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Ceftazidime is the antibiotic of choice for treatment of Burkholderia pseudomallei infections (melioidosis). The chromosomally encoded PenA β-lactamase possesses weak cephalosporinase activity. The wild-type penA gene confers clinically significant ceftazidime resistance only when overexpressed due to a promoter mutation, transcriptional anti-termination or by gene duplication and amplification (GDA). Here we characterize a reversible 33-kb GDA event involving wild-type penA in a ceftazidime resistant clinical isolate from Thailand. We show that duplication arises from exchanges between short (<10 base pairs, bp) chromosomal sequences, which in this example consist of 4 bp repeats flanked by 3 bp inverted repeats. GDA involving β-lactamase may be a common ceftazidime resistance mechanism in B. pseudomallei.

Original publication

DOI

10.1016/j.ijantimicag.2019.01.003

Type

Journal article

Journal

International journal of antimicrobial agents

Publication Date

09/01/2019

Addresses

Department of Molecular Genetics and Microbiology, College of Medicine, Emerging Pathogens Institute, Institute for Therapeutic Innovation, University of Florida, Gainesville, FL, USA.