> 95% Pure. (Multi-step procedure including affinity chromatography.)
Format
Purified
Concentration
Batch dependent - please inquire should you have specific requirements.
Buffer
Tris buffer with salts, pH 7.6.
Preservative
0.09% Sodium Azide
Storage
Store at 2-8°C.
Citations
Publication ()
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Background
Clostridium difficile is a gram-positive bacterium that commonly inhabits the human gastrointestinal tract. It is the primary causative agent of antibiotic-associated diarrhea and pseudomembranous colitis, which can be severe and life-threatening. The detection of specific proteins such as glutamate dehydrogenase (GDH) produced by C. difficile is crucial for diagnosis and understanding the pathogenesis of the infection. C. difficile GDH protein is an enzyme that plays a vital role in the metabolism of glutamate. It catalyzes the reversible reaction between glutamate and α-ketoglutarate, contributing to the conversion of amino acids and the production of energy in the bacterium. GDH is highly conserved among different strains of C. difficile and is produced abundantly during infection. The detection of GDH protein has become an essential component of laboratory diagnostics for C. difficile infection. Enzyme immunoassays (EIAs) targeting GDH have been developed to identify the presence of C. difficile in patient samples, such as stool specimens. These assays utilize antibodies that specifically recognize and bind to GDH protein, allowing for its detection and subsequent diagnosis of C. difficile infection. GDH detection assays are highly sensitive and can provide rapid results, aiding in the prompt identification and management of C. difficile-associated diseases. In addition to its diagnostic significance, GDH protein has also been studied for its potential role in C. difficile virulence. It has been proposed that GDH contributes to the colonization and persistence of C. difficile in the gastrointestinal tract by facilitating the utilization of host-derived nutrients and enhancing the survival of the bacterium. Understanding the function and regulation of GDH protein can shed light on the pathogenesis of C. difficile infection and potentially lead to the development of novel therapeutic interventions.
Alternative Names
Recombinant Clostridium difficile GDH [His] Recombinant C. difficile Glutamate Dehydrogenase (GDH) [His] Recombinant Clostridium difficile Glutamate Dehydrogenase (GDH) [His] C. difficile GDH Recombinant Protein C. difficile Glutamate Dehydrogenase Recombinant Protein Clostridium difficile GDH Recombinant Protein
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References
The Role of Glutamate Dehydrogenase (GDH) Testing Assay in the Diagnosis of Clostridium difficile Infections: A High Sensitive Screening Test and an Essential Step in the Proposed Laboratory Diagnosis Workflow for Developing Countries like China
The incidence and severity of Clostridium difficile infection (CDI) in North America and Europe has increased significantly since the 2000s. However, CDI is not widely recognized in China and other developing countries due to limited laboratory diagnostic capacity and low awareness. Most published studies on laboratory workflows for CDI diagnosis are from developed countries, and thus may not be suitable for most developing countries. Therefore, an alternative strategy for developing countries is needed. In this study, we evaluated the performance of the Glutamate Dehydrogenase (GDH) test and its associated workflow on 416 fecal specimens from suspected CDI cases. The assay exhibited excellent sensitivity (100.0%) and specificity (92.8%), compared to culture based method, and thus could be a good screening marker for C. difficile but not for indication of toxin production. The VIDAS CDAB assay, which can detect toxin A/B directly from fecal specimens, showed good specificity (99.7%) and positive predictive value (97.2%), but low sensitivity (45.0%) and negative predictive value (88.3%), compared with PCR-based toxin gene detection. Therefore, we propose a practical and efficient GDH test based workflow strategy for the laboratory diagnosis of CDI in developing countries like China. By applying this new workflow, the CDI laboratory diagnosis rate was notably improved in our center, yet the increasing cost was kept at a minimum level. Furthermore, to gain some insights into the genetic population structure of C. difficile isolates from our hospital, we performed MLST and PCR toxin gene typing.
Importance of Glutamate Dehydrogenase (GDH) in Clostridium difficile Colonization In Vivo
PLoS One
Authors: Girinathan B P, Braun S, Sirigireddy A R, et al.
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. In this study, we show that glutamate utilization is important for C. difficile to establish itself in the animal gut. When the gluD gene, which codes for glutamate dehydrogenase (GDH), was disrupted, the mutant C. difficile was unable to colonize and cause disease in a hamster model. Further, from the complementation experiment it appears that extracellular GDH may be playing a role in promoting C. difficile colonization and disease progression. Quantification of free amino acids in the hamster gut during C. difficile infection showed that glutamate is among preferred amino acids utilized by C. difficile during its expansion. This study provides evidence of the importance of glutamate metabolism for C. difficile pathogenesis.
