ArticleInfection and immunity2016
Genomic Comparison of Two O111:H- Enterohemorrhagic Escherichia coli Isolates from a Historic Hemolytic-Uremic Syndrome Outbreak in Australia.
Article in Infection and immunity, 2016. 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.
- Pathogenome and Plasmid-Borne Antimicrobial Resistance Phenotypes in a Multidrug-Resistant O111:H8 Shiga Toxin-ProducingbioRxiv : the preprint server for biology · 2026Article
- Impact of Shiga-toxin encoding gene transduction from O80:H2 Shiga toxigenic Escherichia coli (STEC) on non-STEC strains.Scientific reports · 2022Article
- The Characterisation of Diarrhoeagenic Verotoxin Producing Non-O157 Escherichia coli among Young Children in Kuantan, Malaysia.The Malaysian journal of medical sciences : MJMS · 2022Article
- Added Value of Genomic Surveillance of Virulence Factors in Shiga Toxin-ProducingFrontiers in microbiology · 2021Article
- Is Shiga Toxin-ProducingMicroorganisms · 2020Article
- SMRT sequencing reveals differential patterns of methylation in two O111:H- STEC isolates from a hemolytic uremic syndrome outbreak in Australia.Scientific reports · 2019Article
- Article
- Outbreak of multiple strains of non-O157 Shiga toxin-producing and enteropathogenicEuro surveillance : bulletin Europeen sur les maladies transmissibles = European communicable disease bulletin · 2018Article
- Recurrent seasonal outbreak of an emerging serotype of Shiga toxin-producing Escherichia coli (STEC O55:H7 Stx2a) in the south west of England, July 2014 to September 2015.Euro surveillance : bulletin Europeen sur les maladies transmissibles = European communicable disease bulletin · 2017Article
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7 authors.
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Abstract
Enterohemorrhagic Escherichia coli (EHEC) is an important cause of diarrhea and hemolytic-uremic syndrome (HUS) worldwide. Australia's worst outbreak of HUS occurred in Adelaide in 1995 and was one of the first major HUS outbreaks attributed to a non-O157 Shiga-toxigenic E. coli (STEC) strain. Molecular analyses conducted at the time suggested that the outbreak was caused by an O111:H(-) clone, with strains from later in the outbreak harboring an extra copy of the genes encoding the potent Shiga toxin 2 (Stx2). Two decades later, we have used next-generation sequencing to compare two isolates from early and late in this important outbreak. We analyzed genetic content, single-nucleotide polymorphisms (SNPs), and prophage insertion sites; for the latter, we demonstrate how paired-end sequence data can be leveraged to identify such insertion sites. The two strains are genetically identical except for six SNP differences and the presence of not one but two additional Stx2-converting prophages in the later isolate. Isolates from later in the outbreak were associated with higher levels of morbidity, suggesting that the presence of the additional Stx2-converting prophages is significant in terms of the virulence of this clone.
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