Esterly John S, Richardson Chad L, Eltoukhy Noha S, Qi Chao, Scheetz Marc H
John S Esterly PharmD BCPS, at time of writing, Infectious Diseases Pharmacotherapy Fellow, Department of Pharmacy Practice, College of Pharmacy, Midwestern University Chicago, Downers Grove, IL; now, Assistant Professor of Pharmacy Practice, College of Pharmacy, Chicago State University, Chicago, IL; Infectious Diseases Pharmacist, Northwestern Memorial Hospital, Chicago.
Chad L Richardson PharmD, at time of writing, Infectious Diseases Pharmacotherapy Resident, Department of Pharmacy Practice, College of Pharmacy, Midwestern University Chicago; now, Solid Organ Transplant Pharmacist, Northwestern Memorial Hospital.
Ann Pharmacother. 2011 Feb;45(2):218-28. doi: 10.1345/aph.1P084.
To summarize published data identifying known genetic mechanisms of antibiotic resistance in Acinetobacter baumannii and the correlating phenotypic expression of antibiotic resistance.
MEDLINE databases (1966-July 15, 2010) were searched to identify original reports of genetic mechanisms of antibiotic resistance in A. baumannii.
Numerous genetic mechanisms of resistance to multiple classes of antibiotics are known to exist in A. baumannii, a gram-negative bacterium increasingly implicated in nosocomial infections. Mechanisms may be constitutive or acquired via plasmids, integrons, and transposons. Methods of resistance include enzymatic modification of antibiotic molecules, modification of antibiotic target sites, expression of efflux pumps, and downregulation of cell membrane porin channel expression. Resistance to β-lactams appears to be primarily caused by β-lactamase production, including extended spectrum β-lactamases (b/aTEM, blaSHV, b/aTX-M,b/aKPC), metallo-β-lactamases (blaMP, blaVIM, bla, SIM), and most commonly, oxacillinases (blaOXA). Antibiotic target site alterations confer resistance to fluoroquinolones (gyrA, parC) and aminoglycosides (arm, rmt), and to a much lesser extent, β-lactams. Efflux pumps (tet, ade, abe) contribute to resistance against β-lactams, tetracyclines, fluoroquinolones, and aminoglycosides. Finally, porin channel deletion (carO, oprD) appears to contribute to β-lactam resistance and may contribute to rarely seen polymyxin resistance. Of note, efflux pumps and porin deletions as solitary mechanisms may not render clinical resistance to A. baumannii.
A. baumannii possesses copious genetic resistance mechanisms. Knowledge of local genotypes and expressed phenotypes for A. baumannii may aid clinicians more than phenotypic susceptibilities reported in large epidemiologic studies.
总结已发表的数据，确定鲍曼不动杆菌抗生素耐药的已知遗传机制以及抗生素耐药的相关表型表达。
检索MEDLINE数据库（1966年 - 2010年7月15日），以识别鲍曼不动杆菌抗生素耐药遗传机制的原始报告。
已知在鲍曼不动杆菌（一种越来越多地与医院感染相关的革兰氏阴性菌）中存在多种对多类抗生素的耐药遗传机制。这些机制可能是组成性的，也可能是通过质粒、整合子和转座子获得的。耐药方法包括抗生素分子的酶促修饰、抗生素靶位点的修饰、外排泵的表达以及细胞膜孔蛋白通道表达的下调。对β-内酰胺类抗生素的耐药似乎主要由β-内酰胺酶产生引起，包括超广谱β-内酰胺酶（b/aTEM、blaSHV、b/aTX-M、b/aKPC）、金属β-内酰胺酶（blaMP、blaVIM、blaSIM），最常见的是苯唑西林酶（blaOXA）。抗生素靶位点改变赋予对氟喹诺酮类（gyrA、parC）和氨基糖苷类（arm、rmt）的耐药性，对β-内酰胺类抗生素的耐药性影响较小。外排泵（tet、ade、abe）导致对β-内酰胺类、四环素类、氟喹诺酮类和氨基糖苷类抗生素的耐药。最后，孔蛋白通道缺失（carO、oprD）似乎导致β-内酰胺类耐药，也可能导致罕见的多粘菌素耐药。值得注意的是，外排泵和孔蛋白缺失作为单独的机制可能不会使鲍曼不动杆菌产生临床耐药性。
鲍曼不动杆菌拥有丰富的遗传耐药机制。了解鲍曼不动杆菌的局部基因型和表达的表型可能比大型流行病学研究报告的表型敏感性更有助于临床医生。
