Abstract
Escherichia coli is one of the most prevalent pathogens, causing a variety of infections including bloodstream infections. At the same time, it can be found as a commensal, being part of the intestinal microflora. While it is widely accepted that pathogenic strains can evolve from colonizing E. coli strains, the evolutionary route facilitating the commensal-to-pathogen transition is complex and remains not fully understood. Identification of the underlying mechanisms and genetic changes remains challenging. To investigate the factors involved in the transition from intestinal commensal to invasive E. coli causing bloodstream infections, we compared E. coli isolated from blood culture to isolates from the rectal flora of the same individuals by whole genome sequencing to identify clonally related strains and potentially relevant virulence factors. in vitro invasion assays using a Caco- 2 cell intestinal epithelial barrier model and a gut organoid model were performed to compare clonally related E. coli. The experiments revealed a correlation between the presence of an IncFII plasmid carrying hha and the degree of invasiveness. In summary, we provide evidence for the role of an IncFII plasmid in the transition of colonization to invasion in clinical E. coli isolates.
Highlights
Escherichia coli is one of the major pathogens causing hospital-acquired and communityacquired infections such as pneumonia, urinary tract (UTI), and bloodstream infections (BSI) [1]
We identified five patients in the study period with bloodstream infections (BSIs) caused by E. coli (Eco_b) and a corresponding rectal isolate (Eco_r)
Phylogeny based on core genomes (3386 genes) indicated that in 4/5 (80%) of E. coli BSI cases, the rectal isolates were genetically closely related to the E. coli isolate from the blood culture (Figure 1a)
Summary
Escherichia coli is one of the major pathogens causing hospital-acquired and communityacquired infections such as pneumonia, urinary tract (UTI), and bloodstream infections (BSI) [1]. Several virulence factors influencing adhesion, invasion, and biofilm formation, as well as their regulatory networks, have been described for pathogenic E. coli These factors and their regulators, as well as antimicrobial resistance (AMR) genes, can be found on mobile genetic elements such as plasmids, which can be transferred via horizontal gene transfer (HGT) between different bacterial strains and species [3]. Hha is a small (8-kDa) protein, found among enteric bacteria, that enhances repression of a subset of H-NS (histone-like nucleoid structuring) regulated genes [4] This negative regulation of gene expression mostly applies to newly acquired sequences (e.g., via HGT) and might prevent potentially harmful effects of their uncontrolled expression [5]. Hha can be transferred via HGT along with the acquisition of AMR genes
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