Latest Research on Clostridioides difficile

A special issue of Microorganisms (ISSN 2076-2607). This special issue belongs to the section "Medical Microbiology".

Deadline for manuscript submissions: closed (31 October 2024) | Viewed by 1357

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Public Health Ontario Laboratories, Toronto, ON M5G 1M1, Canada
Interests: microbiology; epidemiology; pathology; treatmen; diagnostics
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Special Issue Information

Dear Colleagues,

The pathology of diseases caused by Clostridioides difficile (CD) has been augmented over time by changing population dynamics, healthcare, and agriculture practices and the varied genetics of the organism. Among these changes are the introduction of broad-spectrum antibiotics; the emergence of an outbreak-related strain, NAP1/027; and the consequences of the COVID-19 pandemic. During the pandemic, improved infection control methods decreased the incidence of hospital-acquired CD infection (CDI) but research on the biology, epidemiology, and treatment of CDI stagnated.

Recently, there has been renewed interest in previously developed methods of controlling this infection, including therapy with fecal microbiota transplants; using a mix of beneficial bacteria, therapeutic proteins, antibiotics; and the development of toxoid-based vaccines. The efficiency of these methods and newly developed approaches is also continually affected by the changing characteristics of CDI; its features have changed due to the replacement of hospital-acquired infections with community-acquired cases and more efficient infection control in hospitals.

This Special Issue aims to present new information on various aspects of this pathogen: its biology, the pathology of the disease, existing methods of detection, epidemiology, treatment options and approaches, and the healthcare costs of the disease.

As the Guest Editor of this Special Issue, I invite you to submit research articles, reviews, and short communications related to Clostridioides difficile.

Prof. Dr. George Broukhanski
Guest Editor

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Keywords

  • Clostridioides difficile
  • biology
  • epidemiology
  • pathogenicity
  • detection
  • treatment
  • infection control

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Published Papers (1 paper)

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Research

15 pages, 2335 KiB  
Article
A Mouse Model of Mild Clostridioides difficile Infection for the Characterization of Natural Immune Responses
by Assaf Mizrahi, Gauthier Péan de Ponfilly, Diane Sapa, Antonia Suau, Irène Mangin, Aurélie Baliarda, Sandra Hoys, Benoît Pilmis, Sylvie Lambert, Anaïs Brosse and Alban Le Monnier
Microorganisms 2024, 12(10), 1933; https://doi.org/10.3390/microorganisms12101933 - 24 Sep 2024
Viewed by 715
Abstract
(1) Background: We describe a model of primary mild-Clostridioides difficile infection (CDI) in a naïve host, including gut microbiota analysis, weight loss, mortality, length of colonization. This model was used in order to describe the kinetics of humoral (IgG, IgM) and mucosal [...] Read more.
(1) Background: We describe a model of primary mild-Clostridioides difficile infection (CDI) in a naïve host, including gut microbiota analysis, weight loss, mortality, length of colonization. This model was used in order to describe the kinetics of humoral (IgG, IgM) and mucosal (IgA) immune responses against toxins (TcdA/TcdB) and surface proteins (SlpA/FliC). (2) Methods: A total of 105 CFU vegetative forms of C. difficile 630Δerm were used for challenge by oral administration after dysbiosis, induced by a cocktail of antibiotics. Gut microbiota dysbiosis was confirmed and described by 16S rDNA sequencing. We sacrificed C57Bl/6 mice after different stages of infection (day 6, 2, 7, 14, 21, 28, and 56) to evaluate IgM, IgG against TcdA, TcdB, SlpA, FliC in blood samples, and IgA in the cecal contents collected. (3) Results: In our model, we observed a reproducible gut microbiota dysbiosis, allowing for C. difficile digestive colonization. CDI was objectivized by a mean weight loss of 13.1% and associated with a low mortality rate of 15.7% of mice. We observed an increase in IgM anti-toxins as early as D7 after challenge. IgG increased since D21, and IgA anti-toxins were secreted in cecal contents. Unexpectedly, neither anti-SlpA nor anti-FliC IgG or IgA were observed in our model. (4) Conclusions: In our model, we induced a gut microbiota dysbiosis, allowing a mild CDI to spontaneously resolve, with a digestive clearance observed since D14. After this primary CDI, we can study the development of specific immune responses in blood and cecal contents. Full article
(This article belongs to the Special Issue Latest Research on Clostridioides difficile)
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