Pathogenesis of early lung disease in cystic fibrosis: A window of opportunity to eradicate bacteria

T he patient, a previously asymptomatic 18-year-old man with cysticfibrosts, presented with a chronic, nonproductive cough. His medical history was significant for pancreatic insufficiency and homozygosity for the Delta F508 CFTR mutation. Pancreatic insufficiency was well controlled by enzyme supplementation, and the patient achieved a normal height and weight. He had Pseudomonas aeruginosa detected by bronchoscopy at the age of 5 years and by throat culture at the age of 16years, both of which were successfully eradicated by prolonged courses of antibiotics. Chest radiographs were normal, and he did not have chronic respiratory symptoms until cough 2 months earlier. Bronchoscopy was done to evaluate the patient for respiratory infections and inflammation. The culture of the bronchoalveolar lavage fluid tested positive for I strain Of nonmucoid Pseudomonas aeruginosa in high numbers (1.2 million colony-forming units/mL of bronchoalveolar lavage fluid) and showed increased neutrophils (8016 of leukocytes [normal values <5%6]). Because the patient was not known to have chronic P. aeruginosa infection, he was treated with inhaled and oral antibloticsfor 3 months in an attempt to eradicate this pathogen.