Qureshi Zubair A, Hittle Lauren E, O'Hara Jessica A, Rivera Jesabel I, Syed Alveena, Shields Ryan K, Pasculle Anthony W, Ernst Robert K, Doi Yohei
Division of Infectious Diseases, University of Pittsburgh School of Medicine, Pennsylvania.
Department of Microbial Pathogenesis, School of Dentistry, University of Maryland, Baltimore.
Clin Infect Dis. 2015 May 1;60(9):1295-303. doi: 10.1093/cid/civ048. Epub 2015 Jan 28.
With an increase in the use of colistin methansulfonate (CMS) to treat carbapenem-resistant Acinetobacter baumannii infections, colistin resistance is emerging.
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.
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.
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.
随着多粘菌素甲磺酸盐（CMS）用于治疗耐碳青霉烯类鲍曼不动杆菌感染的情况增多，多粘菌素耐药性正在出现。
在宾夕法尼亚州的一个医院系统中识别出因耐多粘菌素鲍曼不动杆菌导致感染或定植的患者。从电子病历中收集临床数据。进行药敏试验、脉冲场凝胶电泳（PFGE）和多位点序列分型（MLST）。为研究多粘菌素耐药机制，对脂多糖进行基质辅助激光解吸/电离质谱分析。
识别出20例耐多粘菌素鲍曼不动杆菌患者。呼吸机相关性肺炎是最常见的感染类型。19例患者在耐多粘菌素菌株被识别之前，已接受静脉和/或吸入CMS治疗耐碳青霉烯类、对多粘菌素敏感的鲍曼不动杆菌感染。30天全因死亡率为30%。与最低死亡率相关的耐多粘菌素鲍曼不动杆菌感染治疗方案是CMS、一种碳青霉烯类药物和氨苄西林 - 舒巴坦的联合使用。同一患者的多粘菌素敏感和耐药菌株通过PFGE高度相关，但不同患者的菌株则不然，这表明在CMS治疗期间耐药性发生了演变。通过MLST分析，所有分离株均属于国际克隆II型，这是一种在全球流行的谱系。所有耐多粘菌素鲍曼不动杆菌分离株的脂多糖均存在磷酸乙醇胺修饰。
耐多粘菌素鲍曼不动杆菌几乎仅出现在接受CMS治疗耐碳青霉烯类、对多粘菌素敏感的鲍曼不动杆菌感染的患者中。添加磷酸乙醇胺导致的脂多糖修饰是多粘菌素耐药的原因。对于从有CMS治疗经历的患者中分离出的鲍曼不动杆菌，应考虑进行多粘菌素药敏试验。
