURST software. PCR and sequencing techniques were used to analyze the resistance genes (blaOXA-40-like, blaOXA-58-like, blaOXA-23-like, blaOXA-51-like, blaNDM-1), ISAba1, and the mutation sites of adeR, adeS, and trm. The activity of polymyxin B and minocyclinem against tigecycline-non-susceptible A. baumannii were 100% and 25.5%, respectively. The sensitivities of other antibiotics were less than 3.5%, and the sensitivities of imipenem and meropenem totigecycline-nonsusceptible A. baumannii were only 1.1%. A total of 12 ST types were identified, including ST195 (45, 47.9%), ST208 (19, 20.2%) and ST457 (10, 10.6%). EBURST analysis found that 8 of the ST types belonged to the clone complex 92 (Clonal Complex 92, CC92). The blaOXA-23-like type carbapenem gene was identiefied in 93 strains (99% positive); and none of the strains contained the blaNDM-1 gene. The detection rates of adeR and adeS were 73.4% and 91.5% respectively and high frequency mutation sites were located in adeR (Asp26Asn) and adeS (Ala97Glu); The ISAba1 located upstream of the adeS gene was detected in 12 strains of A. baumannii, mainly from the northern region of China. The 240 nucleotide deletion of the trm gene caused a frameshift leading to a premature stop. So the tigecycline-non-susceptible A. baumannii showed high resistance against most antibiotics except polymyxin B. The deletion and mutation of adeR, adeS and trm were the main resistant mechanisms in tigecycline-non-susceptible A. baumannii in China.
为探讨对替加环素不敏感的鲍曼不动杆菌的耐药机制,为控制医院感染及合理使用抗生素提供依据。采用琼脂稀释法和肉汤微量稀释法测定了来自中国12个城市20家医院的94株非重复的对替加环素不敏感的鲍曼不动杆菌的最低抑菌浓度(MIC)。采用多位点序列分型(MLST)和eBURST软件进行分子流行病学研究。采用PCR和测序技术分析耐药基因(blaOXA - 40样、blaOXA - 58样、blaOXA - 23样、blaOXA - 51样、blaNDM - 1)、ISAba1以及adeR、adeS和trm的突变位点。多黏菌素B和米诺环素对替加环素不敏感鲍曼不动杆菌的活性分别为100%和25.5%。其他抗生素的敏感性均低于3.5%,亚胺培南和美罗培南对替加环素不敏感鲍曼不动杆菌的敏感性仅为1.1%。共鉴定出12种ST型,包括ST195(45株,47.9%)、ST208(19株,20.2%)和ST457(10株,10.6%)。EBURST分析发现其中8种ST型属于克隆复合体92(Clonal Complex 92,CC92)。93株菌(阳性率99%)检测到blaOXA - 23样碳青霉烯基因;所有菌株均未检测到blaNDM - 1基因。adeR和adeS的检出率分别为73.4%和91.5%,高频突变位点分别位于adeR(Asp26Asn)和adeS(Ala97Glu);在12株鲍曼不动杆菌中检测到位于adeS基因上游的ISAba1,主要来自中国北方地区。trm基因240个核苷酸的缺失导致移码,提前终止。因此,替加环素不敏感的鲍曼不动杆菌对除多黏菌素B外的大多数抗生素表现出高度耐药。adeR、adeS和trm的缺失和突变是中国替加环素不敏感鲍曼不动杆菌的主要耐药机制。