Evidence map›Paper›PMID 26553467›Full record

ArticleInfection and immunity2016

Discovery and Characterization of Human-Urine Utilization by Asymptomatic-Bacteriuria-Causing Streptococcus agalactiae.

Deepak S Ipe, Nouri L Ben Zakour, Matthew J Sullivan, Scott A Beatson, Kimberly B Ulett, William H Benjamin, Mark R Davies, Samantha J Dando, Nathan P King, Allan W Cripps and 3 more

Open access · bronzeAbstract read
In one paragraph

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 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

19 citing papers in PubMed, 29 citations in OpenAlex.

  1. Descriptive review: global spectrum of invasive group B streptococcal disease in nonpregnant adults: epidemiology, risk factors and clinical presentations.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2026
    Review
  2. Identification of glyoxalase A in group BInfection and immunity · 2025
    Article
  3. Multidrug resistance in group BJournal of medical microbiology · 2025
    Article
  4. Group BMicrobiology (Reading, England) · 2025
    Article
  5. Identification of Glyoxalase A in Group BbioRxiv : the preprint server for biology · 2024
    Article
  6. Article
  7. Review
  8. Variable resistance to zinc intoxication amongFrontiers in immunology · 2023
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Complete Genome Sequence of Serotype IIIGenome announcements · 2017
    Article
  16. Article
  17. Article
  18. Article
  19. The Basics of Bacteriuria: Strategies of Microbes for Persistence in Urine.Frontiers in cellular and infection microbiology · 2016
    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

13 authors at 4 institutions in 3 countries.

Deepak S IpeSchool of Medical Sciences, Menzies Health Institute Queensland, Griffith University, Gold Coast Campus, QLD, Australia.
Nouri L Ben ZakourSchool of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, QLD, Australia.
Matthew J SullivanSchool of Medical Sciences, Menzies Health Institute Queensland, Griffith University, Gold Coast Campus, QLD, Australia.
Scott A BeatsonSchool of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, QLD, Australia.
Kimberly B UlettDepartment of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA.
William H BenjaminDepartment of Microbiology, University of Alabama at Birmingham, Birmingham, Alabama, USA Department of Pathology, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Mark R DaviesSchool of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, QLD, Australia Wellcome Trust Sanger Institute, Hinxton, Cambridge, United Kingdom.
Samantha J DandoInstitute for Glycomics, Griffith University, Gold Coast Campus, QLD, Australia.
Nathan P KingInstitute for Molecular Bioscience, The University of Queensland, Brisbane, QLD, Australia.
Allan W CrippsSchool of Medical Sciences, Menzies Health Institute Queensland, Griffith University, Gold Coast Campus, QLD, Australia.
Mark A SchembriSchool of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, QLD, Australia.ORCID http://orcid.org/0000-0003-4863-9260
Gordon DouganWellcome Trust Sanger Institute, Hinxton, Cambridge, United Kingdom.
Glen C UlettSchool of Medical Sciences, Menzies Health Institute Queensland, Griffith University, Gold Coast Campus, QLD, Australia Department of Microbiology, University of Alabama at Birmingham, Birmingham, Alabama, USA g.ulett@griffith.edu.au.ORCID http://orcid.org/0000-0002-9638-8091
Griffith University · AUThe University of Queensland · AUUniversity of Alabama at Birmingham · USWellcome Sanger Institute · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

Streptococcus agalactiae causes both symptomatic cystitis and asymptomatic bacteriuria (ABU); however, growth characteristics of S. agalactiae in human urine have not previously been reported. Here, we describe a phenotype of robust growth in human urine observed in ABU-causing S. agalactiae (ABSA) that was not seen among uropathogenic S. agalactiae (UPSA) strains isolated from patients with acute cystitis. In direct competition assays using pooled human urine inoculated with equal numbers of a prototype ABSA strain, designated ABSA 1014, and any one of several UPSA strains, measurement of the percentage of each strain recovered over time showed a markedly superior fitness of ABSA 1014 for urine growth. Comparative phenotype profiling of ABSA 1014 and UPSA strain 807, isolated from a patient with acute cystitis, using metabolic arrays of >2,500 substrates and conditions revealed unique and specific l-malic acid catabolism in ABSA 1014 that was absent in UPSA 807. Whole-genome sequencing also revealed divergence in malic enzyme-encoding genes between the strains predicted to impact the activity of the malate metabolic pathway. Comparative growth assays in urine comparing wild-type ABSA and gene-deficient mutants that were functionally inactivated for the malic enzyme metabolic pathway by targeted disruption of the maeE or maeK gene in ABSA demonstrated attenuated growth of the mutants in normal human urine as well as synthetic human urine containing malic acid. We conclude that some S. agalactiae strains can grow in human urine, and this relates in part to malic acid metabolism, which may affect the persistence or progression of S. agalactiae ABU.

Indexed as

AdultAnimalsAsymptomatic InfectionsBacteriuriaCystitisFemaleGene Expression Regulation, BacterialHumansMalatesMaleMetabolic Networks and PathwaysMiceMice, Inbred C57BLRetrospective StudiesStreptococcus agalactiaeUrinary Tract InfectionsMalatesmalic acid

Identifiers

PMID26553467
PMCPMC4694007
OpenAlexW2217737927

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.