Pathogenetic Mechanisms in Lung Diseases Caused by Pseudomonas aeruginosa

Abstract

Pseudomonas aeruginosa has been referred to as a microbial hyena. This seems appropriate. This bacterium, as with the wolf-like carnivore, is a significant pathogen causing disease characterized by hemorrhage and necrosis; yet, like the cowardly hog-like part of this animal, Pseudomonas frequently colonizes the respiratory tract waiting for an opportunity to spring. It is important to recognize that P aeruginosa is not just a few strains of microorganisms grouped within a genus, but each individual typed strain contains microorganisms capable of expressing different invasive properties, toxin and protease production, antigenic markers, pigment production, and, importantly, antibiotic resistance. The ability of PA strains to mutate and change their metabolic behavior to adapt to an often hostile environment reflects one of the more efficient gene pools awaiting microbiologic investigation. Pseudomonas is a superbly adapted organism causing a wide spectrum of human disease. Those studying the pathogenesis of these diseases have increasingly wondered: are some states marked by increased virulence factors and other conditions by decrease in these factors? How are environmental influences translated into expression or regulation of these factors? The recent availability of closed genes for toxin A, phospholipase C, elastase, alginate biosynthesis, and pilus structures are important developments and guarantee that further important developments in our understanding of bacterial pathogenesis will be forthcoming. Understanding the pathogenesis is key to developing rational interventions before extensive and irreversible changes occur.