Sunisa ChirakulNawarat SomprasongMichael H. NorrisVanaporn WuthiekanunNarisara ChantratitaApichai TuanyokHerbert P. SchweizerUniversity of FloridaMahidol University2020-01-272020-01-272019-05-01International Journal of Antimicrobial Agents. Vol.53, No.5 (2019), 582-58818727913092485792-s2.0-85061932818https://repository.li.mahidol.ac.th/handle/20.500.14594/51672© 2019 Elsevier Ltd Ceftazidime (CAZ) is the antibiotic of choice for the treatment of Burkholderia pseudomallei infection (melioidosis). The chromosomally-encoded PenA β-lactamase possesses weak cephalosporinase activity. The wild-type penA gene confers clinically significant CAZ resistance only when overexpressed due to a promoter mutation, transcriptional antitermination or by gene duplication and amplification (GDA). Here we characterise a reversible 33-kb GDA event involving wild-type penA in a CAZ-resistant B. pseudomallei clinical isolate from Thailand. We show that duplication arises from exchanges between short (<10 bp) chromosomal sequences, which in this example consist of 4-bp repeats flanked by 3-bp inverted repeats. GDA involving β-lactamases may be a common CAZ resistance mechanism in B. pseudomallei.Mahidol UniversityMedicineBurkholderia pseudomallei acquired ceftazidime resistance due to gene duplication and amplificationArticleSCOPUS10.1016/j.ijantimicag.2019.01.003