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[肠球菌:西班牙的表型和基因型耐药性及流行病学]

[Enterococcus: phenotype and genotype resistance and epidemiology in Spain].

作者信息

Cercenado Emilia

机构信息

Servicio de Microbiología y Enfermedades Infecciosas, Hospital General Universitario Gregorio Marañón, Madrid, España.

出版信息

Enferm Infecc Microbiol Clin. 2011 Dec;29 Suppl 5:59-65. doi: 10.1016/S0213-005X(11)70045-3.

DOI:10.1016/S0213-005X(11)70045-3
PMID:22305671
Abstract

Enterococci are major nosocomial pathogens due to their intrinsic resistance to many antimicrobials as well as to their ability to acquire new mechanisms of resistance. Acquired resistance to beta-lactams is due to PBP5 overproduction or alterations in this protein. Beta-lactamase production is anecdotal. High-level resistance (HLR) to aminoglycosides is due to the production of aminoglycoside-modifying enzymes that delete synergistic killing in association with cell wall-active agents. The most frequent enzyme is AAC(6')- APH(2"), which inactivates all the aminoglycosides most frequently used in clinical practice. Acquired resistance to glycopeptides is due to the acquisition of gene clusters called vanA, vanB, vanD, vanE, vanG, vanL, vanM and vanN. Linezolid resistance is due to ribosomal mutations or to the acquisition of the cfr gene. Some isolates present diminished susceptibility to daptomycin. In Spain, both enterococcal resistance to beta-lactams and HLR to aminoglycosides are high. E. faecalis is almost uniformly susceptible to ampicillin. Enterococcal resistance to glycopeptides is low, with the exception of occasional outbreaks. The new antimicrobials (linezolid, daptomycin, tigecycline) are almost uniformly active against these microorganisms. Because of the wide dissemination of the high-risk clonal complexes CC2 and CC9 (E. faecalis), and CC17 (E. faecium), surveillance studies are required to detect antimicrobial resistance genes as well as to identify high-risk clonal complexes in order to predict future trends in the acquisition of resistance genes.

摘要

肠球菌是主要的医院病原体,这归因于它们对许多抗菌药物的固有耐药性以及获得新耐药机制的能力。对β-内酰胺类药物的获得性耐药是由于PBP5过度产生或该蛋白发生改变。β-内酰胺酶的产生较为少见。对氨基糖苷类药物的高水平耐药(HLR)是由于产生了氨基糖苷类修饰酶,这些酶消除了与细胞壁活性剂联合使用时的协同杀伤作用。最常见的酶是AAC(6')-APH(2"),它能使临床实践中最常用的所有氨基糖苷类药物失活。对糖肽类药物的获得性耐药是由于获得了称为vanA、vanB、vanD、vanE、vanG、vanL、vanM和vanN的基因簇。利奈唑胺耐药是由于核糖体突变或获得了cfr基因。一些分离株对达托霉素的敏感性降低。在西班牙,肠球菌对β-内酰胺类药物的耐药性和对氨基糖苷类药物的HLR都很高。粪肠球菌几乎对氨苄西林均敏感。肠球菌对糖肽类药物的耐药性较低,偶尔有暴发除外。新型抗菌药物(利奈唑胺、达托霉素、替加环素)几乎对这些微生物均有活性。由于高风险克隆复合体CC2和CC9(粪肠球菌)以及CC17(屎肠球菌)广泛传播,需要进行监测研究以检测抗菌耐药基因并识别高风险克隆复合体,以便预测耐药基因获得的未来趋势。

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