Pseudomonas aeruginosa chronic colonization in cystic fibrosis patients

Purpose of review Chronic infection with Pseudomonas aeruginosa is a leading cause of morbidity and mortality in individuals with cystic fibrosis despite the aggressive use of antibiotics. P. aeruginosa employs a number of strategies that promote chronic pulmonary colonization instead of acute infection. These include biofilm formation, evasion of he host immune system, and conversion to a mucoid phenotype. This review discusses recent advances regarding P. aeruginosa pathogenesis and biofilm behavior in the setting of chronic pulmonary disease. Recent findings Biofilm formation in the cystic fibrosis lung likely occurs under anaerobic conditions, is controlled by bacterial quorum-sensing mechanism, and is enhanced by environmental components in the cystic fibrosis airway. P. aeruginosa possesses regulatory pathways that recognize environmental cues to favor either acute infection or chronic colonization. P. aeruginosa that inhabit the respiratory tract accumulate mutations favoring chronic colonization. Azithromycin, a macrolide with clinical benefit in cystic fibrosis, alter P. aeruginosa biofilm formation include molecules that disrupt quorum sensing. Summary Eradication of P. aeruginosa in cystic fibrosis patients remains problematic. As more information emerges about P. aeruginosa behavior in vivo, potential therapeutics directed against biofilms and mucoid P. aeruginosa are being developed.