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[慢性支气管感染:铜绿假单胞菌问题]

[Chronic bronchial infection: the problem of Pseudomonas aeruginosa].

作者信息

Cantón Rafael, Fernández Olmos Ana, de la Pedrosa Elia Gómez G, del Campo Rosa, Antonia Meseguer María

机构信息

Servicio de Microbiología y CIBER en Epidemiología y Salud Pública, Instituto Ramón y Cajal de Investigación Sanitaria, Hospital Universitario Ramón y Cajal, Madrid, España.

出版信息

Arch Bronconeumol. 2011 Jun;47 Suppl 6:8-13. doi: 10.1016/S0300-2896(11)70029-1.

DOI:10.1016/S0300-2896(11)70029-1
PMID:21703473
Abstract

Pathogenic bronchopulmonary colonizations and the exacerbations produced are among the most important causes of reduced pulmonary function in patients with bronchiectasis. The most frequent pathogens in these patients are Haemophilus influenzae and Pseudomonas aeruginosa. Lesions are produced by the local inflammatory process and the vicious circle developed by antigen stimulation, the release of inflammatory mediators, the presence of neutrophils, the increase of bacterial inoculum and the release of bacterial exoproducts. P. aeruginosa has been demonstrated to affect the patients with bronchiectasis and poorest quality of life and to colonize those with the poorest pulmonary function and the highest number of antimicrobial treatments. In bronchiectasis, as in chronic obstructive pulmonary disease (COPD) or cystic fibrosis, P. aeruginosa is able to colonize the respiratory mucosa chronically. Due to the ecological niche occupied by P. aeruginosa and the multitude of cycles with antimicrobial agents to which these patients are subjected, the development of antimicrobial resistance is highly likely, encouraged by the high proportion of hypermutation variants in existence. Likewise, P. aeruginosa naturally grows in the form of biofilms on the mucosal surface, greatly contributing to its persistence. Antimicrobial treatment in patients with bronchiectasis and P. aeruginosa colonization should be based on antimicrobial agents, alone or in combination, that do not lose activity when acting on biofilms.

摘要

致病性支气管肺定植以及由此引发的病情加重是支气管扩张症患者肺功能下降的最重要原因之一。这些患者中最常见的病原体是流感嗜血杆菌和铜绿假单胞菌。病变是由局部炎症过程以及抗原刺激、炎症介质释放、中性粒细胞存在、细菌接种量增加和细菌外毒素释放所形成的恶性循环导致的。已证实铜绿假单胞菌会影响支气管扩张症患者且这些患者生活质量最差,还会定植于肺功能最差且接受抗菌治疗次数最多的患者体内。在支气管扩张症中,如同在慢性阻塞性肺疾病(COPD)或囊性纤维化中一样,铜绿假单胞菌能够长期定植于呼吸道黏膜。由于铜绿假单胞菌占据的生态位以及这些患者接受多种抗菌药物治疗的周期众多,在现存的高比例超突变变体的推动下,极有可能产生抗菌药物耐药性。同样,铜绿假单胞菌自然地以生物膜形式生长在黏膜表面,这极大地促进了其持续性。对于支气管扩张症合并铜绿假单胞菌定植的患者,抗菌治疗应基于单独或联合使用在作用于生物膜时不会丧失活性的抗菌药物。

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