Journal articles: '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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Uspenskiy, Yu P., and N. V. Baryshnikova. "Antibiotic-associated diarrhea in hospital: frequency and prophylaxis." Medical alphabet, no. 20 (August 18, 2021): 35–37. http://dx.doi.org/10.33667/2078-5631-2021-20-35-37.

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The aim. To analyze the prevalence of antibiotic-associated diarrhea (AAD) caused by Clostridium difficile in a hospital setting.Materials and methods. 93 patients with 3 or more episodes of unformed stool (diarrhea) for two consecutive days or more, developed after the use of antibiotics, were monitored. All patients underwent rapid stool analysis for the presence of Clostridium difficile A and B toxins using the X/pert C. diff toxin A/B test.Results. Toxins A and/or B of Clostridium difficile were detected in 32 patients (34.4 %). The remaining patients (n = 61; 65.6 %) had idiopathic AAD. The most of the patients who were found to have Clostridium difficile toxins in the feces were in the infarction department, cardiology intensive care and trauma departments, i. e. they had severe diseases associated with reduced immunity and inactivity.Conclusions. The prevalence of AAD caused by Clostridium difficile in hospital settings is high. It is recommended to prescribe drugs for the correction of disorders of the gastrointestinal microflora from the first day of antibiotic therapy, since this will significantly reduce the prevalence of clinical manifestation of diarrhea associated with Clostridium difficile.

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Tait, A. Sasha, Monique Dalton, Blandine Geny, Felice D'Agnillo, Michel R. Popoff, and Esther M. Sternberg. "The Large Clostridial Toxins from Clostridium sordellii and C. difficile Repress Glucocorticoid Receptor Activity." Infection and Immunity 75, no. 8 (May 21, 2007): 3935–40. http://dx.doi.org/10.1128/iai.00291-07.

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ABSTRACT We have previously shown that Bacillus anthracis lethal toxin represses glucocorticoid receptor (GR) transactivation. We now report that repression of GR activity also occurs with the large clostridial toxins produced by Clostridium sordellii and C. difficile. This was demonstrated using a transient transfection assay system for GR transactivation. We also report that C. sordellii lethal toxin inhibited GR function in an ex vivo assay, where toxin reduced the dexamethasone suppression of the proinflammatory cytokine tumor necrosis factor alpha (TNF-α). Furthermore, the glucocorticoid antagonist RU-486 in combination with C. sordellii lethal toxin additively prevented glucocorticoid suppression of TNF-α. These findings corroborate the fact that GR is a target for the toxin and suggest a physiological role for toxin-associated GR repression in inflammation. Finally, we show that this repression is associated with toxins that inactivate p38 mitogen-activated protein kinase (MAPK).

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13

Johnson, S. "Clostridium difficile Toxins and Severe C. difficile Infection." Journal of Infectious Diseases 205, no. 3 (December 5, 2011): 353–54. http://dx.doi.org/10.1093/infdis/jir752.

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Stojanovic, Predrag, and Branislava Kocic. "Diarrhoea caused by Clostridium difficile in patients with postoperative subhepatic abscess." Vojnosanitetski pregled 65, no. 3 (2008): 249–54. http://dx.doi.org/10.2298/vsp0803249s.

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Background. Toxigenic strains of Clostridium difficile in the majority of cases cause disease of the intestinal tract of hospitalized patients. For a long time, Clostridium difficile was considered to produce both types of toxins (A+/B+ strain), however, the investigations conducted in the last ten years point to the existence of clinically significant isolates which produce only toxin B, i.e. toxin A negative / toxin B positive (A-/B+ strain) Clostridium difficile. Case report. We presented the case of a patient admitted to the Surgery Clinic, Clinical Center Nis due to the presence of calculus in the ductus choledochus. Twenty-four hours after the surgical intervention for calculus removal, the first signs of the operative wound infection began to appear. In the course of infection treatment, different antibiotics were administered (cefuroxine, ciprofloxacin, vancomycin, imipenem). After making etiological microbiological diagnosis and application of antibiotics according to antibiogram results, the signs of the operative wound infection began to withdraw, but the patient reported the abdominal pain and liquid stools with traces of blood (up to 17 stools per day). By microbiological examination, Clostridium difficile was cultivated and the presence of toxin B was detected in the stool samples. The patient was sent to the Clinic for Infectious Diseases, where the causal therapy of mitronidazol was administered. Liquid and electrolytes were made up by substitution therapy. After the eight-day-treatment, the patient felt much better, and diarrheas stopped on the 10th day of the therapy application. Conclusion. Our results have shown that toxingen strains Clostridium difficile are present in our country so this bacterium sort have to be considered in differential causal diagnosis of diarrhoea syndrom. Considering that it can cause difficult form of the disease, it is an obligation to establish the presence of some toxins of Clostridium difficile in stool samples of patients and/or production of some toxins in liquid culturate of isolates to provide data for the presence of strains which produce only toxin B.

