The Genomic Epidemiology of Clinical <i>Burkholderia pseudomallei</i> Isolates in North Queensland, Australia
Ian Gassiep,
Mark D. Chatfield,
Budi Permana,
Delaney Burnard,
Michelle J. Bauer,
Thom Cuddihy,
Brian M. Forde,
Johanna Mayer-Coverdale,
Robert E. Norton,
Patrick N. A. Harris
Affiliations
Ian Gassiep
UQ Centre for Clinical Research, Faculty of Medicine, The University of Queensland, Royal Brisbane and Women’s Hospital Campus, Herston, Brisbane, QLD 4029, Australia
Mark D. Chatfield
UQ Centre for Clinical Research, Faculty of Medicine, The University of Queensland, Royal Brisbane and Women’s Hospital Campus, Herston, Brisbane, QLD 4029, Australia
Budi Permana
UQ Centre for Clinical Research, Faculty of Medicine, The University of Queensland, Royal Brisbane and Women’s Hospital Campus, Herston, Brisbane, QLD 4029, Australia
Delaney Burnard
Queensland Cyber Infrastructure Foundation, Brisbane, QLD 4067, Australia
Michelle J. Bauer
UQ Centre for Clinical Research, Faculty of Medicine, The University of Queensland, Royal Brisbane and Women’s Hospital Campus, Herston, Brisbane, QLD 4029, Australia
Thom Cuddihy
Institute for Molecular Bioscience (IMB), The University of Queensland, Brisbane, QLD 4067, Australia
Brian M. Forde
UQ Centre for Clinical Research, Faculty of Medicine, The University of Queensland, Royal Brisbane and Women’s Hospital Campus, Herston, Brisbane, QLD 4029, Australia
Johanna Mayer-Coverdale
UQ Centre for Clinical Research, Faculty of Medicine, The University of Queensland, Royal Brisbane and Women’s Hospital Campus, Herston, Brisbane, QLD 4029, Australia
Robert E. Norton
Pathology Queensland, Townsville University Hospital, Townsville, QLD 4814, Australia
Patrick N. A. Harris
UQ Centre for Clinical Research, Faculty of Medicine, The University of Queensland, Royal Brisbane and Women’s Hospital Campus, Herston, Brisbane, QLD 4029, Australia
Background: Burkholderia pseudomallei, the causative agent of melioidosis, is highly genetically recombinant, resulting in significant genomic diversity. Multiple virulence factors have been associated with specific disease presentations. To date, there are limited data relating to genomic diversity and virulence factors associated with melioidosis cases in North Queensland, Australia. Aim: To describe the genetic diversity of B. pseudomallei and identify virulence factors associated with clinical risk factors and patient outcomes. Methods: Whole genome sequencing of clinical isolates was performed and analysed with clinical data obtained from a retrospective melioidosis cohort study. Results: Fifty-nine distinct sequence types (STs) were identified from the 128 clinical isolates. Six STs comprised 64/128 (50%) isolates. Novel STs accounted for 38/59 (64%) STs, with ST TSV-13 as the most prevalent (n = 7), and were less likely to possess an LPS A genotype or YLF gene cluster (p p = 0.001). ST TSV-13 was associated with increased mortality (aOR: 6.1, 95% CI: 1.2–30.9, p = 0.03). Patients with a history of alcohol excess were less likely to be infected by fhaB3 (aOR 0.2, 95% CI: 0.1–0.7, p = 0.01) or YLF (aOR: 0.4, 95% CI: 0.2–0.9, p = 0.04) positive isolates. Conclusions: There are a significant number of novel sequence types in Townsville, Australia. An emerging novel ST appears to have an association with geographic location and mortality. Ongoing investigation is required to further understand the impact of this ST on the Townsville region.
