Evidence map›Paper›PMID 26971047›Full record

ArticleBMC microbiology2016

Comparative genomic analysis of toxin-negative strains of Clostridium difficile from humans and animals with symptoms of gastrointestinal disease.

Piklu Roy Chowdhury, Matthew DeMaere, Toni Chapman, Paul Worden, Ian G Charles, Aaron E Darling, Steven P Djordjevic

Open access · goldAbstract readComparative Study
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. Pangenome-GWAS analysis ofCanadian journal of microbiology · 2026
    Article
  2. Review
  3. Toxin A and B genes expression ofIranian journal of microbiology · 2020
    Article
  4. Article
  5. Article
  6. Antibiotic Resistance and Toxin Production ofFrontiers in microbiology · 2017
    Article
  7. Article
  8. 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

7 authors at 3 institutions in 2 countries.

Piklu Roy ChowdhuryThe ithree institute, University of Technology Sydney, Sydney, 2007, Australia. Piklu.Bhattacharya@uts.edu.au.
Matthew DeMaereThe ithree institute, University of Technology Sydney, Sydney, 2007, Australia.
Toni ChapmanNSW Department of Primary Industries, Elizabeth Macarthur Agricultural Institute, PMB 8, Camden, NSW, 2570, Australia.
Paul WordenThe ithree institute, University of Technology Sydney, Sydney, 2007, Australia.
Ian G CharlesThe ithree institute, University of Technology Sydney, Sydney, 2007, Australia.
Aaron E DarlingThe ithree institute, University of Technology Sydney, Sydney, 2007, Australia.
Steven P DjordjevicThe ithree institute, University of Technology Sydney, Sydney, 2007, Australia. Steven.Djordjevic@uts.edu.au.
University of Technology Sydney · AUNew South Wales Department of Primary Industries · AUQuadram Institute · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundClostridium difficile infections (CDI) are a significant health problem to humans and food animals. Clostridial toxins ToxA and ToxB encoded by genes tcdA and tcdB are located on a pathogenicity locus known as the PaLoc and are the major virulence factors of C. difficile. While toxin-negative strains of C. difficile are often isolated from faeces of animals and patients suffering from CDI, they are not considered to play a role in disease. Toxin-negative strains of C. difficile have been used successfully to treat recurring CDI but their propensity to acquire the PaLoc via lateral gene transfer and express clinically relevant levels of toxins has reinforced the need to characterise them genetically. In addition, further studies that examine the pathogenic potential of toxin-negative strains of C. difficile and the frequency by which toxin-negative strains may acquire the PaLoc are needed.

resultsWe undertook a comparative genomic analysis of five Australian toxin-negative isolates of C. difficile that lack tcdA, tcdB and both binary toxin genes cdtA and cdtB that were recovered from humans and farm animals with symptoms of gastrointestinal disease. Our analyses show that the five C. difficile isolates cluster closely with virulent toxigenic strains of C. difficile belonging to the same sequence type (ST) and have virulence gene profiles akin to those in toxigenic strains. Furthermore, phage acquisition appears to have played a key role in the evolution of C. difficile.

conclusionsOur results are consistent with the C. difficile global population structure comprising six clades each containing both toxin-positive and toxin-negative strains. Our data also suggests that toxin-negative strains of C. difficile encode a repertoire of putative virulence factors that are similar to those found in toxigenic strains of C. difficile, raising the possibility that acquisition of PaLoc by toxin-negative strains poses a threat to human health. Studies in appropriate animal models are needed to examine the pathogenic potential of toxin-negative strains of C. difficile and to determine the frequency by which toxin-negative strains may acquire the PaLoc.

Indexed as

Amino Acid SequenceAnimalsBacterial ProteinsBacterial ToxinsClostridioides difficileClostridium InfectionsGastrointestinal DiseasesHorse DiseasesHorsesHumansMolecular Sequence DataPhylogenySequence AlignmentSwineSwine DiseasesBacterial ProteinsBacterial ToxinsCDIClostridium difficileComparative genomicsToxin-negative isolatesZoonosis

Identifiers

PMID26971047
PMCPMC4789261
OpenAlexW2293304514

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.