Comparison of the β-lactamase stability and the in-vitro activity of cefoperazone, cefotaxime, cefsulodin, ceftazidime, moxalactam and ceftriaxone against Pseudomonas aeruginosa

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Abstract
One hundred clinical isolates of Pseudomonas aeruginosa were tested for susceptibility to β-lactam antibiotics carbenicillin, cefotaxime, moxalactam, ceftriaxone, cefoperazone, cefsulodin and ceftazidime. Mode MICs were found to be 64, 16, 8, 4, 2, 2, 8 and 1 mg/l, respectively. Strains showing resistance to some or all these agents were selected for further study. Two mechanisms of resistance were detected: enzymic and intrinsic. Of the enzymes detected, the universally present Id β-lactamase was unimportant in resistance to any of these compounds. Plasmid-mediated TEM and PSE type β-lactamases did, however, confer resistance to carbenicillin, cefoperazone and cefsulodin but none of the other compounds. This resistance generally correlated with the substrate range of these enzymes. Resistance arose more frequently from intrinsic factors: probably alterations in cell permeability. Unlike enzyme-mediated resistance this mechanism decreased sensitivity to all the β-lactams.