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Abstract

In Aotearoa New Zealand, urinary tract infections in humans are commonly caused by extended-spectrum beta-lactamase (ESBL)-producing . This group of antimicrobial-resistant bacteria are often multidrug resistant. However, there is limited information on ESBL-producing found in the environment and their link with human clinical isolates. In this study, we examined the genetic relationship between environmental and human clinical ESBL-producing and isolates collected in parallel within the same area over 14 months. Environmental samples were collected from treated effluent, stormwater and multiple locations along an Aotearoa New Zealand river. Treated effluent, stormwater and river water sourced downstream of the treated effluent outlet were the main samples that were positive for ESBL-producing (7/14 samples, 50.0%; 3/6 samples, 50%; and 15/28 samples, 54%, respectively). Whole-genome sequence comparison was carried out on 307 human clinical and 45 environmental ESBL-producing isolates. Sequence type 131 was dominant for both clinical (147/307, 47.9%) and environmental isolates (11/45, 24.4%). Only one ESBL gene was detected in each isolate. Among the clinical isolates, the most prevalent ESBL genes were (134/307, 43.6%) and (134/307, 43.6%). Among the environmental isolates, (28/45, 62.2%) was the most prevalent gene. A core SNP analysis of these isolates suggested that some strains were shared between humans and the local river. These results highlight the importance of understanding different transmission pathways for the spread of ESBL-producing .

Funding
This study was supported by the:
  • Hawkes Bay Research Medical Foundation (Award N/A)
    • Principle Award Recipient: SaraA Burgess
  • Palmerston North Medical Research Foundation (Award N/A)
    • Principle Award Recipient: SaraA Burgess
  • This is an open-access article distributed under the terms of the Creative Commons Attribution License. This article was made open access via a Publish and Read agreement between the Microbiology Society and the corresponding author’s institution.
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2025-01-10
2025-01-25
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