Regulatory networks: Linking toxin production and sporulation in Clostridioides difficile.

Clostridioides difficile has been recognized as an important nosocomial pathogen that causes diarrheal disease as a consequence of antibiotic exposure and costs the healthcare system billions of dollars every year. C. difficile enters the host gut as dormant spores, germinates into vegetative cells, colonizes the gut, and produces toxins TcdA and/or TcdB, leading to diarrhea and inflammation.

Role of glycogen metabolism in virulence.

Glycogen plays a vital role as an energy reserve in various bacterial and fungal species. possesses a glycogen metabolism operon that contains genes for both glycogen synthesis and utilization. In our investigation, we focused on understanding the significance of glycogen metabolism in the physiology and pathogenesis of .

Preventing the spread of life-threatening gastrointestinal microbes on the surface of a continuously self-disinfecting block polymer.

Highly persistent, drug-resistant and transmissible healthcare pathogens such as Clostridioides difficile (C. difficile) and Candida auris (C. auris) are responsible for causing antibiotic-associated fatal diarrhea and invasive candidiasis, respectively.

Regulation of Clostridioides difficile toxin production.

Clostridioides difficile produces toxins TcdA and TcdB during infection. Since the severity of the illness is directly correlated with the level of toxins produced, researchers have long been interested in the regulation mechanisms of toxin production. The advent of new genetics and mutagenesis technologies in C.

Phase-variable expression of pdcB, a phosphodiesterase, influences sporulation in Clostridioides difficile.

Clostridioides difficile is the causative agent of antibiotic-associated diarrhea and is the leading cause of nosocomial infection in developed countries. An increasing number of C. difficile infections are attributed to epidemic strains that produce more toxins and spores.

Characterization of an operon required for growth on cellobiose in .

Cellobiose metabolism is linked to the virulence properties in numerous bacterial pathogens. Here, we characterized a putative cellobiose PTS operon of to investigate the role of cellobiose metabolism in pathogenesis. Our gene knockout experiments demonstrated that the putative cellobiose operon enables uptake of cellobiose into and allows growth when cellobiose is provided as the sole carbon source in minimal medium.

Spo0A Suppresses Locus Expression in Clostridioides difficile.

is the leading cause of nosocomial infection and is the causative agent of antibiotic-associated diarrhea. The severity of the disease is directly associated with toxin production, and spores are responsible for the transmission and persistence of the organism. Previously, we characterized locus regulators SinR and SinR' (we renamed it SinI), where SinR is the regulator of toxin production and sporulation.

A simplified method for producing laboratory grade recombinant TEV protease from E. coli.

The tobacco etch virus (TEV) protease has become a popular choice for cleaving fusion proteins because of its high stringency in sequence recognition. Procedures for isolating recombinant protein from the cytoplasm of E. coli require rupturing of the cell wall via enzymatic treatment combined with sonication or French press.

Clostridioides difficile SinR' regulates toxin, sporulation and motility through protein-protein interaction with SinR.

Clostridioides difficile is a Gram-positive, anaerobic bacterium. It is known that C. difficile is one of the major causes of antibiotic associated diarrhea.

Pleiotropic roles of Clostridium difficile sin locus.

Clostridium difficile is the primary cause of nosocomial diarrhea and pseudomembranous colitis. It produces dormant spores, which serve as an infectious vehicle responsible for transmission of the disease and persistence of the organism in the environment. In Bacillus subtilis, the sin locus coding SinR (113 aa) and SinI (57 aa) is responsible for sporulation inhibition.

Effect of Mutation on Sporulation in the Epidemic Strain R20291.

is an important nosocomial pathogen and the leading cause of hospital-acquired diarrhea. Antibiotic use is the primary risk factor for the development of -associated disease because it disrupts normally protective gut flora and enables to colonize the colon. damages host tissue by secreting toxins and disseminates by forming spores.

Correction: Importance of Glutamate Dehydrogenase (GDH) in Clostridium difficile Colonization In Vivo.

[This corrects the article DOI: 10.1371/journal.pone.

Importance of Glutamate Dehydrogenase (GDH) in Clostridium difficile Colonization In Vivo.

