Evidence map›Paper›PMID 25653402›Full record

ArticleJournal of clinical microbiology2015

Emergence of an outbreak-associated Clostridium difficile variant with increased virulence.

Carlos Quesada-Gómez, Diana López-Ureña, Luis Acuña-Amador, Manuel Villalobos-Zúñiga, Tim Du, Rosemayre Freire, Caterina Guzmán-Verri, María del Mar Gamboa-Coronado, Trevor D Lawley, Edgardo Moreno and 5 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of clinical microbiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
6.2field-weighted citation impact, top 3% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. The Global Burden ofInfectious disease reports · 2025
    Review
  4. Article
  5. Advances in diagnostic assays forFrontiers in cellular and infection microbiology · 2024
    Review
  6. Review
  7. Observational
  8. Article
  9. Gut Microbiota and Diarrhea: An Updated Review.Frontiers in cellular and infection microbiology · 2021
    Review
  10. Article
  11. Review
  12. Burden ofIranian journal of public health · 2019
    Review
  13. Toxin B Variants fromToxins · 2019
    Article
  14. Review
  15. Article
  16. The evolving epidemiology ofCMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne · 2018
    Article
  17. Epidemiological aspects of healthcare-associated infections and microbial genomics.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2018
    Review
  18. Article
  19. Article
  20. 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

15 authors at 5 institutions in 4 countries.

Carlos Quesada-GómezFacultad de Microbiología and Centro de Investigación en Enfermedades Tropicales, Universidad de Costa Rica, San José, Costa Rica.
Diana López-UreñaFacultad de Microbiología and Centro de Investigación en Enfermedades Tropicales, Universidad de Costa Rica, San José, Costa Rica.
Luis Acuña-AmadorFacultad de Microbiología and Centro de Investigación en Enfermedades Tropicales, Universidad de Costa Rica, San José, Costa Rica.
Manuel Villalobos-ZúñigaHospital San Juan de Dios, CCSS, San José, Costa Rica.
Tim DuNational Microbiology Laboratory, Public Health Agency of Canada, Winnipeg, Manitoba, Canada.
Rosemayre FreireDepartamento de Morfologia, Universidade Federal do Ceará, Fortaleza, Brazil.
Caterina Guzmán-VerriPrograma de Investigación en Enfermedades Tropicales, Escuela de Medicina Veterinaria, Universidad Nacional, Heredia, Costa Rica.
María del Mar Gamboa-CoronadoFacultad de Microbiología and Centro de Investigación en Enfermedades Tropicales, Universidad de Costa Rica, San José, Costa Rica.
Trevor D LawleyHost-Microbiota Interactions Laboratory, Wellcome Trust Sanger Institute, Hinxton, United Kingdom.
Edgardo MorenoPrograma de Investigación en Enfermedades Tropicales, Escuela de Medicina Veterinaria, Universidad Nacional, Heredia, Costa Rica Instituto Clodomiro Picado, Universidad de Costa Rica, San José, Costa Rica.
Michael R MulveyNational Microbiology Laboratory, Public Health Agency of Canada, Winnipeg, Manitoba, Canada.
Gerly Anne de Castro BritoDepartamento de Morfologia, Universidade Federal do Ceará, Fortaleza, Brazil.
Evelyn Rodríguez-CavalliniFacultad de Microbiología and Centro de Investigación en Enfermedades Tropicales, Universidad de Costa Rica, San José, Costa Rica.
César RodríguezFacultad de Microbiología and Centro de Investigación en Enfermedades Tropicales, Universidad de Costa Rica, San José, Costa Rica.
Esteban Chaves-OlarteFacultad de Microbiología and Centro de Investigación en Enfermedades Tropicales, Universidad de Costa Rica, San José, Costa Rica esteban.chaves@ucr.ac.cr.
Universidad de Costa Rica · CRPublic Health Agency of Canada · CAUniversidade Federal do Ceará · BRUniversidad Nacional · CRWellcome Sanger Institute · GB

Funding

Wellcome TrustWellcome Trust 086418Wellcome Trust 098051
6 · The paper itself

Abstract

The prevalence of Clostridium difficile infections has increased due to the emergence of epidemic variants from diverse genetic lineages. Here we describe the emergence of a novel variant during an outbreak in a Costa Rican hospital that was associated with severe clinical presentations. This C. difficile variant elicited higher white blood cell counts and caused disease in younger patients than did other strains isolated during the outbreak. Furthermore, it had a recurrence rate, a 30-day attributable disease rate, and disease severity as great as those of the epidemic strain NAP1. Pulsed-field gel electrophoresis genotyping indicated that the outbreak strains belong to a previously undescribed variant, designated NAPCR1. Whole-genome sequencing and ribotyping indicated that the NAPCR1 variant belongs to C. difficile ribotype 012 and sequence type 54, as does the reference strain 630. NAPCR1 strains are resistant to fluoroquinolones due to a mutation in gyrA, and they possess an 18-bp deletion in tcdC that is characteristic of the epidemic, evolutionarily distinct, C. difficile NAP1 variant. NAPCR1 genomes contain 10% more predicted genes than strain 630, most of which are of hypothetical function and are present on phages and other mobile genetic elements. The increased virulence of NAPCR1 was confirmed by mortality rates in the hamster model and strong inflammatory responses induced by bacteria-free supernatants in the murine ligated loop model. However, NAPCR1 strains do not synthesize toxin A and toxin B at levels comparable to those in NAP1 strains. Our results suggest that the pathogenic potential of this emerging C. difficile variant is due to the acquisition of hypothetical functions associated with laterally acquired DNA.

Indexed as

Disease OutbreaksAnimalsClostridioides difficileClostridium InfectionsCosta RicaCross InfectionDiarrheaDisease Models, AnimalDNA, BacterialElectrophoresis, Gel, Pulsed-FieldFemaleGene Transfer, HorizontalGenotypeHospitalsHumansIntestinesDNA, BacterialVirulence Factors

Identifiers

PMID25653402
PMCPMC4365207
OpenAlexW2122060112

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.