Department of Pathology and Laboratory Medicine, Taipei Veterans General Hospital, Taipei, Taiwan.
PhD Program of Medical Biotechnology, Taipei Medical University, Taipei, Taiwan.
J Antimicrob Chemother. 2021 Jan 19;76(2):312-321. doi: 10.1093/jac/dkaa432.
Acinetobacter seifertii, a new member of the Acinetobacter baumannii group, has emerged as a cause of severe infections in humans. We investigated the clinical and molecular characteristics of A. seifertii.
This retrospective study enrolled 80 adults with A. seifertii bloodstream infection (BSI) at four medical centres over an 8 year period. Species identification was confirmed by MALDI-TOF MS, rpoB sequencing and WGS. Molecular typing was performed by MLST. Clinical information, antimicrobial susceptibility and the mechanisms of carbapenem and colistin resistance were analysed. Transmissibility of the carbapenem-resistance determinants was examined by conjugation experiments.
The main source of A. seifertii BSI was the respiratory tract (46.3%). The 28 day and in-hospital mortality rates of A. seifertii BSI were 18.8% and 30.0%, respectively. High APACHE II scores and immunosuppressant therapy were independent risk factors for 28 day mortality. The most common MLST type was ST553 (58.8%). Most A. seifertii isolates were susceptible to levofloxacin (86.2%), and only 37.5% were susceptible to colistin. Carbapenem resistance was observed in 16.3% of isolates, mostly caused by the plasmid-borne ISAba1-blaOXA-51-like genetic structure. A. seifertii could transfer various carbapenem-resistance determinants to A. baumannii, Acinetobacter nosocomialis and other A. seifertii isolates. Variations of pmrCAB and lpxCAD genes were not associated with colistin resistance of A. seifertii.
Levofloxacin and carbapenems, but not colistin, have the potential to be the drug of choice for A. seifertii infections. A. seifertii can transfer carbapenem-resistance determinants to other species of the A. baumannii group and warrants close monitoring.
产酸克雷伯菌是鲍曼不动杆菌群的一个新成员,已成为人类严重感染的原因。我们研究了产酸克雷伯菌的临床和分子特征。
这项回顾性研究纳入了 80 名在 8 年内来自四个医疗中心的患有产酸克雷伯菌血流感染(BSI)的成年人。通过基质辅助激光解吸电离飞行时间质谱(MALDI-TOF MS)、rpoB 测序和 WGS 确认物种鉴定。通过 MLST 进行分子分型。分析临床信息、抗菌药物敏感性以及碳青霉烯类和黏菌素耐药的机制。通过接合实验检查碳青霉烯类耐药决定因素的传播性。
产酸克雷伯菌 BSI 的主要来源是呼吸道(46.3%)。产酸克雷伯菌 BSI 的 28 天和住院死亡率分别为 18.8%和 30.0%。高急性生理与慢性健康状况评分Ⅱ(APACHEⅡ)评分和免疫抑制剂治疗是 28 天死亡率的独立危险因素。最常见的 MLST 型是 ST553(58.8%)。大多数产酸克雷伯菌分离株对左氧氟沙星(86.2%)敏感,只有 37.5%对黏菌素敏感。16.3%的分离株表现出碳青霉烯类耐药,主要是由质粒携带的 ISAba1-blaOXA-51 样遗传结构引起的。产酸克雷伯菌可以将各种碳青霉烯类耐药决定因素转移到鲍曼不动杆菌、医院不动杆菌和其他产酸克雷伯菌分离株。pmrCAB 和 lpxCAD 基因的变异与产酸克雷伯菌对黏菌素的耐药性无关。
左氧氟沙星和碳青霉烯类药物,而不是黏菌素,有可能成为产酸克雷伯菌感染的首选药物。产酸克雷伯菌可以将碳青霉烯类耐药决定因素转移到鲍曼不动杆菌群的其他物种,需要密切监测。