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Eur Respir J 2004; 23:493-494
Copyright ©ERS Journals Ltd 2004


Host response to transmissible Pseudomonas aeruginosa

D.W. Reid1, A. Champion2, R. Bradbury2 and S.M. Kirov2

Depts of 1 Respiratory Medicine, and 2 Pathology, University of Tasmania Medical School, Hobart, Tasmania, Australia.

To the Editor:

The recent study by Jones et al. 1 was interesting in that it found no significant difference in local airway or systemic inflammation between cystic fibrosis patients colonised with either transmissible or nontransmissible strains of Pseudomonas aeruginosa. At face value these results appear reassuring, although the authors do rightly raise a note of caution. One factor that was not considered in this article is the effect of bacterial load within the airways, but this must surely be the denominator when one is trying to identify a significant difference in host response. There is also anecdotal evidence that the host inflammatory response at the time of first acquisition of transmissible P. aeruginosa or Burkholderia cepacia may be what determines subsequent outcome i.e. some patients become extremely unwell and die whereas the majority seem to remain relatively well. Presumably some sort of status quo is reached between host and organism and perhaps what we are seeing in the study by Jones et al. 1 is in fact a survivor effect. The experience of Armstrong et al. 2, where a number of deaths occurred shortly after acquisition of a transmissible strain goes some way toward supporting this hypothesis. However, the long-term outcome in those other children in the study by Armstrong et al. 2 who were similarly infected remains unknown, but hopefully longitudinal follow-up in these individuals will add further weight to the reassurance by Jones et al. 1.

In the meantime, until there is evidence to the contrary, efficient segregation based on molecular typing of Pseudomonas aeruginosa would seem be the only appropriate management strategy for our cystic fibrosis patients.

References

  1. Jones AM, Martin L, Bright-Thomas RJ, et al. Inflammatory markers in cystic fibrosis patients with transmissible Pseudomonas aeruginosa. Eur Respir J 2003;22:503–506.[Abstract/Free Full Text]
  2. Armstrong DS, Nixon GM, Carzino R, et al. Detection of a widespread clone of Pseudomonas aeruginosa in a pediatric cystic fibrosis clinic. Am J Respir Crit Care Med 2002;166:983–987.[Abstract/Free Full Text]




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