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Cowardin, Carrie A., Brianna M. Jackman, Zannatun Noor, Stacey L. Burgess, Andrew L. Feig, and William A. Petri. "Glucosylation Drives the Innate Inflammatory Response to Clostridium difficile Toxin A." Infection and Immunity 84, no. 8 (June 6, 2016): 2317–23. http://dx.doi.org/10.1128/iai.00327-16.

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Clostridium difficileis a major, life-threatening hospital-acquired pathogen that causes mild to severe colitis in infected individuals. The tissue destruction and inflammation which characterizeC. difficileinfection (CDI) are primarily due to the Rho-glucosylating toxins A and B. These toxins cause epithelial cell death and induce robust inflammatory signaling by activating the transcription factor NF-κB, leading to chemokine and cytokine secretion. The toxins also activate the inflammasome complex, which leads to secretion of the pyrogenic cytokine IL-1β. In this study, we utilized glucosylation-deficient toxin A to show that activation of the inflammasome by this toxin is dependent on Rho glucosylation, confirming similar findings reported for toxin B. We also demonstrated that tissue destruction andin vivoinflammatory cytokine production are critically dependent on the enzymatic activity of toxin A, suggesting that inhibiting toxin glucosyltransferase activity may be effective in combating this refractory disease.

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Moncrief, J. S., L. A. Barroso, and T. D. Wilkins. "Positive regulation of Clostridium difficile toxins." Infection and immunity 65, no. 3 (1997): 1105–8. http://dx.doi.org/10.1128/iai.65.3.1105-1108.1997.

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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 (1988): 1–18. http://dx.doi.org/10.1128/cmr.1.1.1-18.1988.

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Sun, Xingmin, Tor Savidge, and Hanping Feng. "The Enterotoxicity of Clostridium difficile Toxins." Toxins 2, no. 7 (July 14, 2010): 1848–80. http://dx.doi.org/10.3390/toxins2071848.

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Matchett, William E., Stephanie Anguiano-Zarate, Goda Baddage Rakitha Malewana, Haley Mudrick, Melissa Weldy, Clayton Evert, Alexander Khoruts, Michael Sadowsky, and Michael A. Barry. "A Replicating Single-Cycle Adenovirus Vaccine Effective against Clostridium difficile." Vaccines 8, no. 3 (August 22, 2020): 470. http://dx.doi.org/10.3390/vaccines8030470.

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Clostridium difficile causes nearly 500,000 infections and nearly 30,000 deaths each year in the U.S., which is estimated to cost $4.8 billion. C. difficile infection (CDI) arises from bacteria colonizing the large intestine and releasing two toxins, toxin A (TcdA) and toxin B (TcdB). Generating humoral immunity against C. difficile’s toxins provides protection against primary infection and recurrence. Thus, a vaccine may offer the best opportunity for sustained, long-term protection. We developed a novel single-cycle adenovirus (SC-Ad) vaccine against C. difficile expressing the receptor-binding domains from TcdA and TcdB. The single immunization of mice generated sustained toxin-binding antibody responses and protected them from lethal toxin challenge for up to 38 weeks. Immunized Syrian hamsters produced significant toxin-neutralizing antibodies that increased over 36 weeks. Single intramuscular immunization provided complete protection against lethal BI/NAP1/027 spore challenge 45 weeks later. These data suggest that this replicating vaccine may prove useful against CDI in humans.

