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Exposure of inducible plasmid-mediated AmpC beta-lactamase-producing Klebsiella pneumoniae to cephalosporins and aztreonam leads to increased beta-lactam resistance



Exposure of inducible plasmid-mediated AmpC beta-lactamase-producing Klebsiella pneumoniae to cephalosporins and aztreonam leads to increased beta-lactam resistance



Abstracts of the Interscience Conference on Antimicrobial Agents & Chemotherapy 42: 82



Background: Enterobacteriaceae that acquire plasmid-mediated AmpC beta-lactamases (pAmpCs) may be susceptible to 3rd generation cephs (3GCs) and ATM. It is unknown if therapy with these agents will select resistance. An in vitro study was designed to determine if resistance to 3GCs, ATM and other agents could develop in pAmpC-producing strains of KP after exposure to beta-lactam antibiotics. Methods: Two strains of KP were used. One produced the inducible pAmpC (ipAmpC), DHA-1. The other produced an ACT-1 like ipAmpC. Both strains were susceptible to imipenem (IPM), cefepime (FEP), cefotaxime (CTX), and ceftriaxone (CRO), and either susceptible or intermediate to ATM. Both were exposed to increasing concentrations of CTX, FEP, ATM, and IPM by a gradient plate method. Resulting mutants were tested by NCCLS agar dilution methodology for susceptibility to the above beta-lactam agents and to piperacillin/tazobactam (P/T), ciprofloxacin (CIP), amikacin, and chloramphenicol (CHL). Results: ATM and CTX selected mutants from both strains for which MICs of ATM and 3GCs increased from ltoreq16 to gtoreq128 mug/ml, while MICs of IPM and FEP remained in the susceptible range. FEP selected a similar type of mutant from 1 of the 2 strains. Unlike CTX, FEP and ATM, IPM did not select beta-lactam resistance, but instead selected a mutant from the DHA-1-producing strain that was more resistant to CHL, and mutants from the strain producing the ACT-1-like enzyme that were more susceptible to CIP, P/T, and CHL. Conclusions: These data indicate that IpAmpC-producing strains of KP have the capability to develop broad beta-lactam resistance when exposed to cephs or ATM. The changes in susceptibility to non-beta-lactam agents of the IPM-selected mutants suggest involvement of different resistance mechanisms. These findings may provide insights into the types of resistance that may emerge during therapy of infections caused by pathogens that produce ipAmpCs.

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Accession: 034900829

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