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Academic literature on the topic 'Clostridium difficile toxins'

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Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Clostridium difficile toxins"

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Giesemann, Torsten, Martina Egerer, Thomas Jank, and Klaus Aktories. "Processing of Clostridium difficile toxins." Journal of Medical Microbiology 57, no. 6 (June 1, 2008): 690–96. http://dx.doi.org/10.1099/jmm.0.47742-0.

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The pathogenicity of Clostridium difficile depends on the large clostridial glucosylating toxins A and B (TcdA and TcdB). The proteins accomplish their own uptake by a modular structure comprising a catalytic and a binding/translocation domain. Based on a proteolytic processing step solely the catalytic domain reaches the cytosol. Within the cells, the glucosyltransferases inactivate small GTPases by mono-O-glucosylation. Here, a short overview is given regarding latest insights into the intramolecular processing, which is mediated by an intrinsic protease activity.
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Lyerly, D. M., H. C. Krivan, and T. D. Wilkins. "Clostridium difficile: its disease and toxins." Clinical Microbiology Reviews 1, no. 1 (January 1988): 1–18. http://dx.doi.org/10.1128/cmr.1.1.1.

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Clostridium difficile is the etiologic agent of pseudomembranous colitis, a severe, sometimes fatal disease that occurs in adults undergoing antimicrobial therapy. The disease, ironically, has been most effectively treated with antibiotics, although some of the newer methods of treatment such as the replacement of the bowel flora may prove more beneficial for patients who continue to relapse with pseudomembranous colitis. The organism produces two potent exotoxins designated toxin A and toxin B. Toxin A is an enterotoxin believed to be responsible for the diarrhea and mucosal tissue damage which occur during the disease. Toxin B is an extremely potent cytotoxin, but its role in the disease has not been as well studied. There appears to be a cascade of events which result in the expression of the activity of these toxins, and these events, ranging from the recognition of a trisaccharide receptor by toxin A to the synergistic action of the toxins and their possible dissemination in the body, are discussed in this review. The advantages and disadvantages of the various assays, including tissue culture assay, enzyme immunoassay, and latex agglutination, currently used in the clinical diagnosis of the disease also are discussed.
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Reisinger, Emil Christian, Meinolf Ebbers, and Micha Löbermann. "Clostridium difficile: Antikörpertherapie und Impfungen." DMW - Deutsche Medizinische Wochenschrift 144, no. 12 (June 2019): 842–49. http://dx.doi.org/10.1055/a-0882-7530.

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AbstractHospital-acquired Clostridium difficile infections have become much more frequent in recent years. Besides treatment with antibiotics and fecal microbiota transplant, new preventive strategies are available now. Bezlotoxumab is an antibody against toxin B and may reduce the risk of relapse by roughly 10 %. Several vaccine candidates against toxins A and B and surface-associated antigens were immunogenic and are tested in clinical trials to investigate the efficacy and safety.
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Belyi, Yu F., S. V. Fialkina, and V. I. Troitskii. "Role of toxins in Clostridium difficile pathogenicity." Experimental and Clinical Gastroenterology 160, no. 12 (December 2018): 4–10. http://dx.doi.org/10.31146/1682-8658-ecg-160-12-4-10.

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Wilkins, Tracy D., and David M. Lyerly. "Clostridium difficile toxins attack Rho." Trends in Microbiology 4, no. 2 (February 1996): 49–51. http://dx.doi.org/10.1016/0966-842x(96)81508-3.

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Cimolai, Nevio. "Are Clostridium difficile toxins nephrotoxic?" Medical Hypotheses 126 (May 2019): 4–8. http://dx.doi.org/10.1016/j.mehy.2019.03.002.

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Kelly, C. P., C. Pothoulakis, F. Vavva, I. Castagliuolo, E. F. Bostwick, J. C. O'Keane, S. Keates, and J. T. LaMont. "Anti-Clostridium difficile bovine immunoglobulin concentrate inhibits cytotoxicity and enterotoxicity of C. difficile toxins." Antimicrobial Agents and Chemotherapy 40, no. 2 (February 1996): 373–79. http://dx.doi.org/10.1128/aac.40.2.373.

