# Genomic insights into multidrug resistance in clinical Escherichia albertii: plasmid coexistence, intI1 prevalence, and interspecies dissemination risk

## TL;DR

This study explores how Escherichia albertii becomes resistant to multiple drugs, revealing the role of plasmids and genetic elements in spreading resistance.

## Contribution

The study identifies coexisting plasmids and the role of intI1 in multidrug resistance and interspecies dissemination in E. albertii.

## Key findings

- Five plasmids coexist in E. albertii ESA311, with some carrying resistance genes for seven antibiotic classes.
- Conjugation experiments showed stable co-transfer of plasmids, promoting resistance and virulence co-selection.
- intI1 was found in 19.8% of clinical isolates and strongly linked to multidrug resistance.

## Abstract

Escherichia albertii (E. albertii) is an emerging foodborne pathogen of growing clinical significance and increasing multidrug resistance (MDR). This study characterized the multidrug-resistant clinical strain E. albertii ESA311 to uncover the genetic basis of its resistance and the transmission potential of its mobile genetic elements.

We performed whole-genome sequencing on strain ESA311 to identify plasmids, resistance genes, and virulence factors. Conjugation experiments were conducted to evaluate plasmid transferability. Phylogenetic analysis of the MDR plasmids elucidated their evolutionary history and geographical distribution. The prevalence of intI1 and its correlation with MDR were analyzed across 160 clinical E. albertii isolates.

Whole-genome sequencing identified five plasmids coexisting in ESA311, with pESA311_1 and pESA311_2 harboring diverse antimicrobial resistance genes (ARGs) conferring resistance to seven antibiotic classes, facilitated by mobile genetic elements including insertion sequences (ISs) and a class 1 integron (intI1). Conjugation assays revealed a stable co-transfer consortium of pESA311_1, pESA311_2, and pESA311_5, driving concurrent dissemination of multidrug resistance and virulence (sporadically co-mobilize of pESA311_4) and posing a co-selection risk. Further phylogenetic analysis identified homologous plasmids in other species, such as Salmonella enterica and Escherichia coli. Whereas the pESA311_1 lineage is largely restricted to China, pESA311_2 homologs have dispersed more broadly across different regions. In a broader surveillance of 160 clinical E. albertii isolates, intI1 prevalence was 19.8% and strongly correlated with MDR.

Our findings establish plasmids and intI1 as pivotal drivers of MDR in E. albertii, and highlight the associated risks of resistance-virulence co-selection and interspecies plasmid dissemination.