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High Pseudomonas aeruginosa acquisition rate in CF
  1. B E van Ewijk1,
  2. T F W Wolfs2,
  3. A Fleer2,
  4. J L L Kimpen2,
  5. C K van der Ent3
  1. 1Cystic Fibrosis Centre and Department of Paediatric Respiratory Medicine, Wilhelmina Children’s Hospital/University Medical Centre Utrecht, Utrecht, The Netherlands
  2. 2Department of Paediatric Infectious Diseases, Wilhelmina Children’s Hospital/University Medical Centre Utrecht, Utrecht, The Netherlands
  3. 3Cystic Fibrosis Centre and Department of Paediatric Respiratory Medicine, Wilhelmina Children’s Hospital/University Medical Centre Utrecht, Utrecht, The Netherlands
  1. Correspondence to:
    Dr B E van Ewijk
    Cystic Fibrosis Centre and Department of Paediatric Respiratory Medicine, Wilhelmina Children’s Hospital/University Medical Centre Utrecht, P O Box 85090, 3508 AB Utrecht, Netherlands; b.vanewijk{at}umcutrecht.nl

https://doi.org/10.1136/thx.2006.062372

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    Chronic colonisation of the lungs with Pseudomonas aeruginosa in patients with cystic fibrosis (CF) is associated with reduced lung function and life expectancy. Prevention of chronic colonisation might be achieved by avoidance of, or early and aggressive treatment of, primary P aeruginosa acquisition.1 Segregation of uninfected indivduals from chronically P aeruginosa colonised CF patients is advocated to prevent cross infection.2 As surveillance studies suggest that the airways of healthy children are rarely colonised with P aeruginosa,3 healthy individuals are not regarded as a potential source of P aeruginosa acquisition. In addition, it has been shown that acquisition of P aeruginosa in CF patients is often preceded by a viral respiratory infection.4 We hypothesised that the incidence of P aeruginosa acquisition during periods of acute respiratory infections (ARI) is equal in both healthy and CF individuals, and considerably exceeds the prevalence in …

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    Footnotes

    • This work was supported by the Wilhelmina Children’s Hospital Research Fund (fellowship to B E van Ewijk). The funding source had no role in the design and conduct of the study; in the collection, management, analysis, and interpretation of the data; or in the preparation, review or approval of the manuscript.

    • TW has served as consultant for Pfizer and Abbott; JK has participated in unrestricted educational activities supported by Abbott for which speakers fees were received from 2002 to 2005 and was co-investigator on a clinical trial endorsed by Abbott which was concluded in 2005; CvdE received research grants and speakers fees from GlaxoSmithKline. None of the other authors has any conflict of interest or financial relationships with a commercial entity that has an interest in the subject of this manuscript.