COPD急性加重与气道细菌浓度

Title:Airway Bacterial Concentrations and Exacerbations of Chronic Obstructive Pulmonary Disease

Am. J. Respir. Crit. Care Med. 2007; 176: 356-361.

Author:Sanjay Sethi, Rohin Sethi, Karen Eschberger

Abstract:
Rationale: Increased bacterial concentration (load) in the lower airways and new bacterial strain acquisition have been posited as mechanisms for chronic obstructive pulmonary disease (COPD) exacerbations. Bacterial concentrations are higher during exacerbation than during stable disease; however, these studies are cross sectional and devoid of strain typing.
背景：下气道细菌负荷的增加和新菌株感染被认为是COPD恶化加重的机制。尽管研究表明COPD加重期细菌负荷高于稳定期，但这些研究均为横断面研究，并且缺少对菌株的分类。
Objectives: To determine if the increased bacterial concentrations function as a separate mechanism for exacerbation induction independent of new strain acquisition.
目的：探讨（原有）细菌负荷的增加是否与新菌株感染一样是（COPD）加重的独立机制。
Methods: In a prospective, longitudinal cohort of patients with COPD, the relationship between exacerbation occurrence, sputum bacterial concentrations, and new strain acquisition was examined.
方法：在一项对COPD患者的前瞻性、纵向队列研究中，观察COPD加重的发生与痰细菌浓度和新菌株的获得之间的关系。
Measurements and Main Results: Clinical information, quantitative sputum cultures, and molecular typing of potential bacterial pathogen isolates. Over 81 months, 104 subjects completed 3,009 clinic visits, 560 (19.6%) during exacerbations and 2,449 (80.4%) during stable disease. Among preexisting strains, sputum concentrations of Nontypeable Haemophilus influenzae and Haemophilus haemolyticus were not different in exacerbation versus stable disease. Moraxella catarrhalis (stable, 108.38 ± 0.13 [mean ± SEM] vs. exacerbation, 107.78 ± 0.26; p = 0.02) and Streptococcus pneumoniae (stable, 108.42 ± 0.21 vs. exacerbation, 107.76 ± 0.52; p = 0.07) concentrations were lower during exacerbations compared with stable periods. Concentrations of new strains of H. influenzae (stable, 107.28 ± 0.15 vs. exacerbation, 107.76 ± 0.17; p = 0.04) and M. catarrhalis (stable, 107.85 ± 0.15 vs. exacerbation, 108.37 ± 0.14; p = 0.02), were increased during exacerbations; however, the differences were small.
检测与结果：采集患者临床资料、定量痰培养以及潜在致病菌的分子分型。在81个月中，对104例患者进行了3009次的临床访视，其中加重期560次（19.6%），稳定期2449次（80.4%）。既有菌株中，未分型流感嗜血杆菌和溶血性嗜血杆菌在加重期和稳定期的痰菌浓度无差异；卡他莫拉菌（稳定期108.38 ± 0.13vs. 加重期107.78 ± 0.26，p = 0.02）、肺炎链球菌（稳定期108.42 ± 0.21vs. 加重期107.76 ± 0.52，p = 0.02）痰菌浓度加重期低于稳定期；流感嗜血杆菌（稳定期107.28 ± 0.15vs. 加重期107.76 ± 0.17，p = 0.04）、卡他莫拉菌（稳定期107.85 ± 0.15vs. 加重期108.37± 0.14，p = 0.02）新菌株浓度加重期有少量的增加。
Conclusions: Change in bacterial load is unlikely to be an important mechanism for exacerbations. Better understanding of the host–pathogen interaction, rather than enumerating bacteria in respiratory samples, is required to provide new insights into bacterial infection in COPD.
结论：细菌负荷的改变可能并非COPD加重的主要机制。在认识COPD中的细菌感染时，深入理解宿主－病原菌之间的相互作用可能较之罗列气道标本中的细菌种类更有意义。
Key Words: bacteria • chronic obstructive pulmonary disease • exacerbation
关键词：细菌 慢性阻塞性肺病 加重