Imipenem-rcsistant clinical isolates of Pseudomonas aeruginosa 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 immuneblotting using anti-protein D2 antibody, but not when stained with Coomassie blue and had inducible class 1 /f-lactamase expression; (ii) isolates that were highly resistant to several /Mactams, including meropenem, with no protein D2 by staining or immunoblotting and had stably derepressed /Mactamase. Laboratory strains were isolated and analyzed: (i) mutants lacking protein D2, or (ii) lacking protein D2 and producing stably derepressed /J-lactamase with carbapenem resistance similar to the clinical isolates, (iii) mutants producing undetectable 0-lactamasc which were fourfold more susceptible to imipenem than the mutant producing stably derepressed /J-lactamase or the strain with inducible /J-lactamase. These data suggests that /Mactamase and outer membrane permeability govern meropenem-resistance in P. aeruginosa
