Thorax

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS REGISTER


[Advanced]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this link to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Add article to my folders
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by HØIBY, N
Right arrow Articles by KOCH, C
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by HØIBY, N
Right arrow Articles by KOCH, C
Thorax 2000;55:349-350 ( May )

Editorial

Maintenance treatment of chronic Pseudomonas aeruginosa infection in cystic fibrosis

The first 150 words of the full text of this article appear below.

Thirty years ago Staphylococcus aureus and not Pseudomonas aeruginosa was considered to be the most important lung pathogen in cystic fibrosis.1 Those who believed that P aeruginosa was a pathogen in cystic fibrosis thought that various virulence factors such as exotoxin A, exoenzyme S, elastase, alkaline protease, phospholipase C, lipopolysaccharide and phenazine pigments were responsible for the lung tissue damage by drawing parallels with acute P aeruginosa infections in patients with burns or leukaemia.2 Only acute exacerbations, frequently caused by a virus,3 were therefore treated with antibiotics, although invasive disseminating P aeruginosa infection including bacteraemia was never found in cystic fibrosis.4 However, a very pronounced antibody response to P aeruginosa antigens, including its virulence factors, was detected in patients with cystic fibrosis and the pathogenesis of the lung tissue damage was subsequently found to be caused by immune complex mediated inflammation dominated by polymorphonuclear leucocytes releasing proteolytic enzymes.5-7 Since the . . . [Full text of this article]


This article has been cited by other articles:


Home page
 ThoraxHome page
G A Tramper-Stranders, C K van der Ent, M G Slieker, S W J Terheggen-Lagro, F Teding van Berkhout, J L L Kimpen, and T F W Wolfs
Diagnostic value of serological tests against Pseudomonas aeruginosa in a large cystic fibrosis population
Thorax, August 1, 2006; 61(8): 689 - 693.
[Abstract] [Full Text] [PDF]

Home page
 MicrobiologyHome page
T. B. Rasmussen, M. E. Skindersoe, T. Bjarnsholt, R. K. Phipps, K. B. Christensen, P. O. Jensen, J. B. Andersen, B. Koch, T. O. Larsen, M. Hentzer, et al.
Identity and effects of quorum-sensing inhibitors produced by Penicillium species
Microbiology, May 1, 2005; 151(5): 1325 - 1340.
[Abstract] [Full Text] [PDF]

Home page
 Infect. Immun.Home page
C. Beckmann, M. Brittnacher, R. Ernst, N. Mayer-Hamblett, S. I. Miller, and J. L. Burns
Use of Phage Display To Identify Potential Pseudomonas aeruginosa Gene Products Relevant to Early Cystic Fibrosis Airway Infections
Infect. Immun., January 1, 2005; 73(1): 444 - 452.
[Abstract] [Full Text] [PDF]

Home page
 Eur Respir JHome page
N. Hoiby
Inflammation and infection in cystic fibrosis - hen or egg?
Eur. Respir. J., January 1, 2001; 17(1): 4 - 5.
[Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS REGISTER
Terms and conditions relating to subscriptions purchased online  ¦  Website terms and conditions  ¦  Privacy policy
Copyright © 2000 BMJ Publishing Group Ltd & British Thoracic Society