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Haug, Gerd, Klaus Aktories, and Holger Barth. "The Host Cell Chaperone Hsp90 Is Necessary for Cytotoxic Action of the Binary Iota-Like Toxins." Infection and Immunity 72, no. 5 (May 2004): 3066–68. http://dx.doi.org/10.1128/iai.72.5.3066-3068.2004.

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ABSTRACT The heat shock protein Hsp90 is essential for uptake of the binary actin ADP-ribosylating toxins Clostridium perfringens iota-toxin and Clostridium difficile transferase into eukaryotic cells. Inhibition of Hsp90 by its specific inhibitor radicicol delayed intoxication of Vero cells by these toxins. A common Hsp90-dependent mechanism for their translocation is discussed.

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Genth, Harald, Jörg Selzer, Christian Busch, Jürgen Dumbach, Fred Hofmann, Klaus Aktories, and Ingo Just. "New Method To Generate Enzymatically DeficientClostridium difficile Toxin B as an Antigen for Immunization." Infection and Immunity 68, no. 3 (March 1, 2000): 1094–101. http://dx.doi.org/10.1128/iai.68.3.1094-1101.2000.

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ABSTRACT The family of the large clostridial cytotoxins, encompassingClostridium difficile toxins A and B as well as the lethal and hemorrhagic toxins from Clostridium sordellii, monoglucosylate the Rho GTPases by transferring a glucose moiety from the cosubstrate UDP-glucose. Here we present a new detoxification procedure to block the enzyme activity by treatment with the reactive UDP-2′,3′-dialdehyde to result in alkylation of toxin A and B. Alkylation is likely to occur in the catalytic domain, because the native cosubstrate UDP-glucose completely protected the toxins from inactivation and the alkylated toxin competes with the native toxin at the cell receptor. Alkylated toxins are good antigens resulting in antibodies recognizing only the C-terminally located receptor binding domain, whereas formaldehyde treatment resulted in antibodies recognizing both the receptor binding domain and the catalytic domain, indicating that the catalytic domain is concealed under native conditions. Antibodies against the native catalytic domain (amino acids 1 through 546) and those holotoxin antibodies recognizing the catalytic domain inhibited enzyme activity. However, only antibodies against the receptor binding domain protected intact cells from the cytotoxic activity of toxin B, whereas antibodies against the catalytic domain were protective only when inside the cell.

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Almeida, J. C., R. O. S. Silva, F. C. F. Lobato, and R. A. Mota. "Isolation of Clostridium perfringens and C. difficile in crab-eating fox ( Cerdocyon thous - Linnaeus 1776) from Northeastern Brazil." Arquivo Brasileiro de Medicina Veterinária e Zootecnia 70, no. 6 (December 2018): 1709–13. http://dx.doi.org/10.1590/1678-4162-9895.

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ABSTRACT The aim of the present study was to isolate Clostridium perfringens and C. difficile in crab-eating fox (Cerdocyon thous) from Northeastern Brazil. Stool samples of 18 captive crab-eating foxes from four states of Northeastern Brazil (Alagoas, Bahia, Paraíba e Pernambuco) were collected and subjected to C. perfringens and C. difficile isolation. Suggestive colonies of C. perfringens were then analyzed for genes encoding the major C. perfringens toxins (alpha, beta, epsilon and iota), beta-2 toxin (cpb2), enterotoxin (cpe), and NetB- (netB) and NetF- (netF) encoding genes. C. difficile strains were analyzed by multiplex-PCR for a housekeeping gene (tpi), toxins A (tcdA) and B (tcdB) and a binary toxin gene (cdtB). Unthawed aliquots of stool samples positive for toxigenic C. difficile were subjected to a commercial ELISA to evaluate the presence of A/B toxins. Clostridium perfringens (type A) was isolated from five (27%) samples, and only one sample was positive for beta-2 enconding gene (cpb2). Two (11%) stool samples were positive for C. difficile, but negative for A/B toxins. These two wild canids were also positive for C. perfringens type A. This is the first report of C. difficile in crab-eating fox.