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Clostridium difficile diarrhea and colitis result from the actions of bacterial exotoxins on the colonic mucosa. This study examined the ability of hyperimmune bovine colostral antibodies to neutralize the biological effects of these toxins. Anti-C. difficile bovine immunoglobulin concentrate was prepared from the colostral milk of Holstein cows previously immunized with C. difficile toxoids. The anti-C. difficile bovine immunoglobulin concentrate contained high levels of bovine immunoglobulin G specific for C. difficile toxins A and B, as evaluated by enzyme-linked immunosorbent assay. Anti-C. difficile bovine immunoglobulin concentrate neutralized the cytotoxic effects of purified toxin A and toxin B on cultured human fibroblasts, whereas control bovine immunoglobulin concentrate had little toxin-neutralizing activity. Anti-C. difficile bovine immunoglobulin concentrate also blocked the binding of toxin A to its enterocyte receptor and inhibited the enterotoxic effects of C. difficile toxins on the rat ileum, as measured by an increased rat ileal loop weight/length ratio (63% inhibition; P < 0.01), increased mannitol permeability (92% inhibition; P < 0.01), and histologic grading of enteritis (P < 0.01 versus nonimmune bovine immunoglobulin concentrate). Thus, anti-C. difficile bovine immunoglobulin concentrate neutralizes the cytotoxic effects of C. difficile toxins in vitro and inhibits their enterotoxic effects in vivo. This agent may be clinically useful in the prevention and treatment of C. difficile diarrhea and colitis.
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Salcedo, J., S. Keates, C. Pothoulakis, M. Warny, I. Castagliuolo, J. T. LaMont, and C. P. Kelly. "Intravenous immunoglobulin therapy for severe Clostridium difficile colitis." Gut 41, no. 3 (September 1, 1997): 366–70. http://dx.doi.org/10.1136/gut.41.3.366.

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Background—Many individuals have serum antibodies against Clostridium difficile toxins. Those with an impaired antitoxin response may be susceptible to recurrent, prolonged, or severe C difficile diarrhoea and colitis.Aims—To examine whether treatment with intravenous immunoglobulin might be effective in patients with severe pseudomembranous colitis unresponsive to standard antimicrobial therapy.Patients—Two patients with pseudomembranous colitis not responding to metronidazole and vancomycin were given normal pooled human immunoglobulin intravenously (200–300 mg/kg).Methods—Antibodies against C difficile toxins were measured in nine immunoglobulin preparations by ELISA and by cytotoxin neutralisation assay.Results—Both patients responded quickly as shown by resolution of diarrhoea, abdominal tenderness, and distension. All immunoglobulin preparations tested contained IgG against C difficile toxins A and B by ELISA and neutralised the cytotoxic activity of C difficile toxins in vitro at IgG concentrations of 0.4–1.6 mg/ml.Conclusion—Passive immunotherapy with intravenous immunoglobulin may be a useful addition to antibiotic therapy for severe, refractory C difficile colitis. IgG antitoxin is present in standard immunoglobulin preparations andC difficile toxin neutralising activity is evident at IgG concentrations which are readily achieved in the serum by intravenous immunoglobulin administration.
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McMillin, David E., Lycurgus L. Muldrow, and Shwanda J. Laggette. "Simultaneous detection of toxin A and toxin B genetic determinants of Clostridium difficile using the multiplex polymerase chain reaction." Canadian Journal of Microbiology 38, no. 1 (January 1, 1992): 81–83. http://dx.doi.org/10.1139/m92-013.

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A multiplex polymerase chain reaction was developed to simultaneously detect the presence of toxin A and toxin B genes of Clostridium difficile. A 1050-bp fragment of the toxin B gene and a 1217-bp fragment of the toxin A gene were amplified from 42 toxic strains of C. difficile; however, from 10 nontoxic strains the toxin gene fragments were not amplified; these data demonstrate that this multiplex polymerase chain reaction procedure can be used to differentiate between toxic and nontoxic strains. This sensitive and specific multiplex polymerase chain reaction for C. difficile toxins may prove to be a valuable diagnostic procedure. Key words: Clostridium difficile, polymerase chain reaction, bacterial toxins.
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Govind, Revathi, Govindsamy Vediyappan, Rial D. Rolfe, and Joe A. Fralick. "Evidence that Clostridium difficile TcdC Is a Membrane-Associated Protein." Journal of Bacteriology 188, no. 10 (May 15, 2006): 3716–20. http://dx.doi.org/10.1128/jb.188.10.3716-3720.2006.

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ABSTRACT 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. difficile.
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Dissertations / Theses on the topic "Clostridium difficile toxins"

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Karlsson, Sture. "Toxin production in Clostridium difficile /." Stockholm : Karolinska institutet, 2004. http://diss.kib.ki.se/2004/91-77349-812-2/.

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Mullan, Nivette K. "Mucosal cell responses to Clostridium difficile toxins." Thesis, University of Nottingham, 2011. http://eprints.nottingham.ac.uk/13217/.

