ArticleEuropean journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology2023
Genome-wide association study of hemolytic uremic syndrome causing Shiga toxin-producing Escherichia coli from Sweden, 1994-2018.
Article in European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 14 citations in OpenAlex.
- Comprehensive Genomic Analysis of the pO157 Plasmid in Enterohemorrhagic Escherichia coli O157:H7 Reveals Non-synonymous Variation in Virulence Factors.Current microbiology · 2026Article
- Bacterial genome-wide association studies: exploring the genetic variation underlying bacterial phenotypes.Applied and environmental microbiology · 2025Review
- Case-Control Study of Factors Associated with Hemolytic Uremic Syndrome among Shiga Toxin-Producing Escherichia coli Patients, Ireland, 2017-2020.Emerging infectious diseases · 2025Article
- Whole-Genome Sequence Reveals Genetic Determinants of the Colonization of Shiga Toxin-Producing Escherichia coli O22:H8 Isolates in Cattle.Current microbiology · 2025Article
- Comparative genomics of Shiga toxin-producingFrontiers in veterinary science · 2025Article
- Characterization of Escherichia coli strains producing Shiga Toxin 2f subtype from domestic Pigeon.Scientific reports · 2024Article
- Complex effects of the exo-xis region of the Shiga toxin-converting bacteriophage Φ24Journal of applied genetics · 2024Article
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Authors and funding
9 authors at 6 institutions in 4 countries.
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Abstract
Shiga toxin-producing Escherichia coli (STEC) infection can cause clinical manifestations ranging from diarrhea to potentially fatal hemolytic uremic syndrome (HUS). This study is aimed at identifying STEC genetic factors associated with the development of HUS in Sweden. A total of 238 STEC genomes from STEC-infected patients with and without HUS between 1994 and 2018 in Sweden were included in this study. Serotypes, Shiga toxin gene (stx) subtypes, and virulence genes were characterized in correlation to clinical symptoms (HUS and non-HUS), and pan-genome wide association study was performed. Sixty-five strains belonged to O157:H7, and 173 belonged to non-O157 serotypes. Our study revealed that strains of O157:H7 serotype especially clade 8 were most commonly found in patients with HUS in Sweden. stx2a and stx2a + stx2c subtypes were significantly associated with HUS. Other virulence factors associated with HUS mainly included intimin (eae) and its receptor (tir), adhesion factors, toxins, and secretion system proteins. Pangenome wide-association study identified numbers of accessory genes significantly overrepresented in HUS-STEC strains, including genes encoding outer membrane proteins, transcriptional regulators, phage-related proteins, and numerous genes related to hypothetical proteins. Whole-genome phylogeny and multiple correspondence analysis of pangenomes could not differentiate HUS-STEC from non-HUS-STEC strains. In O157:H7 cluster, strains from HUS patients clustered closely; however, no significant difference in virulence genes was found in O157 strains from patients with and without HUS. These results suggest that STEC strains from different phylogenetic backgrounds may independently acquire genes determining their pathogenicity and confirm that other non-bacterial factors and/or bacteria-host interaction may affect STEC pathogenesis.
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