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<p>Aztreonam-avibactam (ATM-AVI) is one of the few remaining therapeutic options for infections caused by metallo-β-lactamase (MBL)-producing Enterobacterales, yet resistance is increasingly reported. Alternative strategies are therefore critically needed. We investigated the in vitro activity of aztreonam in combination with three marketed β-lactamase inhibitors (avibactam, vaborbactam, relebactam) against 48 well-characterized ATM-resistant MBL-producing <i>Escherichia coli</i>, including 34 ATM-AVI-resistant isolates. Among ATM-AVI-susceptible isolates, ATM-relebactam and ATM-vaborbactam showed reduced activity compared with ATM-AVI (MIC<sub>50/90</sub> 1/4&#xa0;mg/L), with MIC<sub>50/90</sub> values of 8/64&#xa0;mg/L and 64/256&#xa0;mg/L, respectively. Among ATM-AVI-resistant isolates, none of the combinations restored aztreonam susceptibility. CMY-type enzymes seem to play a pivotal role in the failure of both relebactam and vaborbactam to restore aztreonam susceptibility in our collection of isolates.</p>

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In vitro activity of β-lactamase inhibitors avibactam, relebactam and vaborbactam in combination with aztreonam against metallo-β-lactamase producing Escherichia coli clinical isolates

  • 期刊论文

  • 发表日期：

    2026年6月23日

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  • Clément Viguier,
  • Samanta Freire,
  • Maxime Bouvier,
  • Christophe Le Terrier,
  • Laurent Poirel,
  • A. Westers,
  • M. Imperiali,
  • L. Pozzi,
  • D. Balzari,
  • G. Vaninetti,
  • C. Cirillo,
  • V. Gaia,
  • E. Pianezzi,
  • G. Martinetti Lucchini,
  • F. Baggi Menozzi,
  • A. Jayol,
  • C. Guyon,
  • D. Hyden,
  • M. Maitrejean,
  • V. Deggi-Messmer,
  • D. Bandeira,
  • C. Fournier,
  • S. Pfister,
  • C. Nusbaumer,
  • L. Bertaiola Monnerat,
  • J. Schrenzel,
  • G. Renzi,
  • A. Cherkaoui,
  • D. Andrey,
  • S. Emonet,
  • M. Eyer,
  • R. Maret,
  • A. Belo,
  • D. Mabillard,
  • M. Moraz,
  • K. Herzog,
  • V. Gisler,
  • M. Oberle,
  • C. Castelberg,
  • H. Fankhauser,
  • S. Graf,
  • N. Dubey,
  • C. Guler,
  • M. Schoenenberger,
  • U. Karrer,
  • F. Piran,
  • C. Andreutti,
  • M. Dessauges,
  • T. Schmid,
  • B. Suterbuser,
  • I. Mitrovic,
  • V. Bruderer,
  • P. Staehli,
  • B. Schnell,
  • C. O. Marti,
  • I. Steffen,
  • A. Imhof,
  • B. Preiswerk,
  • V. Dilorenzo,
  • C. Payen,
  • D. Boschung,
  • L. Comte,
  • M. Schacher,
  • M. Brandenberger,
  • C. Zowa,
  • C. Zehnder,
  • M. Mathis,
  • L. Basilico,
  • G. Togni,
  • P. Minkova,
  • Y. Born,
  • M. Kuegler,
  • V. Povolo,
  • S. Droz,
  • M. Elzi,
  • C. Casanova,
  • C. Lang,
  • A. Blaich,
  • S. Schmid,
  • B. Ivan,
  • S. Mancini,
  • O. Dubois,
  • K. Narr,
  • S. Schoch,
  • S. Ellenberger,
  • S. Seiffert,
  • Patrice Nordmann

摘要

Aztreonam-avibactam (ATM-AVI) is one of the few remaining therapeutic options for infections caused by metallo-β-lactamase (MBL)-producing Enterobacterales, yet resistance is increasingly reported. Alternative strategies are therefore critically needed. We investigated the in vitro activity of aztreonam in combination with three marketed β-lactamase inhibitors (avibactam, vaborbactam, relebactam) against 48 well-characterized ATM-resistant MBL-producing Escherichia coli, including 34 ATM-AVI-resistant isolates. Among ATM-AVI-susceptible isolates, ATM-relebactam and ATM-vaborbactam showed reduced activity compared with ATM-AVI (MIC50/90 1/4 mg/L), with MIC50/90 values of 8/64 mg/L and 64/256 mg/L, respectively. Among ATM-AVI-resistant isolates, none of the combinations restored aztreonam susceptibility. CMY-type enzymes seem to play a pivotal role in the failure of both relebactam and vaborbactam to restore aztreonam susceptibility in our collection of isolates.