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Colistin-Resistant Acinetobacter baumannii: Beyond Carbapenem Resistance

机译:耐共利斯汀的鲍曼不动杆菌:超越碳青霉烯耐药性

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摘要

>Background. With an increase in the use of colistin methansulfonate (CMS) to treat carbapenem-resistant Acinetobacter baumannii infections, colistin resistance is emerging.>Methods. Patients with infection or colonization due to colistin-resistant A. baumannii were identified at a hospital system in Pennsylvania. Clinical data were collected from electronic medical records. Susceptibility testing, pulsed-field gel electrophoresis (PFGE), and multilocus sequence typing (MLST) were performed. To investigate the mechanism of colistin resistance, lipid A was subjected to matrix-assisted laser desorption/ionization mass spectrometry.>Results. Twenty patients with colistin-resistant A. baumannii were identified. Ventilator-associated pneumonia was the most common type of infection. Nineteen patients had received intravenous and/or inhaled CMS for treatment of carbapenem-resistant, colistin-susceptible A. baumannii infection prior to identification of colistin-resistant isolates. The 30-day all-cause mortality rate was 30%. The treatment regimen for colistin-resistant A. baumannii infection associated with the lowest mortality rate was a combination of CMS, a carbapenem, and ampicillin-sulbactam. The colistin-susceptible and -resistant isolates from the same patients were highly related by PFGE, but isolates from different patients were not, suggesting evolution of resistance during CMS therapy. By MLST, all isolates belonged to the international clone II, the lineage that is epidemic worldwide. Phosphoethanolamine modification of lipid A was present in all colistin-resistant A. baumannii isolates.>Conclusions. Colistin-resistant A. baumannii occurred almost exclusively among patients who had received CMS for treatment of carbapenem-resistant, colistin-susceptible A. baumannii infection. Lipid A modification by the addition of phosphoethanolamine accounted for colistin resistance. Susceptibility testing for colistin should be considered for A. baumannii identified from CMS-experienced patients.
机译:>背景。随着越来越多的粘菌素甲磺酸盐(CMS)用于治疗对碳青霉烯耐药的鲍曼不动杆菌感染,正在产生粘菌素抗性。>方法。感染或定植的患者在宾夕法尼亚州的一家医院系统中发现了对大肠菌素耐药的鲍曼不动杆菌的抗药性。从电子病历中收集临床数据。进行了敏感性测试,脉冲场凝胶电泳(PFGE)和多基因座序列分型(MLST)。为了研究粘菌素耐药的机制,对脂质A进行了基质辅助激光解吸/电离质谱分析。>结果。确定了20例粘菌素耐药的鲍曼不动杆菌。呼吸机相关性肺炎是最常见的感染类型。 19名患者接受了静脉和/或吸入CMS治疗,对碳青霉烯耐药性,对大肠菌素敏感的鲍曼不动杆菌进行了鉴定,然后鉴定了对大肠菌素的耐药菌。 30天全因死亡率为30%。与最低死亡率相关的对大肠菌素耐药的鲍曼不动杆菌感染的治疗方案是CMS,碳青霉烯和氨苄西林舒巴坦联合使用。来自同一患者的对大肠菌素敏感和耐药的分离株与PFGE高度相关,但来自不同患者的分离株却没有相关性,表明CMS治疗期间耐药的演变。通过MLST,所有分离株都属于国际克隆II,即世界范围内流行的血统。 >结论。耐考氏素的鲍曼不动杆菌几乎完全发生在接受CMS的耐碳青霉烯,大肠菌素治疗的患者中。易感染鲍曼不动杆菌。通过添加磷酸乙醇胺进行的脂质A修饰可导致大肠菌素抗性。对于从CMS经验丰富的患者中鉴定出的鲍曼不动杆菌,应考虑对大肠菌素的药敏试验。

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