Evidence map›Paper›PMID 19558711›Full record

ArticleBMC infectious diseases2009

Truncation in the tcdC region of the Clostridium difficile PathLoc of clinical isolates does not predict increased biological activity of Toxin B or Toxin A.

Ruth Murray, Dave Boyd, Paul N Levett, Michael R Mulvey, Michelle J Alfa

Abstract readComparative Study
In one paragraph

Article in BMC infectious diseases, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing 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

38 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Ribotypes and New Virulent Strains Across Europe.Advances in experimental medicine and biology · 2024
    Review
  5. Review
  6. Article
  7. Article
  8. Emergence of Clinical Clostridioides difficile Isolates With Decreased Susceptibility to Vancomycin.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2022
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Phenotypic Characterization of Non-toxigenicFrontiers in microbiology · 2019
    Article
  16. Article
  17. High rate of Clostridium difficile among young adults presenting with diarrhea at two hospitals in Kenya.International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases · 2018
    Article
  18. Binary toxin and its clinical importance in Clostridium difficile infection, Belgium.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2016
    Article
  19. Review
  20. Characterization of Clostridium difficile Strains in British Columbia, Canada: A Shift from NAP1 Majority (2008) to Novel Strain Types (2013) in One Region.The Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale · 2016
    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

5 authors.

Ruth MurraySt. Boniface Research Centre, Winnipeg, MB, Canada. margaretmurray207@hotmail.com
Dave Boyd
Paul N Levett
Michael R Mulvey
Michelle J Alfa

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe increased severity of disease associated with the NAP1 strain of Clostridium difficile has been attributed to mutations to the tcdC gene which codes for a negative regulator of toxin production. To assess the role of hyper-production of Toxins A and B in clinical isolates of Clostridium difficile, two NAP1-related and five NAP1 non-related strains were compared.

methodsSequencing was performed on tcdC, tcdR, and tcdE to determine if there were differences that might account for hyper-production of Toxin A and Toxin B in NAP1-related strains. Biological activity of Toxin B was evaluated using the HFF cell CPE assay and Toxin A biological activity was assessed using the Caco-2 Trans-membrane resistance assay.

resultsOur results confirm that Toxin A and Toxin B production in NAP1-related strains and ATCC 43255 occurs earlier in the exponential growth phase compared to most NAP1-nonrelated clinical isolates. Despite the hyper-production observed in ATCC 43255 it had no mutations in tcdC, tcdR or tcdE. Analysis of the other clinical isolates indicated that the kinetics and ultimate final concentration of Toxin A and B did not correlate with the presence or lack of alterations in tcdC, tcdR or tcdE.

conclusionOur data do not support a direct role for alterations in the tcdC gene as a predictor of hyperproduction of Toxin A and B in NAP1-related strains.

Indexed as

Amino Acid SequenceBacterial ProteinsBacterial ToxinsBacterial Typing TechniquesCaco-2 CellsClostridioides difficileDNA, BacterialEnterotoxinsGene Expression Regulation, BacterialHumansMolecular Sequence DataMutationRepressor ProteinsSequence Analysis, DNABacterial ProteinsBacterial ToxinsDNA, BacterialEnterotoxinsRepressor ProteinstcdA protein, Clostridium difficileTcdC protein, Clostridium difficiletoxB protein, Clostridium difficile

Identifiers

PMID19558711
PMCPMC2707377

What OpenQuestion holds

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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.