Dominance of Escherichia coli sequence types ST73, ST95, ST127 and ST131 in Australian urine isolates: a genomic analysis of antimicrobial resistance and virulence linked to F plasmids

• DOI: 10.1099/mgen.0.001068
• Publication Date: 2023-07-20T16:19:06Z
• Authors: Dmitriy Li; Paarthiphan Elank...; Timothy Kudinha; Amanda K. Kidsley; Darren J. Trott; Veronica Maria Ja...; Steven Philip Djo...
• Keywords: 0301 basic medicine; Genotype; Extraintestinal Pathogenic Escherichia coli; Drug Resistance; 610; UTIs; F Factor; 03 medical and health sciences; Drug Resistance, Bacterial; Escherichia coli; Animals; antimicrobial resistance; Research Articles; Escherichia coli Infections; ExPEC; Virulence; Bacterial; Australia; senB; Genomics; F plasmids; pUTI89; Anti-Bacterial Agents; Urinary Tract Infections

Extraintestinal pathogenic

Escherichia coli

(ExPEC) are the most frequent cause of urinary tract infections (UTIs) globally. Most studies of clinical

E. coli

isolates are selected based on their antimicrobial resistance (AMR) phenotypes; however, this selection bias may not provide an accurate portrayal of which sequence types (STs) cause the most disease. Here, whole genome sequencing (WGS) was performed on 320

E. coli

isolates from urine samples sourced from a regional hospital in Australia in 2006. Most isolates (91%) were sourced from patients with UTIs and were not selected based on any AMR phenotypes. No significant differences were observed in AMR and virulence genes profiles across age sex, and uro-clinical syndromes. While 88 STs were identified, ST73, ST95, ST127 and ST131 dominated. F virulence plasmids carrying senB-cjrABC (126/231; 55%) virulence genes were a feature of this collection. These senB-cjrABC+ plasmids were split into two categories: pUTI89-like (F29:A-:B10 and/or >95 % identity to pUTI89) (n=73) and non-pUTI89-like (n=53). Compared to all other plasmid replicons, isolates with pUTI89-like plasmids carried fewer antibiotic resistance genes (ARGs), whilst isolates with senB-cjrABC+/non-pUTI89 plasmids had a significantly higher load of ARGs and class 1 integrons. F plasmids were not detected in 89 genomes, predominantly ST73. Our phylogenomic analyses identified closely related isolates from the same patient associated with different pathologies and evidence of strain-sharing events involving isolates sourced from companion and wild animals.