ArticleNature2010
The role of toxin A and toxin B in Clostridium difficile infection.
Article in Nature, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 465 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
465 citing papers in PubMed, 1 synthesis or guideline pooled it, 871 citations in OpenAlex.
- Comparing the efficacy and safety of faecal microbiota transplantation with bezlotoxumab in reducing the risk of recurrentBMJ open · 2019Pooled it
- Trial
- A Phase 2 Study Evaluating the Safety, Tolerability, and Immunogenicity of Two 3-Dose Regimens of a Clostridium difficile Vaccine in Healthy US Adults Aged 65 to 85 Years.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2020Trial
- Gut microbiota and diet in colorectal cancer: Converging determinants of carcinogenesis.Gut microbes · 2026Review
- BeyondEmerging microbes & infections · 2026Article
- The prevalence and molecular epidemiology ofEmerging microbes & infections · 2026Observational
- From colonization to infection: Genomic evolution of Clostridioides difficile pathogenesis.Cell reports · 2026Review
- The impact of TcdB conformational dynamics on vaccination against Clostridioides difficile.PLoS pathogens · 2026Article
- Biomarkers for Early Severity Prediction inMedicina (Kaunas, Lithuania) · 2026Review
- Antibiotics promote susceptibility tobioRxiv : the preprint server for biology · 2026Article
- HumanbioRxiv : the preprint server for biology · 2025Article
- Comparison of Gut Microbiome Profile of Chickens Infected with ThreeMicroorganisms · 2025Article
- Global burden and trends of theAnnals of medicine · 2025Observational
- Strategies for engineering domesticated and undomesticated human microbes.Current opinion in biotechnology · 2025Review
- CD44 is a macrophage receptor for TcdB fromGut microbes · 2025Article
- Biliverdin targeting TcdB-DRBD inhibits Clostridioides difficile virulence and restores gut microbiota in Mongolian gerbils (Meriones unguiculatus).Communications biology · 2025Article
- Downregulation of the cysE/cysK genes of Clostridioides difficile induced by cysteine revealed the response of bacteria to iron homeostasis.BMC microbiology · 2025Article
- The monoclonal antibody AZD5148 confers broad protection against TcdB-diverse Clostridioides difficile strains in mice.PLoS pathogens · 2025Article
- The emerging view on the roles of butyrate inInfection and immunity · 2025Review
- Unravelling three-way interactions betweenJournal of medical microbiology · 2025Review
405 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Commented on by
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Clostridium difficile infection is the leading cause of healthcare-associated diarrhoea in Europe and North America. During infection, C. difficile produces two key virulence determinants, toxin A and toxin B. Experiments with purified toxins have indicated that toxin A alone is able to evoke the symptoms of C. difficile infection, but toxin B is unable to do so unless it is mixed with toxin A or there is prior damage to the gut mucosa. However, a recent study indicated that toxin B is essential for C. difficile virulence and that a strain producing toxin A alone was avirulent. This creates a paradox over the individual importance of toxin A and toxin B. Here we show that isogenic mutants of C. difficile producing either toxin A or toxin B alone can cause fulminant disease in the hamster model of infection. By using a gene knockout system to inactivate the toxin genes permanently, we found that C. difficile producing either one or both toxins showed cytotoxic activity in vitro that translated directly into virulence in vivo. Furthermore, by constructing the first ever double-mutant strain of C. difficile, in which both toxin genes were inactivated, we were able to completely attenuate virulence. Our findings re-establish the importance of both toxin A and toxin B and highlight the need to continue to consider both toxins in the development of diagnostic tests and effective countermeasures against C. difficile.
Indexed as
Identifiers
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.