Evidence map›Paper›PMID 26292302›Full record

ArticleJournal of clinical microbiology2015

Simultaneous Presence of Insertion Sequence Excision Enhancer and Insertion Sequence IS629 Correlates with Increased Diversity and Virulence in Shiga Toxin-Producing Escherichia coli.

M Toro, L V Rump, G Cao, J Meng, E W Brown, N Gonzalez-Escalona

Abstract read
In one paragraph

Article in Journal of clinical microbiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Frontiers in microbiology · 2023
    Article
  6. Article
  7. Article
  8. Pathogenomes of Atypical Non-shigatoxigenicFrontiers in microbiology · 2020
    Article
  9. Multi-Year Persistence of VerotoxigenicFrontiers in microbiology · 2018
    Article
  10. Article
  11. Article
  12. Article
  13. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

M ToroDepartment of Nutrition and Food Science, University of Maryland, College Park, Maryland, USA.
L V RumpDepartment of Nutrition and Food Science, University of Maryland, College Park, Maryland, USA.
G CaoDepartment of Nutrition and Food Science, University of Maryland, College Park, Maryland, USA Joint Institute for Food Safety and Applied Nutrition (JIFSAN), University of Maryland, College Park, Maryland, USA.
J MengDepartment of Nutrition and Food Science, University of Maryland, College Park, Maryland, USA Joint Institute for Food Safety and Applied Nutrition (JIFSAN), University of Maryland, College Park, Maryland, USA.
E W BrownDivision of Microbiology, Center for Food Safety and Applied Nutrition, Food and Drug Administration, College Park, Maryland, USA.
N Gonzalez-EscalonaDivision of Microbiology, Center for Food Safety and Applied Nutrition, Food and Drug Administration, College Park, Maryland, USA narjol.gonzalez-escalona@fda.hhs.gov.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although new serotypes of enterohemorrhagic Escherichia coli (EHEC) emerge constantly, the mechanisms by which these new pathogens arise and the reasons emerging serotypes tend to carry more virulence genes than other E. coli are not understood. An insertion sequence (IS) excision enhancer (IEE) was discovered in EHEC O157:H7 that promoted the excision of IS3 family members and generating various genomic deletions. One IS3 family member, IS629, actively transposes and proliferates in EHEC O157:H7 and enterotoxigenic E. coli (ETEC) O139 and O149. The simultaneous presence of the IEE and IS629 (and other IS3 family members) may be part of a system promoting not only adaptation and genome diversification in E. coli O157:H7 but also contributing to the development of pathogenicity among predominant serotypes. Prevalence comparisons of these elements in 461 strains, representing 72 different serotypes and 5 preassigned seropathotypes (SPT) A to E, showed that the presence of these two elements simultaneously was serotype specific and associated with highly pathogenic serotypes (O157 and top non-O157 Shiga toxin-producing Escherichia coli [STEC]) implicated in outbreaks and sporadic cases of human illness (SPT A and B). Serotypes lacking one or both elements were less likely to have been isolated from clinical cases. Our comparisons of IEE sequences showed sequence variations that could be divided into at least three clusters. Interestingly, the IEE sequences from O157 and the top 10 non-O157 STEC serotypes fell into clusters I and II, while less commonly isolated serotypes O5 and O174 fell into cluster III. These results suggest that IS629 and IEE elements may be acting synergistically to promote genome plasticity and genetic diversity among STEC strains, enhancing their abilities to adapt to hostile environments and rapidly take up virulence factors.

Indexed as

Base SequenceDisease OutbreaksDNA, BacterialDNA Transposable ElementsEscherichia coli InfectionsEscherichia coli O157Gene DeletionGenetic VariationGenome, BacterialHumansMolecular Sequence DataPhylogenySequence Analysis, DNASerogroupSerotypingToxins, BiologicalDNA, BacterialDNA Transposable ElementsToxins, BiologicalVirulence Factors

Identifiers

PMID26292302
PMCPMC4609730

What OpenQuestion holds

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Registered trials

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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.