Summary
A bioRxiv preprint analysing 20,331 E. coli genomes identifies ST361 as an emerging carbapenem-resistant clone associated with urinary tract infection. The researchers also link its common surface-polysaccharide type to virulence in mouse infection models.
A bioRxiv preprint reports that Escherichia coli sequence type 361 (ST361) is an emerging carbapenem-resistant clone associated with urinary tract infections (UTIs). The researchers analysed 20,331 E. coli genomes from UTI and urine samples, and linked the clone’s expansion to a common surface-polysaccharide type and the spread of the resistance gene blaNDM-5.
How ST361 spread and resists carbapenems
Phylogenetic and phylodynamic analyses identified two dominant ST361 clades. The authors estimate that they emerged in Asia around 2006 and later spread between continents. ST361 belongs to phylogroup A, one of the major genetic groupings of E. coli.
The preprint describes ST361 as near pan-drug resistant and identifies blaNDM-5 as conferring carbapenem resistance. Carbapenems are an important class of antibiotics used to treat bacterial infections. The researchers also examined mobile genetic elements carrying blaNDM-5 in ST361 and other carbapenem-resistant E. coli. Their analysis points to plasmid transfer and insertion elements as contributors to the gene’s dissemination. This suggests that the spread of resistance involves both the expansion of a bacterial lineage and movement of genetic material.
A shared surface type linked to virulence in mice
Capsules and O antigens are carbohydrate structures on bacterial surfaces; their composition helps define bacterial serotypes. In silico typing found a highly conserved, Klebsiella-like surface-polysaccharide serotype in 95.9% of ST361 genomes. The researchers report that this surface architecture contributes to virulence in mouse models of UTI and catheter-associated UTI.
The findings connect three features of ST361: its growth as a UTI-associated clone, a common surface type, and mobile genetic elements linked to carbapenem resistance. The mouse experiments support a role for the surface polysaccharides in infection in those models; the work is a preprint, and its virulence evidence comes from animals rather than clinical-outcome studies in people.