Different mechanisms of TEM-1 and Oxa-1 mediated resistance to piperacillin in E. coli.

Clinical isolates of Oxa-1 and TEM-1 producing strains of E. coli were studied. Susceptibility to piperacillin was determined by the agar and broth dilution procedure, and beta-lactam hydrolysis rates measured by the iodometric method. The beta-lactamases were identified by isoelectric focusing. Our data on TEM-1 producing strains showed a statistically significant correlation between the MIC, if determined by the agar dilution test, and the specific beta-lactamase activity. The majority of Oxa-1 producing E. coli was resistant to piperacillin although the inactivation rate of piperacillin was usually low. Cell wall permeability of TEM-1 producing strains of E. coli to piperacillin was below the lower limit of detectability, but preincubation of the E. coli strains in piperacillin containing broth led to increased cell wall permeability. Bactericidal kinetics of an Oxa-1 and TEM-1 E. coli were studied. It revealed that regrowth of the Oxa-1 strain in piperacillin containing broth was associated with a 25% decrease of piperacillin concentrations without the formation of degradation products, suggesting binding of piperacillin to bacterial cells. The TEM-1 plasmid bearing strain inactivated piperacillin, and the degradation products (penicilloate) could be detected.