Dataset Information

A Shiga Toxin-Encoding Prophage Recombination Event Confounds the Phylogenetic Relationship Between Two Isolates of Escherichia coli O157:H7 From the Same Patient.

ABSTRACT: We compared genomes from multiple isolations of Shiga toxin-producing Escherichia coli (STEC) O157:H7 from the same patient, in cases notified to Public Health England (PHE) between 2015 and 2019. There were 261 cases where multiple isolates were sequenced from the same patient comprising 589 isolates. Serial isolates from the same patient fell within five single nucleotide polymorphisms (SNPs) of each other for 260/261 (99.6%) of the cases, indicating that there was little evidence of within host variation. The investigation into the 13 SNP discrepancy between one isolate pair revealed the cause to be a recombination event within a stx2a-encoding prophage resulting in the insertion/deletion of a fragment of the genome. This 50 kbp prophage fragment was homologous to a prophage in the reference genome, and the short reads from the isolate that had the 50 kbp fragment, mapped unambiguously to this region. The discrepant variants in the isolate without the 50 kbp fragment were attributed to ambiguous mapping of the short reads from other prophage regions to the 50 kbp fragment in the reference genome. Identification of such recombination events in this dataset appeared to be rare, most likely because the majority of prophage regions in the Sakai reference genome are masked during the analysis. Identification of SNPs under neutral selection, and masking recombination events, is a requirement for phylogenetic analysis used for public health surveillance, and for the detection of point source outbreaks. However, assaying the accessory genome by combining the use of short and long read technologies for public health surveillance may provide insight into how recombination events impact on the evolutionary course of STEC O157:H7.

SUBMITTER: Greig DR

PROVIDER: S-EPMC7645076 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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A Shiga Toxin-Encoding Prophage Recombination Event Confounds the Phylogenetic Relationship Between Two Isolates of <i>Escherichia coli</i> O157:H7 From the Same Patient.

Greig David R DR Jenkins Claire C Dallman Timothy J TJ

Frontiers in microbiology 20201023

We compared genomes from multiple isolations of Shiga toxin-producing <i>Escherichia coli</i> (STEC) O157:H7 from the same patient, in cases notified to Public Health England (PHE) between 2015 and 2019. There were 261 cases where multiple isolates were sequenced from the same patient comprising 589 isolates. Serial isolates from the same patient fell within five single nucleotide polymorphisms (SNPs) of each other for 260/261 (99.6%) of the cases, indicating that there was little evidence of wi ...[more]

PMID: 33193248

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Project description:Escherichia coli O157:H7 is a foodborne pathogen implicated in various multistate outbreaks. It encodes Shiga toxin on a prophage, and Shiga toxin production is linked to phage induction. An E. coli strain, designated 0.1229, that amplified Stx2a production when cocultured with E. coli O157:H7 strain PA2 was identified. Growth of PA2 in 0.1229 cell-free supernatants had a similar effect, even when supernatants were heated to 100°C for 10?min, but not after treatment with proteinase K. The secreted molecule was shown to use TolC for export and the TonB system for import. The genes sufficient for production of this molecule were localized to a 5.2-kb region of a 12.8-kb plasmid. This region was annotated, identifying hypothetical proteins, a predicted ABC transporter, and a cupin superfamily protein. These genes were identified and shown to be functional in two other E. coli strains, and bioinformatic analyses identified related gene clusters in similar and distinct bacterial species. These data collectively suggest that E. coli 0.1229 and other E. coli strains produce a microcin that induces the SOS response in target bacteria. Besides adding to the limited number of microcins known to be produced by E. coli, this study provides an additional mechanism by which stx 2a expression is increased in response to the gut microflora.IMPORTANCE How the gut microflora influences the progression of bacterial infections is only beginning to be understood. Antibiotics are counterindicated for E. coli O157:H7 infections, limiting treatment options. An increased understanding of how the gut microflora directs O157:H7 virulence gene expression may lead to additional treatment options. This work identified E. coli strains that enhance the production of Shiga toxin by O157:H7 through the secretion of a proposed microcin. Microcins are natural antimicrobial peptides that target specific species, can act as alternatives to antibiotics, and mediate microbial competition. This work demonstrates another mechanism by which non-O157 E. coli strains may increase Shiga toxin production and adds to our understanding of microcins, a group of antimicrobials less well understood than colicins.

Dataset Information

A Shiga Toxin-Encoding Prophage Recombination Event Confounds the Phylogenetic Relationship Between Two Isolates of Escherichia coli O157:H7 From the Same Patient.

Publications

A Shiga Toxin-Encoding Prophage Recombination Event Confounds the Phylogenetic Relationship Between Two Isolates of <i>Escherichia coli</i> O157:H7 From the Same Patient.

Similar Datasets

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