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Colonic inflammation in C. difficile infection is mediated by released toxins A and B. I have investigated responses to C. difficile toxin A and B by primary human colonic myofibroblasts, which represent a distinct subpopulation of mucosal cells that are normally located below the intestinal epithelium and epithelial cell lines, Caco-2 and HT29. Myofibroblasts, isolated from normal human colonic mucosal specimens, Caco-2 and HT29 cells incubated with purified toxin A or B displayed a dose dependent response. Myofibroblast morphology changed to a stellate shaped cell, with processes that were immunoreactive for alpha smooth muscle actin. Most of the myofibroblasts remained viable, with persistent stellate morphology, despite exposure to high concentrations (up to 10 μ g/ml) of toxin A for 72 h. In contrast, a majority of the toxin B exposed myofibroblasts lost their processes prior to cell death over 24-72 h. Investigating toxin A+B on myofibroblasts, at low concentrations, toxin A provided protection against toxin B-induced cell death. Most of the intestinal epithelial, HT29 cells remained viable despite exposure to high concentrations of either toxin (up to 10 μ g/mi). By contrast, a significant loss in cell viability was observed in Caco-2 cells exposed to either toxin. Within 4 h, myofibroblast and epithelial cell types exposed to either toxin A or B lost expression of the non-glucosylated form of Racl, but total intracellular RhoA remained unchanged in myofibroblasts and Caco-2 cells. A time-dependent reduction in RhoA expression was seen in HT29 in response to toxin A or B. Active RhoA expression was lost within 4h in myofibroblasts exposed to either toxin. Despite pre-exposure to high concentrations of toxin A for 3 h, colonic myofibroblasts were able to recover their morphology and proliferative capacity during prolonged culture in medium. This was also shown when pre-exposure to toxin A was extended to 48 h. However, toxin B-pre-exposed myofibroblasts were not able to recover. In conclusion, primary human colonic mucosal myofibroblasts are resistant to toxin A (but not toxin B)-induced cell death. Responses by colonic myoflbroblasts may play an important role in mucosal protection, repair, and regeneration in colitis due to C. difficile infection. Investigation into the apparent resilience of HT29 cells has highlighted the importance of cell specific substrate specificity by C. difficile toxins.
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Hussack, Greg. "Single-domain Antibody Inhibitors of Clostridium difficile Toxins." Thèse, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/20362.

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Clostridium difficile is a leading cause of nosocomial infection in North America and a considerable challenge to healthcare professionals in hospitals and nursing homes. The Gram-positive bacterium produces two exotoxins, toxin A (TcdA) and toxin B (TcdB), which are the major virulence factors responsible for C. difficile-associated disease (CDAD) and are targets for CDAD therapy. In this work, recombinant single-domain antibody fragments (VHHs) which target the cell receptor binding domains of TcdA or TcdB were isolated from an immune, llama phage display library and characterized. Four VHHs (A4.2, A5.1, A20.1, and A26.8) were potent neutralizers of the cytopathic effects of TcdA in an in vitro assay and the neutralizing potency was enhanced when VHHs were administered in combinations. Epitope mapping experiments revealed that some synergistic combinations consisted of VHHs recognizing overlapping epitopes, an indication that factors other than mere epitope blocking are responsible for the increased neutralization. Binding assays revealed TcdA-specific VHHs neutralized TcdA by binding to sites other than the carbohydrate binding pocket of the toxin. The TcdB-specific VHHs failed to neutralize TcdB, as did a panel of human VL antibodies isolated from a synthetic library. To enhance the stability of the C. difficile TcdA-specific VHHs for oral therapeutic applications, the VHHs were expressed with an additional disulfide bond by introducing Ala/Gly54Cys and Ile78Cys mutations. The mutant VHHs were found to be well expressed, were non-aggregating monomers, retained low nM affinity for TcdA, and were capable of in vitro TcdA neutralization. Digestion of the VHHs with the major gastrointestinal proteases, at biologically relevant concentrations, revealed a significant increase in pepsin resistance for all mutants and an increase in chymotrypsin resistance for the majority of mutants without compromising inherent VHH trypsin resistance. Collectively, the second disulfide not only increased VHH thermal stability at neutral pH, as previously shown, but also represents a generic strategy to increase VHH stability at low pH and impart protease resistance. These are all desirable characteristics for the design of protein-based oral therapeutics. In conclusion, llama VHHs represent a class of novel, non-antibiotic inhibitors of infectious disease virulence factors such as C. difficile toxins.
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Shilling, Michael P. "Optimizing detection and control of Clostridium difficile and its toxins." Thesis, Kent State University, 2014. http://pqdtopen.proquest.com/#viewpdf?dispub=3618927.

