Colistin-Resistant Acinetobacter baumannii: Beyond Carbapenem Resistance
Colistin-Resistant Acinetobacter baumannii: Beyond Carbapenem Resistance
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DOI：
10.1093/cid/civ048
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发表时间：
2015-05-01
影响因子：
11.8
通讯作者：
Doi, Yohei
中科院分区：
文献类型：
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作者：
Qureshi, Zubair A.;Hittle, Lauren E.;Doi, Yohei
背景。随着多粘菌素甲磺酸盐（CMS）治疗耐碳青霉烯不动杆菌感染的增加，多粘菌素耐药性正在出现。在宾夕法尼亚州的一家医院系统中发现了因耐粘菌素鲍曼不动杆菌感染或定植的患者。临床数据从电子病历中收集。进行药敏试验、脉冲场凝胶电泳（PFGE）和多位点序列分型（MLST）。为了研究粘菌素耐药机制，采用基质辅助激光解吸/电离质谱法对脂质A进行了研究。共鉴定出20例耐粘菌素鲍曼不动杆菌。呼吸机相关性肺炎是最常见的感染类型。在鉴定出耐粘菌素分离株之前，19例患者接受静脉注射和/或吸入CMS治疗碳青霉烯耐药、粘菌素敏感鲍曼不动杆菌感染。30天全因死亡率为30%。死亡率最低的耐粘菌素鲍曼杆菌感染的治疗方案是联合使用CMS、碳青霉烯和氨苄西林-舒巴坦。来自同一患者的粘菌素敏感和耐药菌株与PFGE高度相关，但来自不同患者的分离株与PFGE高度相关，提示在CMS治疗期间耐药性进化。经MLST鉴定，所有分离株均属于流行于全球的ⅱ型国际克隆。在所有耐粘菌素鲍曼不动杆菌分离株中均存在磷酸乙醇胺修饰的脂质A。耐粘菌素鲍曼不动杆菌几乎全部发生在接受CMS治疗碳青霉烯耐药、粘菌素敏感鲍曼不动杆菌感染的患者中。添加磷酸乙醇胺修饰脂质A是导致粘菌素耐药的原因。对于从cms患者中鉴定出的鲍曼不动杆菌，应考虑进行粘菌素药敏试验。
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.