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铜绿假单胞菌中β-内酰胺类耐药机制。

Mechanisms of β-lactam resistance among Pseudomonas aeruginosa.

机构信息

Department of Pediatrics, University of Washington, Seattle, WA, USA.

出版信息

Curr Pharm Des. 2013;19(2):209-22.

Abstract

Treatment of serious P. aeruginosa infections becomes more challenging with each passing year. As this pathogen acquires more transferrable resistance mechanisms and continues to rapidly adapt and emerge resistant during the course of antimicrobial therapy, we face the growing threat of pan-resistance. This review has focused on those mechanisms that directly impact the future of β-lactam antibiotics, including the production of β-lactamases, porin-mediated resistance, and/or the overexpression of RND efflux pumps. With the pipeline of new anti-pseudomonal agents diminishing, it is essential that novel therapeutic strategies be explored. These include targeting biofilm formation and maintenance, virulence factors, and resistance mechanisms. Furthermore, we must continue to search for effective antibacterial combinations to not only prevent further emergence of resistance but also treat resistant strains already in the environment.

摘要

随着时间的推移,严重的铜绿假单胞菌感染的治疗变得更加具有挑战性。由于这种病原体获得了更多可转移的耐药机制,并在抗微生物治疗过程中继续快速适应和出现耐药性,我们面临着泛耐药性日益增长的威胁。本综述重点关注了那些直接影响β-内酰胺类抗生素未来的机制,包括β-内酰胺酶的产生、孔蛋白介导的耐药性和/或 RND 外排泵的过度表达。随着新型抗假单胞菌药物的研发管道不断减少,探索新的治疗策略至关重要。这些策略包括针对生物膜形成和维持、毒力因子和耐药机制。此外,我们必须继续寻找有效的抗菌联合治疗方法,不仅要防止进一步出现耐药性,还要治疗已经存在于环境中的耐药菌株。

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