Clostridioides (Clostridium) difficile-associated disease: Epidemiology among patients in a general hospital in Saudi Arabia
AMERICAN JOURNAL OF INFECTION CONTROL
Authors: Al-Tawfiq, Jaffar A.; Rabaan, Ali A.; Bazzi, Ali M.; Raza, Safia; Noureen, Madeeha
Background: Clostridioides (Clostridium) difficile infection (CDI) is an important health care-associated infection with variable incidence and prevalence across the globe. There are limited data from Saudi Arabia on the epidemiology of C. difficile-associated diarrhea (CDAD). In this study, we present the epidemiology and incidence of CDAD in a hospital in Saudi Arabia. Methods: This study included all stool samples from 2001 to 2018 that were tested for C. difficile. C. difficile toxins were detected by enzyme-linked immunosorbent assay in 2001-2012 and the diagnosis was based on PCR testing (2013-2018). Results: There was a total of 577 distinctive episodes of CDAD representing 5.2% of 10,995 tested stool samples with an annual positivity rate of 0.9%-11.8%. Of all CDAD cases, there were 230 (39.9%) community associated-CDAD, 105 (18.2%) community onset-health care facility associated disease, and 242 (42%) health care facility onset health care facility-associated disease (HCFO-HCFAD). There was a trend of increasing percentage of community onset-health care facility associated disease cases from 17% in 2001 to 20% in 2018 of all cases, and a trend towards less cases of community associated-CDAD from 85% to 50% over time. However, the percentages of HCFO-HCFAD percentages remained relatively stable. The rate of HCFO-HCFAD per 1,000 patient-days increased from 0.009 to 0.22 from 2001 to 2018, respectively. Conclusions: The rate of CDAD was 5.15% among all tested samples and that there is a large proportion of community associated-CDAD. The findings parallel the data from developed countries and deserve further studies in the risk factors for community-associated CDAD. (C) 2020 Association for Professionals in Infection Control and Epidemiology, Inc. Published by Elsevier Inc. All rights reserved.
Evaluation of Addition of Intravenous Metronidazole to Oral Vancomycin Therapy in Critically Ill Patients with Non-Fulminant Severe Clostridioides difficile Infection
PHARMACOTHERAPY
Authors: Vega, Ana D.; Heil, Emily L.; Blackman, Alison L.; Banoub, Mary; Johnson, Jennifer Kristie; Leekha, Surbhi; Claeys, Kimberly C.
Background Data on the impact of combination therapy (intravenous metronidazole [IV MTZ] plus oral vancomycin [PO VAN]) on clinical outcomes in intensive care unit (ICU) patients with severe non-fulminant Clostridioides difficile infection (CDI), including NAP1-positive samples, are lacking. Methods Retrospective observational cohort of adult patients who developed CDI in the ICU diagnosed with severe non-fulminant CDI who received PO VAN. Patients with an order for IV MTZ started within 72 hours of PO VAN and who received at least 72 hours of combined therapy composed the combination therapy group. A subset of patients had stool samples collected for NAP1 testing. An additional subset was matched by Acute Physiology and Chronic Health Evaluation (APACHE) II scores. The primary outcome was inpatient all-cause mortality within 30 days of CDI diagnosis. Results A total of 138 patients were included with 60 (43.5%) patients in the combination group. Compared with the PO VAN group, those in the combination group had higher white blood cell counts at diagnosis (15.9 [interquartile range (IQR) 10.2-21.1] vs 20.9 [IQR 16.2-29] cells/mm(3), p<0.001), respectively. Overall inpatient mortality was higher in the combination group, but 30-day mortality was not significantly different between groups (12.8% monotherapy vs 18.3% combination, p=0.371). This finding was the same for the 96 patients in the APACHE II-matched subgroup, 14.6% monotherapy versus 18.8% combination, p=0.785. NAP1 testing was completed in 42 patients; 11 were positive (26.2%). Patients who were NAP1 positive were more likely to receive IV MTZ (54.5% vs 19.4%, p=0.026). Conclusion Compared with PO VAN, combination therapy with IV MTZ was not associated with better clinical outcomes in severe non-fulminant CDI in ICU patients.