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45. Pseudomonas aeruginosa : résistance et options thérapeutiques à l'aube du troisième millénaire

Author

Mesaros, N., Nordmann, P., Plésiat, P., Roussel-Delvallez, M., Van Eldere, J., Glupczynski, Y., Van Laethem, Y., Jacobs, F., Lebecque, P., Malfroot, A., Tulkens, P.M., Van Bambeke, F., Humbert, Murielle, Agents pathogènes et inflammation - UFC (EA 4266) (API), Université de Franche-Comté (UFC), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC), Unité de Pharmacologie cellulaire et moléculaire, and Université Catholique de Louvain = Catholic University of Louvain (UCL)

Subjects
[SDV.MP.BAC] Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, [SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, ComputingMilieux_MISCELLANEOUS
Abstract

National audience

Published
2007

47. Pharmacodynamics of ceftazidime/avibactam against extracellular and intracellular forms of Pseudomonas aeruginosa.

Author

Buyck, J. M., Luyckx, C., Muccioli, G. G., Krause, K. M., Nichols, W. W., Tulkens, P. M., and Van Bambeke, F.

Subjects
PHARMACODYNAMICS, PSEUDOMONAS aeruginosa, BETA lactamases, PHAGOCYTOSIS, EXTRACELLULAR enzymes, ANTIBIOTICS, CYTOPLASM, DYNAMICS, ENZYME inhibitors, MASS spectrometry, MICROBIAL sensitivity tests, ORGANIC compounds, PSEUDOMONAS, CEFTAZIDIME, MONONUCLEAR leukocytes
Abstract

Objectives: When tested in broth, avibactam reverses ceftazidime resistance in many Pseudomonas aeruginosa that express ESBLs. We examined whether similar reversal is observed against intracellular forms of P. aeruginosa .Methods: Strains: reference strains; two engineered strains with basal non-inducible expression of AmpC and their isogenic mutants with stably derepressed AmpC; and clinical isolates with complete, partial or no resistance to reversion with avibactam. Pharmacodynamic model: 24 h concentration-response to ceftazidime [0.01-200 mg/L alone or with avibactam (4 mg/L)] of bacteria in broth or bacteria phagocytosed by THP-1 monocytes, with calculation of ceftazidime relative potency ( C s : concentration yielding a static effect) and maximal relative effect [ E max : cfu decrease at infinitely large antibiotic concentrations (efficacy in the model)] using the Hill equation. Cellular content of avibactam: quantification by LC-MS/MS.Results: For both extracellular and intracellular bacteria, ceftazidime C s was always close to its MIC. For ceftazidime-resistant strains, avibactam addition shifted ceftazidime C s to values close to the MIC of the combination in broth. E max was systematically below the detection limit (-5 log 10 ) for extracellular bacteria, but limited to -1.3 log 10 for intracellular bacteria (except for two isolates) with no effect of avibactam. The cellular concentration of avibactam reflected extracellular concentration and was not influenced by ceftazidime (0-160 mg/L).Conclusions: The potential for avibactam to inhibit β-lactamases does not differ for extracellular and intracellular forms of P. aeruginosa , denoting an unhindered access to its target in both situations. The loss of maximal relative efficacy of ceftazidime against intracellular P. aeruginosa was unrelated to resistance via avibactam-inhibitable β-lactamases. [ABSTRACT FROM AUTHOR]

Published
2017
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