Pseudomonas aeruginosa is the major pathogen in the cystic fibrosis (CF) lung. Prevalence is high and, once acquired, chronic infection will almost always ensue. Several hypotheses related to the underlying molecular defects in CF have been suggested to explain this high rate of prevalence. These include abnormalities of airway surface liquid leading to impaired mucociliary clearance or malfunction of antibacterial peptides, increased availability of bacterial receptors, reduced ingestion of pathogens by CF cells and impaired defence related to low levels of molecules such as nitric oxide or glutathione. Further work is needed to identify which of these mechanisms is important in the early stages of infection. Once the organisms have gained a foothold in the CF airway they have a wide array of properties that enhance their survival and allow them to evade host defences and antibiotic agents successfully. Conversion to mucoidy and the formation of biofilms are two of the main mechanisms by which this is achieved. Understanding the steps involved in both initial infection and in establishing chronicity may help in the development of new treatment strategies.
Copyright 2002 Elsevier Science Ltd.