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Clostridium difficile infection (CDI) is a bacterial disease affecting the lower gastrointestinal tract of patients whose normal colonic microbiota are altered, generally by administration of antibiotic therapies. C. difficile produces toxins that cause severe diarrhea, with potentially fatal complications in the immunocompromised. CDI has spread unabated despite the best prevention efforts of clinical practitioners. This dissertation is a broad-based study of several factors of importance in prevention and control CDI. In clinical environments, transport media are used to maintain the integrity of clinical samples for later laboratory testing. A transport medium for enteric bacteria was assessed as a preservative in outpatient fecal samples submitted for CDI testing. The transport medium used preserved C. difficile toxin out to five days. The possible effect of fecal pH and trypsin content on toxin stability was investigated. Fecal pH was ruled out as a factor due to CDI selected samples tending toward neutral pH. Trypsin was found to degrade toxin in controlled experiments; however, results from clinical samples were mixed. Oils and fatty acids, including virgin coconut oil (VCO), have antimicrobial effects on a variety of human pathogens. Use of natural products like VCO may reduce or prevent CDI by killing C. difficile while preserving the protective bowel flora. Virgin coconut oil (VCO) and three of its constituent fatty acids were evaluated for their toxic effect on C. difficile and were found to have bactericidal activity, the most potent of which was lauric acid. The outer surface of C. difficile spores is thought to contain proteins that are critical for attachment of the spores to surfaces, including human hands. This strong attachment assists in transmission of infectious spores; however, the source of this strong attachment in the spore remains unknown. Transmission electron micrography shows that C. difficile lacks a true exosporium, rather, they are coated in the remains of the mother cell. Results from subsequent fluorescence microscopy and ELISA with antibodies raised against spore coat proteins confirm that this residue is not part of the spore coat and can be easily removed by chemical treatment, increasing spore binding to anti-coat antibodies.

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Shilling, Michael. "OPTIMIZING DETECTION AND CONTROL OF CLOSTRIDIUM DIFFICILE AND ITS TOXINS." Kent State University / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=kent1374852321.

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Tsuchiya, Ana Claudia 1987. "Avaliação de métodos e ocorrência de Clostridium difficile em carnes." [s.n.], 2012. http://repositorio.unicamp.br/jspui/handle/REPOSIP/255444.

