Emergence of a carbapenem-resistant atypical uropathogenic Escherichia coli clone as an increasing cause of urinary tract infection
- Lachlan L. Walker
- Minh-Duy Phan
- Budi Permana
- Zheng Jie Lian
- Nguyen Thi Khanh Nhu
- Thom Cuddihy
- Kate M. Peters
- Kay A. Ramsay
- Chelsea Stewart
- Niels Pfennigwerth
- Timothy J. Kidd
- Patrick N. A. Harris
- David L. Paterson
- Matthew J. Sweet
- Brian M. Forde
- Mark A. Schembri
2025-09-02
Carbapenem-resistant Enterobacterales pose a critical global health threat, exemplified by increasing resistance of uropathogenic E. coli (UPEC) that cause urinary tract infections (UTIs). Here, we investigate the publicly available EnteroBase dataset and identify a signal of increasing UTI caused by phylogroup A E. coli sequence type 167 (ST167). Phylogenetic analysis of ST167 based on whole genome sequence data reveal three major clades (A, B, C), with clade C further resolving into several subclades, notably subclade C2 that possessed high carriage rates of carbapenem and cephalosporin resistance genes. Hierarchical clustering of core genome multi-locus sequence typing reveals ~77% of subclade C2 strains contain <20 allelic differences in 2,513 core genes and harbour two distinct group 1 capsule types, KL124 and KL30, likely originating from Klebsiella . Subclade C2 was predominantly sequenced in North America, and we provide evidence for clonal expansion since 2016. Analysis of UPEC virulence factors reveals complete loss of the type 1 fimbriae genes in strains from clades B and C. Two subclade C2 isolates exhibit significantly reduced capacity to colonise the bladder compared to the reference UPEC strain CFT073 in a murine UTI model. Collectively, our data identifies ST167 as an atypical UPEC clone associated with UTI.