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Bartlett, John G. "Detection of Clostridium difficile Infection." Infection Control & Hospital Epidemiology 31, S1 (November 2010): S35—S37. http://dx.doi.org/10.1086/655999.

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There has been a recent surge of interest in Clostridium difficile infection, which reflects an impressive increase in the number and severity of these infections. This review addresses some of the newer methods for detection of C. difficile infection at the bedside and in the laboratory. Particularly important are the new rapid diagnostic tests that detect toxigenic C. difficile using polymerase chain reaction and the combination tests that, either simultaneously or sequentially, screen for C. difficile and test for toxins A and B. It is expected that these new testing methods will largely supplant the enzyme immunoassays for toxins, which are used by most laboratories, departments, and divisions. The present goal is to combine clinical, laboratory, and animal research related to C. difficile that reflects issues that are considered to be major contemporary challenges. Among this work is the pursuit of studies of immune mechanisms to better control this disease.

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Klyuchnikova, I. A., I. N. Petukhova, Z. V. Grigorievskaya, N. S. Bagirova, I. V. Tereshchenko, and N. V. Dmitrieva. "Infections caused by Clostridium difficile in cancer patients." Siberian journal of oncology 17, no. 6 (January 1, 2019): 92–96. http://dx.doi.org/10.21294/1814-4861-2018-17-6-92-96.

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The purpose of the studywas to determine the role of antibiotics as a risk factor of Clostridium difficile-associated diarrhea in hospitalized cancer patients.Material and Methods. The study included 844 hospitalized cancer patients with diarrhea. The presence of Clostridium difficile toxins A and B in the fecal samples was determined by enzyme immunoassay.Results.Clostridium difficile toxins A and B were detected in 100 cancer patients (42 % men and 58 % women). The incidence of Clostridium difficile-associated diarrhea was higher in women than in men (р<0.02). Patients with hemoblastosis and gastrointestinal tumors were more susceptible to the development of Clostridium difficile associated diarrhea (p<0.02). The use of cephalosporin antibiotics was the main risk factor (р<0.001). In our study, 46 % of the patients took antibiotics.Conclusion.Clostridium difficile was shown to play a significant role in the development of diarrhea in cancer patients, and early detection of Clostridium difficile infection contributes to the early onset of therapy.

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Wang, Haiying, Xingmin Sun, Yongrong Zhang, Shan Li, Kevin Chen, Lianfa Shi, Weijia Nie, et al. "A Chimeric Toxin Vaccine Protects against Primary and Recurrent Clostridium difficile Infection." Infection and Immunity 80, no. 8 (May 21, 2012): 2678–88. http://dx.doi.org/10.1128/iai.00215-12.

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ABSTRACTThe global emergence ofClostridium difficileinfection (CDI) has contributed to the recent surge in severe antibiotic-associated diarrhea and colonic inflammation.C. difficileproduces two homologous glucosylating exotoxins, TcdA and TcdB, both of which are pathogenic and require neutralization to prevent disease occurrence. However, because of their large size and complex multifunctional domain structures, it has been a challenge to produce native recombinant toxins that may serve as vaccine candidates. Here, we describe a novel chimeric toxin vaccine that retains major neutralizing epitopes from both toxins and confers complete protection against primary and recurrent CDI in mice. Using a nonpathogenicBacillus megateriumexpression system, we generated glucosyltransferase-deficient holotoxins and demonstrated their loss of toxicity. The atoxic holotoxins induced potent antitoxin neutralizing antibodies showing little cross-immunogenicity or protection between TcdA and TcdB. To facilitate simultaneous protection against both toxins, we generated an active clostridial toxin chimera by switching the receptor binding domain of TcdB with that of TcdA. The toxin chimera was fully cytotoxic and showed potent proinflammatory activities. This toxicity was essentially abolished in a glucosyltransferase-deficient toxin chimera, cTxAB. Parenteral immunization of mice or hamsters with cTxAB induced rapid and potent neutralizing antibodies against both toxins. Complete and long-lasting disease protection was conferred by cTxAB vaccinations against both laboratory and hypervirulentC. difficilestrains. Finally, prophylactic cTxAB vaccination prevented spore-induced disease relapse, which constitutes one of the most significant clinical issues in CDI. Thus, the rational design of recombinant chimeric toxins provides a novel approach for protecting individuals at high risk of developing CDI.