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Orientador: Arnaldo Yoshiteru Kuaye
Dissertação (mestrado) - Universidade Estadual de Campionas, Faculdade de Engenharia de Alimentos
Made available in DSpace on 2018-08-20T10:25:27Z (GMT). No. of bitstreams: 1 Tsuchiya_AnaClaudia_M.pdf: 449310 bytes, checksum: 3afe68453ac7a3b16148cef90be5c03f (MD5) Previous issue date: 2012
Resumo: Clostridium difficile é um bacilo anaeróbio responsável por doença intestinal associada ao tratamento prévio com antibióticos, manifestando desde uma diarreia leve até casos graves de colite pseudomembranosa causada principalmente pelas toxinas A (TcdA) e B (TcdB). Os casos de infecção estão relacionados à contaminação em hospitais, porém pesquisas recentes sugerem possível associação ao consumo de alimentos contaminados, pois C. difficile já foi isolado de bovinos, suínos e aves e suas carnes sugerindo os animais como reservatórios. Desta forma, os estudos são de suma importância para o entendimento da transmissão da doença causada por C. difficile. Diante de poucas pesquisas de C. difficile e da inexistência de método padronizado para seu isolamento a partir dos alimentos, o trabalho consistiu em três etapas: 1) avaliação de metodologia [utilizando dois procedimentos (tratamento com álcool e plaqueamento direto) e dois meios seletivos (ágar Clostridium difficile moxalactan norfloxacina ¿ CDMNA e ágar cicloserina cefoxitina frutose ¿ CCFA)] de detecção de C. difficile em carnes (bovina moída e peito de frango [Peitoralis profundus e superficialis]); 2) avaliação da ocorrência de C. difficile em amostras de carnes resfriadas (bovina moída, bovina peça [Semimembranosus], suína [Longuisimus dorsi] e frango [Peitoralis profundus e superficialis]), compreendendo detecção, isolamento e identificação dos isolados; 3) avaliação do perfil toxigênico dos isolados através da detecção de genes tcdA e tcdB codificadores de TcdA e TcdB e respectivamente avaliação de produção do toxinas pelos isolados. A partir da comparação de dois procedimentos, observou-se que o plaqueamento direto foi mais eficaz e recuperou uma maior quantidade de C. difficile se comparado com o tratamento com álcool e o ágar Clostridium difficile moxalactan norfloxacina (CDMNA) apresentou maior taxa de recuperação em relação ao ágar cicloserina cefoxitina frutose (CCFA). A ocorrência de C. difficile foi observada em 11,5% (17/147) das amostras analisadas, totalizando 80 isolados, destes 41,2% (33/83) apresentaram positivo para pelo menos um gene de virulência (A-B+), ou para ambos os genes (A+B+). Houve concordância de 70,5% entre os testes fenotípicos e genotípicos utilizados para detecção de toxinas. Desta forma, sugere-se que alimentos de origem animal são uma potencial fonte de transmissão de C. difficile para humanos
Abstract: Clostridium difficile is an anaerobic bacillus responsible for intestinal deseases in individuals previouslly treated with antibiocs, who can manifest from a mild diarrhea to severe cases of pseudomembranous colitis, mainly caused by toxins A (TcdA) and B (TcdB). The infections are related to contamination in hospitals, but recent researches sugests a possible association with the consumiption of contaminated foods as C. difficile has been isolated from bovines, suines and poultries and their meat, sugesting animals as reservatories. Thus, studies are extremelly important to elucidate the transmition of the desease caused by C. difficile. Faced with few researches about this bacteria and the lack of a standard method for its isolation from food, this work is divided in three steps: 1) Evaluation of the methodology for C. difficile detection in meet (commercial bovine mince and chicken breast ¿ [Peitoralis superficialis and Peitoralis profundus] [using two procedures (treatment with alcohol and direct plating) and two selective mediums (agar Clostridium difficile moxalactan norfloxacin ¿ CDMNA and cycloserine cefoxitin fructose agar¿ CCFA)]; 2) Assessing of the occurrence of C. difficile in samples of chilled meat (bovine: commercial mince and the whole Semimembranosus; suine: whole Longuisimus dorsi; chicken: Peitoralis profundus and Peitoralis superficialis) by detection, isolation and identification of the isolated; 3) Evaluation of the toxicogenic profile of the isolated by the detection of the genes tcdA and tcdB, which are encoding of TcdA and TcdB respectivelly, and the capacity of toxine production by the isolated bacterias. From the comparison of the two proceeding above it was observed that the direct plating was more efficient and recovered a larger aumont of C. difficile than the treatment with alcohol. Furthermore, the CDMNA agar presented a higher recovery rate compared to CCFA agar. It was observed the occurrence of C. difficile in 11,5% (17/147) of the analyzed samples, comprising 80 isolates, of which 41,2% (33/83) showed a positive response for at least one virulence gene (A-B+), or for both genes (A+B-). In addition, there was a 70,5% concordance between the phenotypic and genotypic tests used to detect toxins. In this way, it is suggested that foods of animal origin are a potential source of transmission of C. difficile for humans
Mestrado
Tecnologia de Alimentos
Mestre em Tecnologia de Alimentos
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Davies, Abigail. "Structure and biochemical analysis of toxins from the superbug Clostridium difficile." Thesis, University of Bath, 2014. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.619282.

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Clostridium difficile is a gram positive, anaerobic bacterium that is the leading cause of antibiotic-associated pseudomembranous colitis worldwide. C. difficile is an extremely infectious bacterium that produces spores that are highly resistant to standard disinfectant agents and can survive on surfaces for long periods of time. Both the resistance of the spores combined with multiple patients with low-immune systems has lead to an increase in hospital-acquired C. difficile infection, which has had a severe economic impact on the healthcare system. Due to the emerging antibiotic resistance problems and the common occurrence of patient relapse using the current drugs of choice, alternative therapeutic avenues are being explored. C.difficile produces two potent exotoxins; Toxin A and Toxin B that are the causative agents of infection. These toxins have multi-modular domain organisations, with each domain playing a role in cytotoxicity. Some of these domains have been characterised structurally using X-ray crystallography. In this thesis, the low resolution SAXS structure of Toxin A will be presented along with the advances made towards determining the X-ray crystallographic structure of the full-length Toxin A. In addition to Toxins A and B, some strains of C. difficile produce a binary toxin, CDT, which is made up of two individually produced components, CDTa and CDTb. The CDTa component is the enzymatically active component, whereas CDTb is the transport component, directly involved in translocating CDTa into target cells. The precise role of CDT in pathogenesis is unclear, however there is evidence that CDT ADP-ribosylates monomeric actin in target cells, but the detailed mechanism by which this reaction takes place is unknown. Here site directed mutagenesis of key residues of the active site of CDTa was performed and the effect of these mutations on the enzyme’s cytotoxicity tested. By separately mutating three active site residues, the cytotoxic effect of CDTa can be completely eradicated, details of which will be discussed in this thesis. Additionally, the progress made towards determining the X-ray crystallographic structure of the transport component, CDTb, will be discussed.
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Martinez, Ramon D. "Purification and characterization of Clostridium sordellii toxins HT and LT and comparison to toxins A and B of Clostridium difficile." Diss., Virginia Polytechnic Institute and State University, 1989. http://hdl.handle.net/10919/54238.

