ReviewGut microbes2015
Shiga toxin 2a and Enteroaggregative Escherichia coli--a deadly combination.
Review in Gut microbes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 45 citations in OpenAlex.
- Pathogenesis and therapeutic strategies in the interaction between gut microbiota and enterohemorrhagic Escherichia coli infection.FEMS microbiology reviews · 2026Review
- EnteroaggregativeEcoSal Plus · 2025Review
- Overview of pathogenic Escherichia coli, with a focus on Shiga toxin-producing serotypes, global outbreaks (1982-2024) and food safety criteria.Gut pathogens · 2024Review
- O-Antigen Diversification Masks Identification of Highly Pathogenic Shiga Toxin-Producing Escherichia coli O104:H4-Like Strains.Microbiology spectrum · 2023Article
- Prevalence and Implications of Shiga Toxin-ProducingPathogens (Basel, Switzerland) · 2022Review
- EnterohemorrhagicInternational journal of molecular sciences · 2022Review
- Article
- Article
- Pathogenic potential assessment of the Shiga toxin-producingProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Continuous Genomic Surveillance Monitored themSystems · 2021Article
- In Silico Characterization of a Hypothetical Protein fromBioinformatics and biology insights · 2021Article
- QseC Signaling in the Outbreak O104:H4Journal of bacteriology · 2019Article
- Organization and architecture of AggR-dependent promoters from enteroaggregative Escherichia coli.Molecular microbiology · 2019Article
- Type VI Secretion System in PathogenicFrontiers in microbiology · 2019Review
- Novel type of pilus associated with a Shiga-toxigenic E. coli hybrid pathovar conveys aggregative adherence and bacterial virulence.Emerging microbes & infections · 2018Article
- Protection against Shiga Toxins.Toxins · 2017Review
- Whole Genome Sequencing for Public Health Surveillance of Shiga Toxin-Producing Escherichia coli Other than Serogroup O157.Frontiers in microbiology · 2016Article
- Characterization of Shiga Toxin Subtypes and Virulence Genes in Porcine Shiga Toxin-Producing Escherichia coli.Frontiers in microbiology · 2016Article
- Comparative Genome Analysis of an Extensively Drug-Resistant Isolate of Avian Sequence Type 167mSystemsArticle
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
In 2011, a Shiga toxin (Stx) type 2a-producing enteroaggregative E. coli (EAEC) strain of serotype O104:H4 caused a large lethal outbreak in Northern Europe. Until recently, the pathogenic mechanisms explaining the high virulence of the strain have remained unclear. Our laboratories have shown that EAEC genes encoded on the pAA virulence plasmid, particularly the AggR-regulated AAF/I fimbriae, enhance inflammation and enable the outbreak strain to both adhere to epithelial cells and translocate Stx2a across the intestinal epithelium, possibly explaining the high incidence of the life threatening post-diarrheal sequelae of hemolytic uremic syndrome. Epidemiologic evidence supports a model of EAEC pathogenesis comprising the concerted action of multiple virulence factors along with induction of inflammation. Here, we suggest a model for the pathogenesis of the O104:H4 outbreak strain that includes contributions from EAEC alone, but incorporating additional injury induced by Stx2a.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.