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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 IS 26 -flanked pseudo-compound transposon, PTn 6762 , which harbours  bla  TEM-1B . The TU re-inserts into the chromosome adjacent to IS 26  and forms a tandem array of TUs, which increases the copy number of  bla  TEM-1B,  leading to TEM-1B hyperproduction and TZP resistance. Despite a significant increase in  bla  TEM-1B  copy number, the TZP-resistant isolate does not incur a fitness cost compared to the TZP-susceptible ancestor. This mechanism of amplification of  bla  TEM-1B  is an important consideration when using genomic data to predict susceptibility to TZP.

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