Clostridium difficile is the principal cause of antibiotic-associated diarrhea. Major metabolic requirements for colonization and expansion of C. difficile after microbiota disturbance have not been fully determined.

Enhanced D-lactic acid production from renewable resources using engineered Lactobacillus plantarum.

D-lactic acid is used as a monomer in the production of poly-D-lactic acid (PDLA), which is used to form heat-resistant stereocomplex poly-lactic acid. To produce cost-effective D-lactic acid by using all sugars derived from biomass efficiently, xylose-assimilating genes encoding xylose isomerase and xylulokinase were cloned into an L-lactate-deficient strain, Lactobacillus plantarum. The resulting recombinant strain, namely L.

Observations on the Role of TcdE Isoforms in Clostridium difficile Toxin Secretion.

Unlabelled: Clostridium difficile is a major nosocomial pathogen and the principal causative agent of antibiotic-associated diarrhea. The toxigenic C. difficile strains that cause disease secrete virulence factors, toxin A and toxin B, that cause colonic injury and inflammation.

Clostridium difficile glutamate dehydrogenase is a secreted enzyme that confers resistance to H2O2.

Clostridium difficile produces an NAD-specific glutamate dehydrogenase (GDH), which converts l-glutamate into α-ketoglutarate through an irreversible reaction. The enzyme GDH is detected in the stool samples of patients with C. difficile-associated disease and serves as one of the diagnostic tools to detect C.

Identification and characterization of Clostridium sordellii toxin gene regulator.

Toxigenic Clostridium sordellii causes uncommon but highly lethal infections in humans and animals. Recently, an increased incidence of C. sordellii infections has been reported in women undergoing obstetric interventions.

Secretion of Clostridium difficile toxins A and B requires the holin-like protein TcdE.

The pathogenesis of Clostridium difficile, the major cause of antibiotic-associated diarrhea, is mainly associated with the production and activities of two major toxins. In many bacteria, toxins are released into the extracellular environment via the general secretion pathways. C.

The anti-sigma factor TcdC modulates hypervirulence in an epidemic BI/NAP1/027 clinical isolate of Clostridium difficile.

Nosocomial infections are increasingly being recognised as a major patient safety issue. The modern hospital environment and associated health care practices have provided a niche for the rapid evolution of microbial pathogens that are well adapted to surviving and proliferating in this setting, after which they can infect susceptible patients. This is clearly the case for bacterial pathogens such as Methicillin Resistant Staphylococcus aureus (MRSA) and Vancomycin Resistant Enterococcus (VRE) species, both of which have acquired resistance to antimicrobial agents as well as enhanced survival and virulence properties that present serious therapeutic dilemmas for treating physicians.

In vivo lysogenization of a Clostridium difficile bacteriophage ФCD119.

Clostridium difficile is a nosocomial pathogen identified as the cause of antibiotic-associated diarrhea and colitis. In this study, we have documented the lysogeny of a C. difficile bacteriophage in hamsters during C.

Bacteriophage-mediated toxin gene regulation in Clostridium difficile.

Clostridium difficile has been identified as the most important single identifiable cause of nosocomial antibiotic-associated diarrhea and colitis. Virulent strains of C. difficile produce two large protein toxins, toxin A and toxin B, which are involved in pathogenesis.

Evidence that Clostridium difficile TcdC is a membrane-associated protein.

Clostridium difficile produces two toxins, A and B, which act together to cause pseudomembraneous colitis. The genes encoding these toxins, tcdA and tcdB, are part of the pathogenicity locus, which also includes tcdC, a putative negative regulator of the toxin genes. In this study, we demonstrate that TcdC is a membrane-associated protein in C.

Genomic organization and molecular characterization of Clostridium difficile bacteriophage PhiCD119.

In this study, we have isolated a temperate phage (PhiCD119) from a pathogenic Clostridium difficile strain and sequenced and annotated its genome. This virus has an icosahedral capsid and a contractile tail covered by a sheath and contains a double-stranded DNA genome. It belongs to the Myoviridae family of the tailed phages and the order Caudovirales.