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How much do Pseudomonas biofilms contribute to symptoms of pulmonary exacerbation in cystic fibrosis?
Author(s) -
VanDevanter Donald R.,
Van Dalfsen Jill M.
Publication year - 2005
Publication title -
pediatric pulmonology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.866
H-Index - 106
eISSN - 1099-0496
pISSN - 8755-6863
DOI - 10.1002/ppul.20220
Subject(s) - pseudomonas aeruginosa , antibiotics , cystic fibrosis , exacerbation , medicine , microbiology and biotechnology , biofilm , bacteria , immunology , biology , genetics
Recent studies suggest that chronic Pseudomonas aeruginosa lung infections in cystic fibrosis (CF) involve anaerobic biofilms, and that these biofilms are the reason chronic infections are rarely eradicated by antibiotic therapy, regardless of the in vitro susceptibility of infecting bacteria. These observations led to the development of an in vitro method for testing antibiotic susceptibility of CF clinical isolates in biofilms (Moskowitz et al., J Clin Microbiol 2004;42:1915–1922) and unearthed an apparent paradox. Antibiotics that remain cornerstones of clinical management of CF pulmonary exacerbations (e.g., beta‐lactam antibiotics) appear to have little to no activity at clinically achievable concentrations when tested in vitro against clinical P. aeruginosa isolates growing in biofilms. The proven clinical efficacy of beta‐lactam antibiotics in treating exacerbations, and the selection for beta‐lactam resistance in vivo, suggest that planktonic bacteria play a significant role in pulmonary exacerbations of CF. A model of infection architecture is proposed in which biofilm and planktonic compartments each play a role in infection persistence and pulmonary exacerbation, respectively. Infection architecture may partially account for the observed lack of correlation between in vitro antibiotic susceptibility testing and clinical response to antibiotic therapy. © 2005 Wiley‐Liss, Inc.