caa a22 4500 397593422 CHVBK 20180308164945.0 cr unu---uuuuu 161202e199605 xx s 000 0 eng 10.1093/jac/37.5.931 doi (NATIONALLICENCE)oxford-10.1093/jac/37.5.931 In-vitro susceptibility of Klebsiella oxytoca strains to 13 β-lactams in the presence and absence of β-lactamase inhibitors [Elektronische Daten] [Bénédicte Fournier, Philippe H. Lagrange, Alain Philippon] The susceptibility of Klebsiella oxytoca isolates was tested by an agar diffusion method (167 strains collected in six countries) and an agar dilution method (38 strains). Multivariate analysis of inhibition zone diameters by principal component analysis clearly individualised four susceptibility patterns, including the phenotype of strains overproducing β-lactamase and resistant to penicillins, first-generation cephalosporins, cefuroxime and aztreonam, but susceptible to ceftazidime. This phenotype was different from that conferred by plasmid-mediated extended-spectrum β-lactamases; strains expressing these enzymes were also resistant to ceftazidime and cefotaxime. The blaoxy gene from K. oxytoca was introduced into Escherichia coli and K. oxytoca recipients and conferred increased resistance to β-lactams in the recipient cells. Clavulanic acid was effective in association with piperacillin (MIC decreased 36-fold), ceftriaxone (35-fold) and aztreonam (19-fold) against overproducing strains, in spite of a relatively high IC50 (0.3 μm). Sulbactam (IC50, 400 μm) was ineffective in this context when combined with piperacillin (MIC decreased 1.5-fold), ceftriaxone (1.6-fold) and aztreonam (1.6-fold). The inhibitory activity of tazobactam (IC50, 8.2 μm) was heterogeneous depending on the strain and the β-lactam with which it was combined. When combined with piperacillin or ceftriaxone little potentiation in antibiotic activity occurred (MIC decreased 3.9-fold and 4.5-fold, respectively); however, tazobactam plus aztreonam resulted in a 50-fold decrease in MIC of antibiotic. © 1996 The British Society for Antimicrobial Chemotherapy Original articles nationallicence Fournier Bénédicte Laboratoire de Microbiologie, Höpital Saint-Louis (Université Paris VII), 75010 Paris, France aut Lagrange Philippe H. Laboratoire de Microbiologie, Höpital Saint-Louis (Université Paris VII), 75010 Paris, France aut Philippon Alain Laboratoire de Microbiologie, Höpital Saint-Louis (Université Paris VII), 75010 Paris, France aut Journal of Antimicrobial Chemotherapy Oxford University Press 37/5(1996-05), 931-942 0305-7453 37:5<931 1996 37 jac https://doi.org/10.1093/jac/37.5.931 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1093/jac/37.5.931 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Fournier Bénédicte Laboratoire de Microbiologie, Höpital Saint-Louis (Université Paris VII), 75010 Paris, France aut NATIONALLICENCE 700 1- Lagrange Philippe H. Laboratoire de Microbiologie, Höpital Saint-Louis (Université Paris VII), 75010 Paris, France aut NATIONALLICENCE 700 1- Philippon Alain Laboratoire de Microbiologie, Höpital Saint-Louis (Université Paris VII), 75010 Paris, France aut NATIONALLICENCE 773 0- Journal of Antimicrobial Chemotherapy Oxford University Press 37/5(1996-05), 931-942 0305-7453 37:5<931 1996 37 jac Metadata rights reserved CC BY-NC-4.0 http://creativecommons.org/licenses/by-nc/4.0 nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-oxford