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Updated: Oct 14, 2025

Characterization of a Pathogenic Escherichia coli Strain Derived from Oreochromis spp. Farms Using Whole-Genome Sequencing
Published on: December 23, 2022
Genome structural variation in Escherichia coli O157:H7
Stephen F Fitzgerald1, Nadejda Lupolova1, Sharif Shaaban1
1Division of Infection and Immunity, The Roslin Institute and R(D)SVS, The University of Edinburgh, Easter Bush, Midlothian, EH25 9RG, UK.
Large-chromosomal rearrangements (LCRs) driven by prophage are a key source of genomic variation in Escherichia coli O157:H7. These rearrangements impact virulence factors and highlight the pathogen's adaptability.
Area of Science:
- Microbiology
- Genomics
- Pathogen Evolution
Background:
- Escherichia coli O157:H7 is a significant human zoonotic pathogen.
- Prophages within E. coli O157:H7 encode virulence factors like Shiga toxin and drive genomic instability.
- Large-chromosomal rearrangements (LCRs) are generated by prophage-mediated homologous recombination.
Purpose of the Study:
- To investigate the types and frequencies of LCRs across major E. coli O157:H7 lineages.
- To determine if LCRs are generated during laboratory culture and present in cattle.
- To assess the impact of LCRs on virulence gene expression and phenotypes.
Main Methods:
- Optical mapping
- Oxford Nanopore long-read sequencing
- RNA transcriptional profiling
- Phenotyping of structural variants
Main Results:
- LCRs are a major source of genomic variation in all E. coli O157:H7 lineages.
- LCRs are generated in vitro from single colonies and found in cattle.
- LCRs are concentrated near the genome terminus and flanked by homologous prophage sequences.
- LCRs influence Shiga-toxin production, type-3 secretion, and motility.
Conclusions:
- Prophage activity continually generates structural genome variants in E. coli O157:H7.
- Prophage-mediated genome plasticity is crucial for pathogen adaptability.
- This genomic contingency raises questions about E. coli O157:H7 evolution and adaptation strategies.
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