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Respiratory Research 2008, 9:48doi:10.1186/1465-9921-9-48

Research

Severe asthma exacerbation: role of acute Chlamydophila pneumoniae and Mycoplasma pneumoniae infection

 

Roberto Cosentini 1 , Paolo Tarsia 2 , Ciro Canetta 1 , Giovanna Graziadei 1 , Anna Maria Brambilla 1 , Stefano Alibert 2 , Maria Pappalettera 2 , Francesca Tantardini 1 and Francesco Blasi 2

 

  1. Emergency Medicine Department, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena, Gruppo NIV Policlinico, Milan, Italy
  2. Institute of Respiratory Diseases, University of Milan, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena, Gruppo NIV Policlinico, Milan, Italy

 

The electronic version of this article is the complete one and can be found online at:
http://respiratory-research.com/content/9/1/48

 

Published: 30 May 2008

 

© 2008 Cosentini et al; licensee BioMed Central Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

 

Background

Chlamydophila pneumoniae and Mycoplasma pneumoniae are associated with acute exacerbation of bronchial asthma (AEBA). The aim of this study was to evaluate the correlation between these acute bacterial infections and the severity of AEBA.

Methods

We prospectively analysed consecutive patients admitted to the Emergency Department with acute asthma exacerbation. In every patient peak expiratory flow (PEF) measurement was performed on admission, and spirometry during follow-up. Serology for Chlamydophila and Mycoplasma pneumoniae was performed on admission and after 4–8 weeks.

Results

Fifty-eight patients completed the study. Acute atypical infections (AAI) was observed in 22/58 cases; we found single acute C. pneumoniae in 19 cases, single acute M. pneumoniae in 2 cases, and double acute infection in one case. Functional impairment on admission was greater in patients with AAI than in patients without AAI (PEF 205 ± 104 L/min vs 276 ± 117 p = 0.02) and persisted until visit 2 (FEV1% 76.30 ± 24.54 vs FEV1% 92.91 ± 13.89, p = 0.002). Moreover, the proportion of patients who presented with severe AEBA was significantly greater in the group with AAI than in the group without AAI (15/22 vs 12/36, p = 0.01; OR 4.29, 95% CI 1.38–13.32).

Conclusion

Our data suggest an association between acute atypical infection and a more severe AEBA.

 

Full Text article at : http://respiratory-research.com/content/9/1/48

 

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