Evidence map›Paper›PMID 24816604›Full record

ArticleJournal of bacteriology2014

Tolerance of a phage element by Streptococcus pneumoniae leads to a fitness defect during colonization.

Hilary K DeBardeleben, Elena S Lysenko, Ankur B Dalia, Jeffrey N Weiser

Open access · bronzeAbstract read
In one paragraph

Article in Journal of bacteriology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.5field-weighted citation impact, top 12% of its field
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

22 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Wild-typeFrontiers in microbiology · 2023
    Article
  4. Article
  5. Article
  6. Lysogeny inMicroorganisms · 2020
    Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Puzzling Over the Pneumococcal Pangenome.Frontiers in microbiology · 2018
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

4 authors at 2 institutions in 1 country.

Hilary K DeBardelebenDepartment of Microbiology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA.
Elena S LysenkoDepartment of Microbiology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA.
Ankur B DaliaDepartment of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts, USA.
Jeffrey N WeiserDepartment of Microbiology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA Department of Pediatrics, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA weiser@mail.med.upenn.edu.
University of Pennsylvania · USTufts University · US

Funding

TRANSGENIC AND CHIMERIC MOUSE COREP30DK050306 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI Ken Hashigiwa Cadwell · 1997 to 2026
$32.5M
Early Events in Pneumococcal ColonizationR01AI105168 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI WEISER, JEFFREY NEAL · 2014 to 2018
$2.1M
Training in bacteriologyT32AI060516 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI GOULIAN, MARK D, ZHU, JUN · 2006 to 2015
$2.0M
Bacterial and host factors in pneumococcal competitionR01AI078538 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI WEISER, JEFFREY NEAL · 2009 to 2013
$1.9M
NIAID NIH HHS R01 AI078538NIAID NIH HHS R01 AI105168NIAID NIH HHS T32 AI060516NIDDK NIH HHS P30 DK050306PHS HHS T32 A1060516
6 · The paper itself

Abstract

The pathogenesis of the disease caused by Streptococcus pneumoniae begins with colonization of the upper respiratory tract. Temperate phages have been identified in the genomes of up to 70% of clinical isolates. How these phages affect the bacterial host during colonization is unknown. Here, we examined a clinical isolate that carries a novel prophage element, designated Spn1, which was detected in both integrated and episomal forms. Surprisingly, both lytic and lysogenic Spn1 genes were expressed under routine growth conditions. Using a mouse model of asymptomatic colonization, we demonstrate that the Spn1(-) strain outcompeted the Spn1(+) strain >70-fold. To determine if Spn1 causes a fitness defect through a trans-acting factor, we constructed an Spn1(+) mutant that does not become an episome or express phage genes. This mutant competed equally with the Spn1(-) strain, indicating that expression of phage genes or phage lytic activity is required to confer this fitness defect. In vitro, we demonstrate that the presence of Spn1 correlated with a defect in LytA-mediated autolysis. Furthermore, the Spn1(+) strain displayed increased chain length and resistance to lysis by penicillin compared to the Spn(-) strain, indicating that Spn1 alters the cell wall physiology of its host strain. We posit that these changes in cell wall physiology allow for tolerance of phage gene products and are responsible for the relative defect of the Spn1(+) strain during colonization. This study provides new insight into how bacteria and prophages interact and affect bacterial fitness in vivo.

Indexed as

AnimalsBacterial ProteinsCarrier StateMiceMicrobial Sensitivity TestsMolecular Sequence DataPenicillin ResistancePenicillinsPneumococcal InfectionsProphagesStreptococcus PhagesStreptococcus pneumoniaeBacterial ProteinsPenicillins

Identifiers

PMID24816604
PMCPMC4097588
OpenAlexW2151886256

What OpenQuestion holds

Textmetadata
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.