Role of ompD2 and chromosomal β-lactamase in carbapenem resistance in clinical isolates of pseudomonas aeruginosa

Imipenem-resistant clinical isolata of Pseudomonas aeruginaso were divided into two categories: (i) isolates that were moderately resistant to imipenem (MIC 6·25 mg/L) that produced trace amounts of protein D2 detected with immunoblotting using anti-protein D2 antibody, but not when stained with Coomassie blue and had inducible class 1 β-lactamase expression; (ii) isolates that were highly resistant to several β-lactamase, including meropenem, with no protein D2 by staining or immunoblotting and had stably derepressed β-lactamase. Laboratory strains were isolated and analyzed: (i) mutants lacking protein D2, or (ii) Lacking protein D2 and producing stably derepressed β-lactamase with carbapenem resistance similar to the clinical isolates. (iii) mutants producing undetectable β-lactamase which were four-fold more susceptible to imipenem than the mutant producing stably derepressed β-lactamase or the strain with inducible β-lactamase. These data suggests that β-lactamase and outer membrane permeability govern meropenem-resistance in P. aeruginosa