Clostridium difficile and Clostridium perfringens research

This study investigates how strand-swapping in GerS, a LolA-like protein in C. difficile, affects its dimerization and ability to activate the amidase CwlD.

This study identifies Clostridium novyi type B as the cause of fatal hemorrhagic disease in wild Asian elephants through molecular diagnostic methods.

This study examines biofilm formation and properties of C. difficile undomesticated strains, finding that ribotype 009 strains form highly adhesive biofilms and show increased vancomycin tolerance.

The paper determines the structures of intermediate stages of pore formation by the Iota toxin's membrane-binding component using cryo-EM, revealing a stepwise maturation mechanism.

This study identifies caffeic acid phenethyl ester (CAPE) as an inhibitor of TcdB, a key toxin in Clostridioides difficile infection, showing reduced pathology and microbiota modulation in mice.

The paper reveals an allosteric mechanism in Clostridioides difficile toxins using MD simulations and mutagenesis, showing a switchable interaction network that drives conformational changes.

This study investigates whether inhibiting EGFR/ErbB receptors protects against C. difficile toxin B, finding no protective effect.

The paper characterizes the genome of a hypervirulent C. difficile strain, identifying genes associated with pathogenesis and antibiotic resistance.

The paper discusses the use of genomic resources for spore-forming pathogens like Clostridia to improve outbreak detection, disease prevention, and understanding of their persistence and virulence across environments.

The paper develops a systems biology pipeline to design bacterial consortia that protect against severe Clostridioides difficile infection by targeting amino acid cross-feeding.

The paper uses microbial community-scale metabolic models to predict C. difficile engraftment risk and assess probiotic therapy efficacy in the human gut.

The paper analyzes genetic diversity and antibiotic resistance of Clostridium perfringens isolates from humans, animals, and food in China using MLST, cgMLST, and cgSNP, revealing high genetic diversity and potential transmission events.

This study identifies microbial interactions affecting C. difficile's antibiotic response using human gut communities and transcriptional profiling.

The paper compares core genome MLST (cgMLST) with CE-PCR ribotyping and SNP analysis for C. difficile typing, finding cgMLST offers better discrimination but may require adjusted thresholds for outbreak detection.

The paper identifies SEMA6A and SEMA6B as receptors for C. sordellii lethal toxin and shows how mutations can switch receptor specificity between related toxins.

This paper identifies CD31 as the receptor for Clostridium perfringens β-toxin, explaining its cell type specificity and toxicity.

This study shows that certain antibiotics increase CDAD risk through host-driven changes, not just microbiome disruption, by impairing mucosal barriers and immune function in human gut models.

This study characterizes the epigenome of C. difficile and identifies a conserved DNA methyltransferase that impacts sporulation and other biological processes.

The paper compares gut microbiota composition in ICU patients with Clostridium difficile-positive diarrhea and different C. difficile types using 16S rDNA and metagenome sequencing.