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Davies, Abigail H., April K. Roberts, Clifford C. Shone, and K. Ravi Acharya. "Super toxins from a super bug: structure and function of Clostridium difficile toxins." Biochemical Journal 436, no. 3 (May 27, 2011): 517–26. http://dx.doi.org/10.1042/bj20110106.

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Clostridium difficile, a highly infectious bacterium, is the leading cause of antibiotic-associated pseudomembranous colitis. In 2009, the number of death certificates mentioning C. difficile infection in the U.K. was estimated at 3933 with 44% of certificates recording infection as the underlying cause of death. A number of virulence factors facilitate its pathogenicity, among which are two potent exotoxins; Toxins A and B. Both are large monoglucosyltransferases that catalyse the glucosylation, and hence inactivation, of Rho-GTPases (small regulatory proteins of the eukaryote actin cell cytoskeleton), leading to disorganization of the cytoskeleton and cell death. The roles of Toxins A and B in the context of C. difficile infection is unknown. In addition to these exotoxins, some strains of C. difficile produce an unrelated ADP-ribosylating binary toxin. This toxin consists of two independently produced components: an enzymatic component (CDTa) and the other, the transport component (CDTb) which facilitates translocation of CDTa into target cells. CDTa irreversibly ADP-ribosylates G-actin in target cells, which disrupts the F-actin:G-actin equilibrium leading to cell rounding and cell death. In the present review we provide a summary of the current structural understanding of these toxins and discuss how it may be used to identify potential targets for specific drug design.

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Kaiser, Eva, Claudia Kroll, Katharina Ernst, Carsten Schwan, Michel Popoff, Gunter Fischer, Johannes Buchner, Klaus Aktories, and Holger Barth. "Membrane Translocation of Binary Actin-ADP-Ribosylating Toxins from Clostridium difficile and Clostridium perfringens Is Facilitated by Cyclophilin A and Hsp90." Infection and Immunity 79, no. 10 (July 18, 2011): 3913–21. http://dx.doi.org/10.1128/iai.05372-11.

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ABSTRACTSome hypervirulent strains ofClostridium difficileproduce the binary actin-ADP-ribosylating toxinC. difficiletransferase (CDT) in addition to Rho-glucosylating toxins A and B. It has been suggested that the presence of CDT increases the severity ofC. difficile-associated diseases, including pseudomembranous colitis. CDT contains a binding and translocation component, CDTb, that mediates the transport of the separate enzyme component CDTa into the cytosol of target cells, where CDTa modifies actin. Here we investigated the mechanism of cellular CDT uptake and found that bafilomycin A1 protects cultured epithelial cells from intoxication with CDT, implying that CDTa is translocated from acidified endosomal vesicles into the cytosol. Consistently, CDTa is translocated across the cytoplasmic membranes into the cytosol when cell-bound CDT is exposed to acidic medium. Radicicol and cyclosporine A, inhibitors of the heat shock protein Hsp90 and cyclophilins, respectively, protected cells from intoxication with CDT but not from intoxication with toxins A and B. Moreover, both inhibitors blocked the pH-dependent membrane translocation of CDTa, strongly suggesting that Hsp90 and cyclophilin are crucial for this process. In contrast, the inhibitors did not interfere with the ADP-ribosyltransferase activity, receptor binding, or endocytosis of the toxin. We obtained comparable results with the closely related iota-toxin fromClostridium perfringens. Moreover, CDTa and Ia, the enzyme component of iota-toxin, specifically bound to immobilized Hsp90 and cyclophilin Ain vitro. In combination with our recently obtained data on the C2 toxin fromC. botulinum, these results imply a common Hsp90/cyclophilin A-dependent translocation mechanism for the family of binary actin-ADP-ribosylating toxins.

