Evidence map›Paper›PMID 26160165›Full record

ArticleGenome research2015

Genome specialization and decay of the strangles pathogen, Streptococcus equi, is driven by persistent infection.

Simon R Harris, Carl Robinson, Karen F Steward, Katy S Webb, Romain Paillot, Julian Parkhill, Matthew T G Holden, Andrew S Waller

Open access · bronzeAbstract read
In one paragraph

Article in Genome research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing 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

35 citing papers in PubMed, 76 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Progressive evolution ofMicrobial genomics · 2025
    Article
  7. Geographic diversity of theFrontiers in veterinary science · 2025
    Article
  8. Article
  9. Article
  10. Pathogens (Basel, Switzerland) · 2023
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

8 authors at 3 institutions in 1 country.

Simon R HarrisThe Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, United Kingdom;
Carl RobinsonThe Animal Health Trust, Lanwades Park, Kentford, Newmarket CB8 7UU, United Kingdom;
Karen F StewardThe Animal Health Trust, Lanwades Park, Kentford, Newmarket CB8 7UU, United Kingdom;
Katy S WebbThe Animal Health Trust, Lanwades Park, Kentford, Newmarket CB8 7UU, United Kingdom;
Romain PaillotThe Animal Health Trust, Lanwades Park, Kentford, Newmarket CB8 7UU, United Kingdom;
Julian ParkhillThe Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, United Kingdom;
Matthew T G HoldenThe Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, United Kingdom; School of Medicine, University of St Andrews, North Haugh, St. Andrews KY16 9TF, United Kingdom.
Andrew S WallerThe Animal Health Trust, Lanwades Park, Kentford, Newmarket CB8 7UU, United Kingdom;
Animal Health Trust · GBWellcome Sanger Institute · GBUniversity of St Andrews · GB

Funding

Wellcome TrustWellcome Trust 098051
6 · The paper itself

Abstract

Strangles, the most frequently diagnosed infectious disease of horses worldwide, is caused by Streptococcus equi. Despite its prevalence, the global diversity and mechanisms underlying the evolution of S. equi as a host-restricted pathogen remain poorly understood. Here, we define the global population structure of this important pathogen and reveal a population replacement in the late 19th or early 20th Century. Our data reveal a dynamic genome that continues to mutate and decay, but also to amplify and acquire genes despite the organism having lost its natural competence and become host-restricted. The lifestyle of S. equi within the horse is defined by short-term acute disease, strangles, followed by long-term infection. Population analysis reveals evidence of convergent evolution in isolates from post-acute disease samples as a result of niche adaptation to persistent infection within a host. Mutations that lead to metabolic streamlining and the loss of virulence determinants are more frequently found in persistent isolates, suggesting that the pathogenic potential of S. equi reduces as a consequence of long-term residency within the horse post-acute disease. An example of this is the deletion of the equibactin siderophore locus that is associated with iron acquisition, which occurs exclusively in persistent isolates, and renders S. equi significantly less able to cause acute disease in the natural host. We identify several loci that may similarly be required for the full virulence of S. equi, directing future research toward the development of new vaccines against this host-restricted pathogen.

Indexed as

Genome, BacterialHost-Pathogen InteractionsAnimalsDisease OutbreaksGene AmplificationGene DeletionGene OrderGenetic LociGenomicsHorse DiseasesHorsesMutagenesis, InsertionalPhylogenyPolymorphism, Single NucleotideStreptococcal InfectionsStreptococcus equi

Identifiers

PMID26160165
PMCPMC4561494
OpenAlexW2164238430

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.