ArticleInfection and immunity2009
Analysis of the genome of the Escherichia coli O157:H7 2006 spinach-associated outbreak isolate indicates candidate genes that may enhance virulence.
Article in Infection and immunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.
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94 citing papers in PubMed, 151 citations in OpenAlex.
- Global expression profile of enterohemorrhagic Escherichia coli O157:H7 in phagosome of murine macrophages.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2026Article
- Comprehensive Genomic Analysis of the pO157 Plasmid in Enterohemorrhagic Escherichia coli O157:H7 Reveals Non-synonymous Variation in Virulence Factors.Current microbiology · 2026Article
- Digital holographic microscopy for rapid bacteria segmentation and counting in microfluidic cartridges: basic considerations and limitations for diagnostic application.Journal of biomedical optics · 2025Article
- Centriflaken: An automated data analysis pipeline for assembly and in silico analyses of foodborne pathogens from metagenomic samples.PloS one · 2025Article
- In Silico Analysis of Shiga Toxin-ProducingToxins · 2024Article
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- Differences in the Shiga Toxin (Stx) 2a Phage Regulatory Switch Region Influence Stx2 Localization and Virulence of Stx-ProducingMicroorganisms · 2023Article
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- Pathogenomes and variations in Shiga toxin production among geographically distinct clones ofMicrobial genomics · 2022Article
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- Genomic Diversity, Virulence Gene, and Prophage Arrays of Bovine and Human Shiga Toxigenic and EnteropathogenicFrontiers in microbiology · 2022Article
- Flavorubredoxin, a Candidate Trigger Related to Thrombotic Thrombocytopenic Purpura: Screening of the Complete Genome of aFrontiers in cellular and infection microbiology · 2022Review
- Proteomic Advances in Cereal and Vegetable Crops.Molecules (Basel, Switzerland) · 2021Review
- Review
- Comparative Pathogenomics ofInfection and immunity · 2021Article
- Variability in the Occupancy ofToxins · 2021Article
- Strain and host-cell dependent role of type-1 fimbriae in the adherence phenotype of super-shed Escherichia coli O157:H7.International journal of medical microbiology : IJMM · 2021Article
- Bacteriophages of Shiga Toxin-ProducingPathogens (Basel, Switzerland) · 2021Review
- Comparative Whole Genome Analysis ofFrontiers in microbiology · 2021Article
34 more citing papers are in PubMed but not listed here.
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Authors and funding
23 authors at 4 institutions in 1 country.
Funding
Abstract
In addition to causing diarrhea, Escherichia coli O157:H7 infection can lead to hemolytic-uremic syndrome (HUS), a severe disease characterized by hemolysis and renal failure. Differences in HUS frequency among E. coli O157:H7 outbreaks have been noted, but our understanding of bacterial factors that promote HUS is incomplete. In 2006, in an outbreak of E. coli O157:H7 caused by consumption of contaminated spinach, there was a notably high frequency of HUS. We sequenced the genome of the strain responsible (TW14359) with the goal of identifying candidate genetic factors that contribute to an enhanced ability to cause HUS. The TW14359 genome contains 70 kb of DNA segments not present in either of the two reference O157:H7 genomes. We identified seven putative virulence determinants, including two putative type III secretion system effector proteins, candidate genes that could result in increased pathogenicity or, alternatively, adaptation to plants, and an intact anaerobic nitric oxide reductase gene, norV. We surveyed 100 O157:H7 isolates for the presence of these putative virulence determinants. A norV deletion was found in over one-half of the strains surveyed and correlated strikingly with the absence of stx(1). The other putative virulence factors were found in 8 to 35% of the O157:H7 isolates surveyed, and their presence also correlated with the presence of norV and the absence of stx(1), indicating that the presence of norV may serve as a marker of a greater propensity for HUS, similar to the correlation between the absence of stx(1) and a propensity for HUS.
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