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Aronsson, B., M. Granström, R. Möllby, and C. E. Nord. "Serum antibody response to clostridium difficile toxins in patients with clostridium difficile diarrhoea." Infection 13, no. 3 (May 1985): 97–101. http://dx.doi.org/10.1007/bf01642866.

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Chen, Shuyi, Huawei Gu, Chunli Sun, Haiying Wang, and Jufang Wang. "Rapid detection of Clostridium difficile toxins and laboratory diagnosis of Clostridium difficile infections." Infection 45, no. 3 (September 6, 2016): 255–62. http://dx.doi.org/10.1007/s15010-016-0940-9.

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Taha, Medhat M. "Optimal Conditions for Clostridium difficile Toxins Production." International Journal of Current Microbiology and Applied Sciences 9, no. 10 (2020): 3469–74. http://dx.doi.org/10.20546/ijcmas.2020.910.400.

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Wilkins, Tracy D. "Role of Clostridium difficile toxins in disease." Gastroenterology 93, no. 2 (August 1987): 389–91. http://dx.doi.org/10.1016/0016-5085(87)91031-6.

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Hinkson, Paul L., Carol Dinardo, Daniel DeCiero, Jeffrey D. Klinger, and Robert H. Barker. "Tolevamer, an Anionic Polymer, Neutralizes Toxins Produced by the BI/027 Strains of Clostridium difficile." Antimicrobial Agents and Chemotherapy 52, no. 6 (April 7, 2008): 2190–95. http://dx.doi.org/10.1128/aac.00041-08.

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ABSTRACTClostridium difficile-associated diarrhea (CDAD) is caused by the toxins the organism produces when it overgrows in the colon as a consequence of antibiotic depletion of normal flora. Conventional antibiotic treatment of CDAD increases the likelihood of recurrent disease by again suppressing normal bacterial flora. Tolevamer, a novel toxin-binding polymer, was developed to ameliorate the disease without adversely affecting normal flora. In the current study, tolevamer was tested for its ability to neutralize clostridial toxins produced by the epidemic BI/027 strains, thereby preventing toxin-mediated tissue culture cell rounding. The titers of toxin-containingC. difficileculture supernatants were determined using confluent cell monolayers, and then the supernatants were used in assays containing dilutions of tolevamer to determine the lowest concentration of tolevamer that prevented ≥90% cytotoxicity. Tolevamer neutralized toxins in the supernatants of allC. difficilestrains tested. Specific antibodies against the large clostridial toxins TcdA and TcdB also neutralized the cytopathic effect, suggesting that tolevamer is specifically neutralizing these toxins and that the binary toxin (whose genes are carried by the BI/027 strains) is not a significant source of cytopathology against tissue culture cells in vitro.

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Govind, Revathi, Govindsamy Vediyappan, Rial D. Rolfe, Bruno Dupuy, and Joe A. Fralick. "Bacteriophage-Mediated Toxin Gene Regulation in Clostridium difficile." Journal of Virology 83, no. 23 (September 23, 2009): 12037–45. http://dx.doi.org/10.1128/jvi.01256-09.

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ABSTRACT 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. In this study, we examined the effect of lysogeny by ΦCD119 on C. difficile toxin production. Transcriptional analysis demonstrated a decrease in the expression of pathogenicity locus (PaLoc) genes tcdA, tcdB, tcdR, tcdE, and tcdC in ΦCD119 lysogens. During this study we found that repR, a putative repressor gene of ΦCD119, was expressed in C. difficile lysogens and that its product, RepR, could downregulate tcdA::gusA and tcdR::gusA reporter fusions in Escherichia coli. We cloned and purified a recombinant RepR containing a C-terminal six-His tag and documented its binding to the upstream regions of tcdR in C. difficile PaLoc and in repR upstream region in ΦCD119 by gel shift assays. DNA footprinting experiments revealed similarities between the RepR binding sites in tcdR and repR upstream regions. These findings suggest that presence of a CD119-like temperate phage can influence toxin gene regulation in this nosocomially important pathogen.

