Evidence map›Paper›PMID 29048477›Full record

ReviewFEMS microbiology reviews2017

The role of toxins in Clostridium difficile infection.

Ramyavardhanee Chandrasekaran, D Borden Lacy

Open access · bronzeAbstract readReview
In one paragraph

Review in FEMS microbiology reviews, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 219 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
219citing papers in PubMed, 1 pooled it
12.5field-weighted citation impact, top 1% 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

219 citing papers in PubMed, 1 synthesis or guideline pooled it, 340 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. P2X7R+CD8αβiScience · 2026
    Article
  6. Review
  7. A programmed reset mechanism primesScience advances · 2026
    Article
  8. Phase variable colony morphotypes ofInfection and immunity · 2026
    Article
  9. bioRxiv : the preprint server for biology · 2026
    Article
  10. Review
  11. Colonization Dynamics ofVeterinary sciences · 2026
    Article
  12. Current status and future perspectives of fecal immunological markers in the differential diagnosis of Clostridioides difficile infection in children.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2026
    Review
  13. Article
  14. Article
  15. Development of a high-throughput screening platform forAntimicrobial agents and chemotherapy · 2026
    Article
  16. Article
  17. Article
  18. Phase variable colony morphotypes ofbioRxiv : the preprint server for biology · 2026
    Article
  19. Review
  20. Review

159 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Ramyavardhanee ChandrasekaranDepartment of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.
D Borden LacyDepartment of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.
Vanderbilt University · US

Funding

Structural mechanisms of Clostridium difficile pathogenesisR01AI095755 · NIAID · VANDERBILT UNIVERSITY MEDICAL CENTER · PI LACY, DANA BORDEN · 2011 to 2020
$3.9M
Structural Mechanisms of Clostridioides difficile pathogenesisR37AI095755 · NIAID · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Dana Borden Lacy · 2021 to 2026
$3.2M
The role of toxins in Clostridium difficile infection pathogenesisI01BX002943 · VA · VETERANS HEALTH ADMINISTRATION · PI LACY, DANA BORDEN · 2016 to 2025
–
BLRD VA I01 BX002943NIAID NIH HHS R01 AI095755NIAID NIH HHS R37 AI095755
6 · The paper itself

Abstract

Clostridium difficile is a bacterial pathogen that is the leading cause of nosocomial antibiotic-associated diarrhea and pseudomembranous colitis worldwide. The incidence, severity, mortality and healthcare costs associated with C. difficile infection (CDI) are rising, making C. difficile a major threat to public health. Traditional treatments for CDI involve use of antibiotics such as metronidazole and vancomycin, but disease recurrence occurs in about 30% of patients, highlighting the need for new therapies. The pathogenesis of C. difficile is primarily mediated by the actions of two large clostridial glucosylating toxins, toxin A (TcdA) and toxin B (TcdB). Some strains produce a third toxin, the binary toxin C. difficile transferase, which can also contribute to C. difficile virulence and disease. These toxins act on the colonic epithelium and immune cells and induce a complex cascade of cellular events that result in fluid secretion, inflammation and tissue damage, which are the hallmark features of the disease. In this review, we summarize our current understanding of the structure and mechanism of action of the C. difficile toxins and their role in disease.

Indexed as

Bacterial ToxinsClostridioides difficileClostridium InfectionsHumansImmunityIntestinal MucosaBacterial Toxinsactin cytoskeletonbacterial toxinsClostridium difficilecolitisglucosyltransferaseinflammationintestinal epitheliumpore formation

Identifiers

PMID29048477
PMCPMC5812492
OpenAlexW2765868029

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.