Genome evolution and the emergence of pathogenicity in avian Escherichia coli

Leonardos Mageiros, Guillaume Méric, Sion C. Bayliss, Johan Pensar, Ben Pascoe, Evangelos Mourkas, Jessica K. Calland, Koji Yahara, Susan Murray, Thomas S. Wilkinson, Lisa K. Williams, Matthew D. Hitchings, Jonathan Porter, Kirsty Kemmett, Edward J. Feil, Keith A. Jolley, Nicola J. Williams, Jukka Corander and Samuel K. Sheppard ()
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Leonardos Mageiros: University of Bath, Claverton Down
Guillaume Méric: University of Bath, Claverton Down
Sion C. Bayliss: University of Bath, Claverton Down
Johan Pensar: University of Oslo
Ben Pascoe: University of Bath, Claverton Down
Evangelos Mourkas: University of Bath, Claverton Down
Jessica K. Calland: University of Bath, Claverton Down
Koji Yahara: National Institute of Infectious Diseases
Susan Murray: Uppsala University
Thomas S. Wilkinson: Institute of Life Science
Lisa K. Williams: Institute of Life Science
Matthew D. Hitchings: Institute of Life Science
Jonathan Porter: Environment Agency
Kirsty Kemmett: University of Liverpool, Leahurst Campus
Edward J. Feil: University of Bath, Claverton Down
Keith A. Jolley: South Parks Road
Nicola J. Williams: University of Liverpool, Leahurst Campus
Jukka Corander: University of Oslo
Samuel K. Sheppard: University of Bath, Claverton Down

Nature Communications, 2021, vol. 12, issue 1, 1-13

Abstract: Abstract Chickens are the most common birds on Earth and colibacillosis is among the most common diseases affecting them. This major threat to animal welfare and safe sustainable food production is difficult to combat because the etiological agent, avian pathogenic Escherichia coli (APEC), emerges from ubiquitous commensal gut bacteria, with no single virulence gene present in all disease-causing isolates. Here, we address the underlying evolutionary mechanisms of extraintestinal spread and systemic infection in poultry. Combining population scale comparative genomics and pangenome-wide association studies, we compare E. coli from commensal carriage and systemic infections. We identify phylogroup-specific and species-wide genetic elements that are enriched in APEC, including pathogenicity-associated variation in 143 genes that have diverse functions, including genes involved in metabolism, lipopolysaccharide synthesis, heat shock response, antimicrobial resistance and toxicity. We find that horizontal gene transfer spreads pathogenicity elements, allowing divergent clones to cause infection. Finally, a Random Forest model prediction of disease status (carriage vs. disease) identifies pathogenic strains in the emergent ST-117 poultry-associated lineage with 73% accuracy, demonstrating the potential for early identification of emergent APEC in healthy flocks.

Date: 2021
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DOI: 10.1038/s41467-021-20988-w

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