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Clostridium sordellii cause gas gangrene in man and animals, and more recently it has been implicated as a causal agent of diarrhea and enterotoxemia in domestic animals. This organism was once believed to cause pseudomembranous colitis (PMC) in humans, however, Clostridium difficile, not C. sordellii, was found to be the causative agent of this disease. It is now known that C. difficile produces two toxins, designated A and B, that are implicated in the pathogenesis of the disease. C. sordellii produces two toxins, designated HT (Hemorrhagic Toxin) and LT (Lethal Toxin), that are similar to toxins A and B of C. difficile. The goal of my research was to purify and characterize the two toxins of C. sordellii, and compare their properties to those of C. difficile. Toxin HT was purified from C. sordellii (VPI strain 9048) culture filtrate by ultrafiltration through an XM-100 membrane filter and immunoaffinity chromatography using a monoclonal antibody to toxin A of C. difficile as the ligand. Toxin LT was purified to 80% homogeneity by ultrafiltration on an XM-100 membrane filter and ion-exchange chromatography. Toxin HT migrated as a major band with molecular weight of 525,000 and a minor band at 450,000 on non-denaturing PAGE. By SDS-PAGE the molecular weight was estimated at 300,000. Isoelectric focusing indicated a pI of 6.1. Like toxin A, toxin HT was cytotoxic to cultured cells, lethal for mice, and elicited an accumulation of hemorrhagic fluid in rabbit ileal loops. Toxin LT exhibited properties similar to toxin B, although LT was about a 1000-fold less cytotoxic than toxin B. By SDS-PAGE the molecular weight was estimated at 260,000. Immunodiffusion analysis revealed a reaction of partial identity between these toxins and their amino-terminal sequences were very similar. Toxins HT and LT of C. sordellii have retained remarkable immunological similarities as well as physicochemical and biological properties with toxins A and B of Q. difficult however the toxins are not identical.
Ph. D.
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Vohra, Prerna. "Clostridium difficile : expression of virulence factors, resistance to disinfectants and interactions with human cells." Thesis, University of Edinburgh, 2012. http://hdl.handle.net/1842/6490.

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Clostridium difficile is the most common cause of nosocomial diarrhoea today. Through the changing epidemiology of C. difficile infection, the emergence and decline of different strains of varying virulence and a broad spectrum of disease from asymptomatic carriage and mild infection to severe pseudomembranous colitis have been observed. The main aim of this three-part thesis was to identify bacterial factors that might explain these variations by comparing five C. difficile strains - strain 630, an historic strain, strain VPI 10463, a reference strain, the hypervirulent ribotype 027 and the current locally endemic ribotypes 001 and 106. The first study focussed on the growth-related phenotypic and genotypic expression of virulence factors in C. difficile. Growth was studied over twenty-four hours, with simultaneous assessment of toxin and spore production. Total toxin production was measured by a commercial ELISA, while a quantitative ELISA for toxin A and a quantitative cytotoxicity assay for toxin B were developed for individual toxin levels, and spores were enumerated by viable counts. Ribotype 027 produced large amounts of toxin A and toxin B and was the second highest spore producer after ribotype 106. Growth may not affect virulence, but the ability to produce more toxins and spores could. To study the transcription of the genes involved in these processes, a real-time RT-PCR was developed. The transcription of the pathogenicity locus (tcdA-E) that regulates toxin production in C. difficile, and of spo0A, the initiator of sporulation, was studied. There were three key observations: firstly, the transcription of tcdC, the negative regulator of toxin production, did not decrease over time, suggesting it has a modulatory rather than repressive effect on the process. Secondly, tcdE expression was highest in ribotype 027, which might explain its hypertoxicity by greater toxin release. Thirdly, there was almost steady state expression of spo0A during the exponential growth phase in ribotypes 106 and 027, the highest spore producers, suggesting prolonged activation of sporulation. Thus, distinct inter-strain differences exist between C. difficile strains in vitro, which could mirror their virulence in vivo, and several traits contribute synergistically to the hypervirulence of ribotype 027. The second study aimed to identify suitable laboratory disinfectants against C. difficile. The efficacy of four commonly-used disinfectants and one decontaminant was tested; one disinfectant was a chlorine-based agent commonly used in hospitals. In conventional susceptibility tests, all five agents were effective against vegetative cells and spores of C. difficile. However, only the chlorine-based disinfectant was effective against spores dried onto surfaces, but this too required more than two minutes of treatment. The presence of organic matter significantly impaired the efficacy of the non-chlorine agents. The spores of epidemic strains were destroyed less effectively and exposure to sub-MIC levels of disinfectant increased sporulation, especially in ribotype 001, a common outbreak strain. Environmental sampling of the laboratory and surrounding areas showed considerable dissemination of C. difficile, highlighting the need for effective decontamination in conjunction with basic hygiene methods like hand-washing. The third study examined the biological activity of C. difficile. Macrophages were challenged in vitro with S-layer proteins, flagella, heat-shock proteins and culture supernatants of the five strains and cytokine production was measured by specially developed ELISAs. No significant inter-strain differences were observed, although the epidemic strains generally elicited a slightly greater cytokine response. Using epithelial cell lines it was observed that epidemic strains showed greater adherence; from inhibition assays, flagella and S-layer proteins were found to contribute equally to this. Through these studies, inter-strain differences between epidemic and historic isolates were identified with respect to virulence factors, survival in the environment and possible behaviour within the host. A sum of these observations suggests increased virulence in contemporary versus historical C. difficile strains. Finally, a supplementary study characterising a collection of ribotype 027 strains isolated in Scotland and the Netherlands by typing schemes, gene sequencing, susceptibility testing and phenotypic studies was performed. In agreement with other studies, the clonality of these hypervirulent strains was observed.
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10

