Urease production as a marker of virulence in Pseudomonas aeruginosa

Strains show a gradual but marked change over time towards mucoid, non-motile and antibiotic resistant phenotypes.3 In recent decades, multidrug-resistant clonal strains of this organism have been described infecting CF patients on several continents.4 10 At least one clonal strain (Australian epidemic strain 3; AES3) has been shown to result in adverse clinical outcomes for patients.10 The mechanisms by which such clonal strains establish infection in the CF lung, and sometimes supplant other non-clonal isolates of P. aeruginosa, remain to be fully elucidated. Ceftazidime resistance was noted as a marker for the Liverpool epidemic strain (LES) in 1996,6 but not all LES strains are resistant to this antibiotic,11 and non-clonal CF isolates may often express such resistance.12 P. aeruginosa isolates from CF respiratory infections also gradually cease to express virulence factors over time, leading to a less virulent phenotype, as demonstrated by immunoblot analysis of type III secretion system effector enzyme expression13 and whole cell virulence in a Dictyostelium discoideum eukaryotic virulence model.14 The progressive nature of whole cell virulence loss has also been demonstrated in a D. discoideum eukaryotic virulence model.15 Almost all non-CF isolates of P. aeruginosa express the enzyme urease