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George Trad, Varun Sodhi, Matthew Brockway, Nazanin Sheikhan, Abdul Gader Gheriani, Olivia Astor, and Hatim Gemil. "Clostridioides (Clostridium) difficile infection: Review of literature." World Journal of Advanced Research and Reviews 14, no. 2 (May 30, 2022): 146–55. http://dx.doi.org/10.30574/wjarr.2022.14.2.0366.

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Clostridioides (Clostridium) difficile (C. difficile) is a gram-positive bacterium that infects the large intestine. The number of clostridium difficile infections has increased in the recent years due to multiple risk factors including frequent use of antibiotics and proton pump inhibitors. The virulence of C. difficile comes from its production of toxins. Treatment for C. difficile infection includes the use of antibiotics, monoclonal antibodies, or a fecal transplant.

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Huelsenbeck, Johannes, Stefanie Dreger, Ralf Gerhard, Holger Barth, Ingo Just, and Harald Genth. "Difference in the Cytotoxic Effects of Toxin B from Clostridium difficile Strain VPI 10463 and Toxin B from Variant Clostridium difficile Strain 1470." Infection and Immunity 75, no. 2 (December 4, 2006): 801–9. http://dx.doi.org/10.1128/iai.01705-06.

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ABSTRACT Glucosylation of RhoA, Rac1, and Cdc42 by Clostridium difficile toxin B from strain VPI 10463 (TcdB) results in actin reorganization (cytopathic effect) and apoptosis (cytotoxic effect). Toxin B from variant C. difficile strain 1470 serotype F (TcdBF) differs from TcdB with regard to substrate proteins, as it glucosylates Rac1 and R-Ras but not RhoA and Cdc42. In this study, we addressed the question of whether the cellular effects of the toxins depend on their protein substrate specificity. Rat basophilic leukemia (RBL) cells were synchronized using the thymidine double-block technique. We show that cells were most sensitive to the cytotoxic effect of TcdB in S phase, as analyzed in terms of phosphatidyl serine externalization, fragmentation of nuclei, and activation of caspase-3; in contrast, TcdBF induced only a marginal cytotoxic effect, suggesting that inactivation of RhoA (but not of Rac1) was required for the cytotoxic effect. The glucosylation of Rac1 was correlated to the cytopathic effect of either toxin, suggesting a close connection of the two effects. The cytotoxic effect of TcdB was executed by caspase-3, as it was responsive to inhibition by acetyl-Asp-Met-Gln-Asp-aldehyde (Ac-DMQD-CHO), an inhibitor of caspase-3. The viability of TcdB-treated RBL cells was reduced, whereas the viability of TcdBF-treated cells was unchanged, further confirming that inactivation of RhoA is required for the cytotoxic effect. In conclusion, the protein substrate specificity of the glucosylating toxins determines their biological activity.

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Chumbler, Nicole M., Melissa A. Farrow, Lynne A. Lapierre, Jeffrey L. Franklin, and D. Borden Lacy. "Clostridium difficile Toxins TcdA and TcdB Cause Colonic Tissue Damage by Distinct Mechanisms." Infection and Immunity 84, no. 10 (July 25, 2016): 2871–77. http://dx.doi.org/10.1128/iai.00583-16.

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As the major cause of antibiotic-associated diarrhea,Clostridium difficileis a serious problem in health care facilities worldwide.C. difficileproduces two large toxins, TcdA and TcdB, which are the primary virulence factors in disease. The respective functions of these toxins have been difficult to discern, in part because the cytotoxicity profiles for these toxins differ with concentration and cell type. The goal of this study was to develop a cell culture model that would allow a side-by-side mechanistic comparison of the toxins. Conditionally immortalized, young adult mouse colonic (YAMC) epithelial cells demonstrate an exquisite sensitivity to both toxins with phenotypes that agree with observations in tissue explants. TcdA intoxication results in an apoptotic cell death that is dependent on the glucosyltransferase activity of the toxin. In contrast, TcdB has a bimodal mechanism; it induces apoptosis in a glucosyltransferase-dependent manner at lower concentrations and glucosyltransferase-independent necrotic death at higher concentrations. The direct comparison of the responses to TcdA and TcdB in cells and colonic explants provides the opportunity to unify a large body of observations made by many independent investigators.

