Springer Online Journal Archives 1860-2000
Abstract The contribution of induction and stable derepression of chromosomal class I β-lactamases to β-lactam antibiotic resistance was studied in clinical isolates ofPseudomonas aeruginosa collected from patients treated with β-lactam antibiotics. Multiple isolates from the same patient were characterized by O-serotyping as a primary screen, combined with pyocin typing. Sonicated extracts of cells were assayed for chromosomal and plasmid-mediated β-lactamases by isoelectric focusing and cloxacillin inhibition studies. The specific β-lactamase activity, basal and induced, with cefoxitin was determined to differentiate strains with inducible or derepressed production of the enzyme. Beta-lactamase induction was performed in each strain against the β-lactam agents used in the therapy of each patient. The observations showed that induction against older penicillins such as penicillin, amoxicillin, and amoxicillin/clavulanate resulted in a moderate to strong increase in β-lactamase activity, whereas the results obtained with first-generation cephalosporins varied with the β-lactam agent tested. Third-generation cephalosporins were weak inducers of β-lactamases, and their use as therapy preceded the appearance of strains that produce chromosomal group I β-lactamases constitutively. These strains showed a remarkable reduction in sensitivity to ureidopenicillins, carboxipenicillins, third-generation cephalosporins, and monobactams, but not to carbapenems.
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