Jefferson, Kimberly Kay. "Clostridium difficile toxins A and B: exploring the possible mechanism of action." Thesis, Virginia Tech, 1995. http://hdl.handle.net/10919/45056.

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Clostridium difficile is a common cause of antibiotic-associated diarrhea and occasionally causes the life-threatening disease pseudomembranous colitis. The pathogenicity of the organism has been attributed to the production of two large exotoxins, toxin A (308,000 daltons) and toxin B (269,000 daltons). Toxin A is a powerful enterotoxin and is generally thought to play the more important role in the pathology of the disease. Toxin B may exert its effect after the initial tissue damage by toxin A. Both toxins cause rounding of mammalian culture cells by disrupting the cytoskeletal system. The similar biological activities and high percentage of sequence homology between the two toxins suggest that they have a similar mechanism of action. I found that purified preparations of both toxins cleave skeletal muscle actin at a single site, producing a 38,000 dalton actin fragment, and that the toxins are capable of autodigestion. The proteolytic activity may be involved in the mechanism of action of the toxins. I also analyzed an aberrant strain of C. difficile which reportedly lacked the gene for toxin B. Such a strain would be very useful for the study of the mechanism of toxin A. I concluded however, that the strain contained the genes for both toxin A and toxin B. The toxin genes and resulting proteins appear, however, to be slightly different from those of other strains.
Master of Science

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Books on the topic "Clostridium difficile toxins"

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Ketley, Julian Mark. Studies on toxins A and B of Clostridium difficile. Birmingham: University of Birmingham, 1986.

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Papatheodorou, Panagiotis. Clostridium difficile binary toxin CDT induces clustering of the lipolysis-stimulated lipoprotein receptor into lipid rafts. Freiburg: Universität, 2013.

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Mitchell, Timothy John. Studies on the mode of action of Clostridium difficile toxin A. Birmingham: University of Birmingham, 1986.

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Urtz, Bruce E. Purification and characterization Clostridium difficile toxin A. 1987.

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Masnyk, Michael. The interactions of Clostridium Difficile Toxin B with mammalian cells. 1988.

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Katirji, Bashar. Case 24. Edited by Bashar Katirji. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603434.003.0028.

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Botulism is an extremely rare neuromuscular disorder, caused by botulinum toxin which is produced by the anaerobic bacteria Clostridium botulinum. It has several forms: classic foodborne, infantile, wound, intestinal, and iatrogenic forms. The presentation is often acute and severe but may be occasionally subacute and moderate. The diagnosis may be difficult and requires a high index of suspicion. This case presents an adult with classic foodborne botulism and highlights the clinical and electrodiagnostic findings that distinguish this disorder from other neuromuscular junction disorders including myasthenia gravis and Lambert-Eaton myasthenic syndrome. Specifically, the findings on repetitive nerve stimulation are discussed and distinguished from the results seen in other neuromuscular junction disorders.
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Book chapters on the topic "Clostridium difficile toxins"

1

Moncrief, J. S., and T. D. Wilkins. "Genetics of Clostridium difficile Toxins." In Current Topics in Microbiology and Immunology, 35–54. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-662-06272-2_2.

