Why is Pseudomonas the colonizer and why does it persist?

Abstract

Pseudomonas aeruginosa is currently the major cause of morbidity and mortality in cystic fibrosis. Studies to understand why this particular organism is a problem and why host defenses fail to clear it, are beginning to provide some answers. Implicit in any working hypothesis are the prerequisites that: (i) P. aeruginosa should have a tropism for the respiratory tract; (ii) there should be a physical clearance defect; and (iii) there should be an acquired immune clearance defect. Studies from many laboratories support these contentions. This organism exhibits its tropism by adhering to tracheal cells and to tracheobronchial mucins by means of pili or the mucoid exopolysacharide of mucoid strains. The receptors on both cells and mucins contain sialic acid as the dominant sugar moiety. Many factors contribute to its persistence, chief among which is the failure of phagocytic defenses caused by microbial or host enzymes and even by mucins which inhibit the opsonophagocytosis of P. aeruginosa. Injury to the mucociliary system, again caused by microbial or host factors, is also a prominent factor in the persistence of P. aeruginosa. We hypothesize that this organism is the dominant pathogen because of the existence of receptors in the respiratory tract for it and that it persists because bacteria in stagnant mucus cannot be cleared physically or immunologically. We are doubtful that conventional vaccination approaches will yield a solution to this problem.