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Piperacillin/tazobactam resistance in a clinical isolate of Escherichia coli due to IS26-mediated amplification of blaTEM-1B

Author

Listed:
  • Alasdair T. M. Hubbard

    (Liverpool School of Tropical Medicine, Pembroke Place)

  • Jenifer Mason

    (Liverpool University Hospital Foundation Trust)

  • Paul Roberts

    (Liverpool University Hospital Foundation Trust
    University of Wolverhampton, Wulfruna Building MA)

  • Christopher M. Parry

    (Alder Hey Children’s NHS Foundation Trust
    University of Liverpool
    Clinical Sciences, Liverpool School of Tropical Medicine, Pembroke Place
    University of Nagasaki)

  • Caroline Corless

    (Liverpool University Hospital Foundation Trust)

  • Jon Aartsen

    (Liverpool University Hospital Foundation Trust)

  • Alex Howard

    (Liverpool University Hospital Foundation Trust)

  • Issra Bulgasim

    (Liverpool School of Tropical Medicine, Pembroke Place)

  • Alice J. Fraser

    (Liverpool School of Tropical Medicine, Pembroke Place)

  • Emily R. Adams

    (Liverpool School of Tropical Medicine, Pembroke Place)

  • Adam P. Roberts

    (Liverpool School of Tropical Medicine, Pembroke Place)

  • Thomas Edwards

    (Liverpool School of Tropical Medicine, Pembroke Place)

Abstract

A phenotype of Escherichia coli and Klebsiella pneumoniae, resistant to piperacillin/tazobactam (TZP) but susceptible to carbapenems and 3rd generation cephalosporins, has emerged. The resistance mechanism associated with this phenotype has been identified as hyperproduction of the β-lactamase TEM. However, the mechanism of hyperproduction due to gene amplification is not well understood. Here, we report a mechanism of gene amplification due to a translocatable unit (TU) excising from an IS26-flanked pseudo-compound transposon, PTn6762, which harbours blaTEM-1B. The TU re-inserts into the chromosome adjacent to IS26 and forms a tandem array of TUs, which increases the copy number of blaTEM-1B, leading to TEM-1B hyperproduction and TZP resistance. Despite a significant increase in blaTEM-1B copy number, the TZP-resistant isolate does not incur a fitness cost compared to the TZP-susceptible ancestor. This mechanism of amplification of blaTEM-1B is an important consideration when using genomic data to predict susceptibility to TZP.

Suggested Citation

  • Alasdair T. M. Hubbard & Jenifer Mason & Paul Roberts & Christopher M. Parry & Caroline Corless & Jon Aartsen & Alex Howard & Issra Bulgasim & Alice J. Fraser & Emily R. Adams & Adam P. Roberts & Thom, 2020. "Piperacillin/tazobactam resistance in a clinical isolate of Escherichia coli due to IS26-mediated amplification of blaTEM-1B," Nature Communications, Nature, vol. 11(1), pages 1-9, December.
    • Handle: RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-18668-2
    DOI: 10.1038/s41467-020-18668-2
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