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Warny, Michel, and Ciarán P. Kelly. "Pathogenicity of Clostridium difficile Toxins." In Microbial Pathogenesis and the Intestinal Epithelial Cell, 503–24. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555817848.ch27.

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Delmée, Michel, and Michel Warny. "Antibody response to Clostridium difficile toxins." In Ökosystem Darm Special, 83–91. Paris: Springer Paris, 1996. http://dx.doi.org/10.1007/978-2-8178-0903-8_9.

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Delmée, Michel, and Michel Warny. "Antibody response to Clostridium difficile toxins." In Ökosystem Darm Special, 83–91. Paris: Springer Paris, 1996. http://dx.doi.org/10.1007/978-2-8178-0924-3_9.

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von Eichel-Streiber, Christoph. "Molecular Biology of the Clostridium difficile Toxins." In Brock/Springer Series in Contemporary Bioscience, 264–89. New York, NY: Springer New York, 1993. http://dx.doi.org/10.1007/978-1-4615-7087-5_19.

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Thelestam, M., and E. Chaves-Olarte. "Cytotoxic Effects of the Clostridium difficile Toxins." In Current Topics in Microbiology and Immunology, 85–96. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-662-06272-2_4.

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Borriello, S. P. "Structure and Function of Clostridium difficile Toxins." In Molecular Pathogenesis of Gastrointestinal Infections, 161–67. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-5982-1_21.

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López-Ureña, Diana, Carlos Quesada-Gómez, César Rodríguez, and Esteban Chaves-Olarte. "Role of Clostridium difficile Toxins in Antibiotic-Associated Diarrhea and Pseudomembranous Colitis." In Microbial Toxins, 1–18. Dordrecht: Springer Netherlands, 2016. http://dx.doi.org/10.1007/978-94-007-6725-6_17-1.

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Barbut, Frédéric, and Jean-Claude Petit. "Laboratory methods for detecting the toxins of Clostridium difficile." In Ökosystem Darm Special, 93–104. Paris: Springer Paris, 1996. http://dx.doi.org/10.1007/978-2-8178-0903-8_10.

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Barbut, Frédéric, and Jean-Claude Petit. "Laboratory methods for detecting the toxins of Clostridium difficile." In Ökosystem Darm Special, 93–104. Paris: Springer Paris, 1996. http://dx.doi.org/10.1007/978-2-8178-0924-3_10.

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Conference papers on the topic "Clostridium difficile toxins"

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Monaghan, TM, O. Negm, B. MacKenzie, M. Hamed, CC Shone, DP Humphreys, KR Acharya, and MH Wilcox. "PWE-017 High prevalence of subclass-specific binding and neutralising antibodies against clostridium difficile toxins in adult cystic fibrosis sera: possible mode of protection against symptomatic clostridium difficile infection." In British Society of Gastroenterology, Annual General Meeting, 19–22 June 2017, Abstracts. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2017. http://dx.doi.org/10.1136/gutjnl-2017-314472.262.

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Matos, Eduarda Syhara Rocha, Costa, D.V.S., Martins, C.S., Oliveira, L.C., Silva, A.M.H.P., Martins, D.S., Pimentel, P.V.S., and Brito, G.A.C. "Alterações neuroimunes induzidas por toxinas do Clostridium difficile." In II Encontro do Programa de Pós-Graduação em Ciências Farmacêuticas da Universidade Federal do Ceará e I Simpósio Norte-Nordeste de Ciências Farmacêuticas. Fortaleza - CE, Brazil: Galoa, 2017. http://dx.doi.org/10.17648/ppgcf-2017-64895.

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Prohaska, C., and M. F. Ragland. "A Toxic Combination: Clostridium Difficile Infection Leading to Miscarriage." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a6573.

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Reports on the topic "Clostridium difficile toxins"

1

Muldrow, Lycurgus L., and Joe Johnson. Genetic Engineering of Clostridium Difficile Toxin A Vaccine. Fort Belvoir, VA: Defense Technical Information Center, September 1991. http://dx.doi.org/10.21236/ada242265.

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Muldrow, Lycurgus L., and Joe Johnson. Genetic Engineering of Clostridium Difficile Toxin a Vaccine. Fort Belvoir, VA: Defense Technical Information Center, August 1990. http://dx.doi.org/10.21236/ada230411.

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