ArticleEmerging infectious diseases2017
Evolutionary Context of Non-Sorbitol-Fermenting Shiga Toxin-Producing Escherichia coli O55:H7.
Article in Emerging infectious diseases, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Phylogenomic framework and virulence gene boundaries of emerging Shiga toxin-producingVirulence · 2026Article
- Pathogenomes of Shiga Toxin Positive and NegativeMicroorganisms · 2024Article
- Prevalence and Virulent Gene Profiles of Sorbitol Non-Fermenting Shiga Toxin-ProducingTropical medicine and infectious disease · 2022Article
- SARS-CoV-2 and Emerging Foodborne Pathogens: Intriguing Commonalities and Obvious Differences.Pathogens (Basel, Switzerland) · 2022Review
- Epidemiological investigation of recurrent outbreaks of haemolytic uraemic syndrome caused by Shiga toxin-producingEpidemiology and infection · 2021Article
- Comparison of Shiga toxin-encoding bacteriophages in highly pathogenic strains of Shiga toxin-producingMicrobial genomics · 2020Article
- Pathogenomes of Atypical Non-shigatoxigenicFrontiers in microbiology · 2020Article
- A sensitive method for the recovery of Escherichia coli serogroup O55 including Shiga toxin-producing variants for potential use in outbreaks.Journal of applied microbiology · 2019Article
- Genomic Characterization of β-Glucuronidase-Positive Escherichia coli O157:H7 Producing Stx2a.Emerging infectious diseases · 2018Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In July 2014, an outbreak of Shiga toxin-producing Escherichia coli (STEC) O55:H7 in England involved 31 patients, 13 (42%) of whom had hemolytic uremic syndrome. Isolates were sequenced, and the sequences were compared with publicly available sequences of E. coli O55:H7 and O157:H7. A core-genome phylogeny of the evolutionary history of the STEC O55:H7 outbreak strain revealed that the most parsimonious model was a progenitor enteropathogenic O55:H7 sorbitol-fermenting strain, lysogenized by a Shiga toxin (Stx) 2a-encoding phage, followed by loss of the ability to ferment sorbitol because of a non-sense mutation in srlA. The parallel, convergent evolutionary histories of STEC O157:H7 and STEC O55:H7 may indicate a common driver in the evolutionary process. Because emergence of STEC O157:H7 as a clinically significant pathogen was associated with acquisition of the Stx2a-encoding phage, the emergence of STEC O55:H7 harboring the stx2a gene is of public health concern.
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Registered trials
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