Therapy With Macrolides in Patients With Cystic Fibrosis

Allyson S. Gaylor, Pharm.D., Joan C. Reilly, Pharm.D.

Pharmacotherapy. 2002;22(2) 

In This Article

Pseudomonas aeruginosa and Biofilm Formation

Chronic infections, especially with mucoid strains of P. aeruginosa, contribute to lung inflammation in patients with cystic fibrosis. The most crucial finding linked to a poor prognosis is chronic endobronchial infection with these mucoid strains.[50] Mucoid P. aeruginosa obstructs phagocytosis since the microcolonies are dispersed in a biofilm. The surrounding biofilm also makes the organism more resistant to antibiotic therapy.[51] The major component of biofilm is alginate, which induces a continuous antigen-antibody reaction on the surface of small airways.[51,52] Excess antigen resulting from persistent colonization of mucoid alginate-producing P. aeruginosa triggers host immune complexes. Deposition of lung immune complexes stimulates neutrophil chemotaxis. Neutrophils combine with immune complexes deposited in airway tissue and may cause deterioration of lung tissue.[53]Pseudomonas aeruginosa also produces virulent exoproducts such as exotoxin A, protease, and elastase, which impair phagocytosis and lead to lung tissue damage.[44,51,54]

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