Affiliations 

  • 1 School of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, 4072, Queensland, Australia
  • 2 Division of Microbiology and Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, 84132, UT, USA
  • 3 Genitourinary Injury and Reconstructive Urology, Department of Surgery, University of Utah, Salt Lake City, 84132, UT, USA
  • 4 ARUP Laboratories and Department of Pathology, University of Utah, Salt Lake City, 84112, UT, USA
  • 5 Division of Genetics and Molecular Biology, Institute of Biological Sciences, Faculty of Science, University of Malaya, Kuala Lumpur, 50603, Malaysia
  • 6 School of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, 4072, Queensland, Australia. m.schembri@uq.edu.au
  • 7 Division of Microbiology and Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, 84132, UT, USA. mulvey@path.utah.edu
  • 8 School of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, 4072, Queensland, Australia. s.beatson@uq.edu.au
Nat Commun, 2019 08 13;10(1):3643.
PMID: 31409795 DOI: 10.1038/s41467-019-11571-5

Abstract

Recurrent urinary tract infections (rUTIs) are extremely common, with ~ 25% of all women experiencing a recurrence within 1 year of their original infection. Escherichia coli ST131 is a globally dominant multidrug resistant clone associated with high rates of rUTI. Here, we show the dynamics of an ST131 population over a 5-year period from one elderly woman with rUTI since the 1970s. Using whole genome sequencing, we identify an indigenous clonal lineage (P1A) linked to rUTI and persistence in the fecal flora, providing compelling evidence of an intestinal reservoir of rUTI. We also show that the P1A lineage possesses substantial plasmid diversity, resulting in the coexistence of antibiotic resistant and sensitive intestinal isolates despite frequent treatment. Our longitudinal study provides a unique comprehensive genomic analysis of a clonal lineage within a single individual and suggests a population-wide resistance mechanism enabling rapid adaptation to fluctuating antibiotic exposure.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.