ReviewClinical microbiology reviews2005
Clostridium difficile toxins: mechanism of action and role in disease.
Review in Clinical microbiology reviews, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 528 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
528 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,114 citations in OpenAlex.
- Pooled it
- Double-Blind, Placebo-Controlled Study of Bezlotoxumab in Children Receiving Antibacterial Treatment for Clostridioides difficile Infection (MODIFY III).Journal of the Pediatric Infectious Diseases Society · 2023Trial
- A possible association between statin use and improved Clostridioides difficile infection mortality in veterans.PloS one · 2019Trial
- Naturally Occurring CodY Variants Alter Ligand Binding, DNA Target Affinity, and Virulence in Clostridioides difficile.Molecular microbiology · 2026Article
- Novel endogenous protein-based strategies to inhibit clinically relevant bacterial AB-type toxins including pertussis toxin.Archives of toxicology · 2026Review
- Clostridioides difficile as a Zoonotic and Foodborne Pathogen: Reviewing the Global Evidence and South African Data.MicrobiologyOpen · 2026Review
- Mechanistic insights on spatiotemporal control of Ras-signaling.Biological chemistry · 2026Review
- Sub-inhibitory concentrations of metronidazole alter the proteomic profile and biological effects of extracellular vesicles from Clostridioides difficile.BMC microbiology · 2026Article
- The Use of Bacteria and Their Toxins as Antitumor Agents: Present and Future.Microorganisms · 2026Review
- High-fat diet rewires gut host-microbiota relationship to derive worse outcomes followingbioRxiv : the preprint server for biology · 2026Article
- Clostridioides difficile : A suspected pro-carcinogenic bacterium for gastrointestinal tumors.Chinese medical journal · 2026Review
- Gut microecology in critical illness: mechanisms, biomarkers, and therapeutic strategies - a critical appraisal.Frontiers in gastroenterology (Lausanne, Switzerland) · 2026Review
- Gut microbiota dysbiosis: Pathogenic drivers and emerging phage-based therapeutics.AIMS microbiology · 2026Review
- Diagnostic challenges and treatment approaches forFrontiers in microbiology · 2026Review
- Gut-microbiota-mediated host immune modulation: mechanisms, pathological dysbiosis, and therapeutic frontiers.Frontiers in cellular and infection microbiology · 2026Review
- Article
- Epitope Conservation of AZD5148, a Broadly Neutralizing Anti-Toxin B Monoclonal Antibody, Among Diverse and Global Contemporary Clostridioides difficile Isolates.The Journal of infectious diseases · 2025Article
- Polysaccharide lyase PL3.3 possibly potentiating Clostridioides difficile clinical symptoms based on complete genome analysis of RT046/ST35 and RT012/ST54.International microbiology : the official journal of the Spanish Society for Microbiology · 2025Article
- Cysteine proteases and how YabG fits into clan CD of the MEROPS database.Journal of bacteriology · 2025Review
- Clostridioides difficile Infection in Healthy Children After Antibiotic Use: A Report of Two Cases.Cureus · 2025Article
468 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As the leading cause of hospital-acquired diarrhea, Clostridium difficile colonizes the large bowel of patients undergoing antibiotic therapy and produces two toxins, which cause notable disease pathologies. These two toxins, TcdA and TcdB, are encoded on a pathogenicity locus along with negative and positive regulators of their expression. Following expression and release from the bacterium, TcdA and TcdB translocate to the cytosol of target cells and inactivate small GTP-binding proteins, which include Rho, Rac, and Cdc42. Inactivation of these substrates occurs through monoglucosylation of a single reactive threonine, which lies within the effector-binding loop and coordinates a divalent cation critical to binding GTP. By glucosylating small GTPases, TcdA and TcdB cause actin condensation and cell rounding, which is followed by death of the cell. TcdA elicits effects primarily within the intestinal epithelium, while TcdB has a broader cell tropism. Important advances in the study of these toxins have been made in the past 15 years, and these are detailed in this review. The domains, subdomains, and residues of these toxins important for receptor binding and enzymatic activity have been elegantly studied and are highlighted herein. Furthermore, there have been major advances in defining the role of these toxins in modulating the inflammatory events involving the disruption of cell junctions, neuronal activation, cytokine production, and infiltration by polymorphonuclear cells. Collectively, the present review provides a comprehensive update on TcdA and TcdB's mechanism of action as well as the role of these toxins in disease.
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What OpenQuestion holds
Registered trials
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.