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Vohra, Prerna, and Ian R. Poxton. "Comparison of toxin and spore production in clinically relevant strains of Clostridium difficile." Microbiology 157, no. 5 (May 1, 2011): 1343–53. http://dx.doi.org/10.1099/mic.0.046243-0.

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Clostridium difficile is a major cause of nosocomial diarrhoea. The toxins that it produces (TcdA and TcdB) are responsible for the characteristic pathology of C. difficile infection (CDI), while its spores persist in the environment, causing its widespread transmission. Many different strains of C. difficile exist worldwide and the epidemiology of the strains is ever-changing: in Scotland, PCR ribotype 012 was once prevalent, but currently ribotypes 106, 001 and 027 are endemic. This study aimed to identify the differences among these ribotypes with respect to their growth, and toxin and spore production in vitro. It was observed that the hypervirulent ribotype 027 produces significantly more toxin than the other ribotypes in the exponential and stationary phases of growth. Further, the endemic strains produce significantly more toxins and spores than ribotype 012. Of note was the observation that tcdC expression did not decrease into the stationary phase of growth, implying that it may have a modulatory rather than repressive effect on toxin production. Further, the increased expression of tcdE in ribotype 027 suggests its importance in the release of the toxins. It can thus be concluded that several genotypic and phenotypic traits might synergistically contribute to the hypervirulence of ribotype 027. These observations might suggest a changing trend towards increased virulence in the strains currently responsible for CDI.

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Venkatasubramanian, Prashanna Balaji, Els Oosterink, Monic M. M. Tomassen, Maria Suarez-Diez, Jurriaan J. Mes, Edoardo Saccenti, and Nicole J. W. de Wit. "Transcriptome-based identification of the beneficial role of blackcurrant, strawberry and yellow onion to attenuate the cytopathic effects of Clostridium difficile toxins." Journal of Berry Research 11, no. 2 (June 14, 2021): 231–48. http://dx.doi.org/10.3233/jbr-200646.

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BACKGROUND: Clostridium difficile Infection (CDI) can lead to diarrhea and fulminant colitis. C. difficile infects the host using toxins. Recent studies report prevalence of CDI in the small intestine. Berries are known to contain antioxidants and phenolic compounds that might mitigate bacterial infection. OBJECTIVE: We explored the impact of C. difficile toxins on the small intestine using an in vitro approach and used systems biology techniques together with data integration to identify food compounds that can reduce their cytopathic impact. METHODS: Differentiated Caco-2 cells were exposed to C. difficile toxins and the transcriptomic changes were studied. To identify foods with potential beneficial counteracting effects, the transcriptomic profiles were integrated with transcriptomics data from Caco-2 cells exposed to various food compounds and analyzed using multivariate analysis. RESULTS: Beneficial food candidates, selected by multivariate analysis, such as blackcurrant, strawberry and yellow onion were further examined for their potential to counteract the effect of the toxin-induced disruption of cell integrity and toxin translocation. Our results confirmed effects of food compounds, on the cytopathic effects of toxins in the small intestine. CONCLUSION: Blackcurrant, strawberry and yellow onion can counteract C. difficile toxins induced effects.

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NIKOLAEVA, I. V., S. V. KHALIULLINA, G. Kh MURTAZINA, and V. A. ANOKHIN. "Clostridioides (Clostridium) difficile infection. Review of current clinical guidelines." Practical medicine 18, no. 6 (2020): 106–12. http://dx.doi.org/10.32000/2072-1757-2020-6-106-112.

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Clostridioides difficile (CDI) infection is a disease associated with a disruption of the gut microbiome with over-colonization of C. difficile, the toxins of which cause inflammation and damage to the colon. A dynamic assessment of the CDI prevalence indicates a significant increase in laboratory-confirmed cases of infection and a high mortality associated with it. C. difficile is recognized as the main causative agent of nosocomial infections in Europe, USA, Canada and Australia, which develops 48 hours after hospitalization in a medical facility and within 12 weeks after discharge. The severity of CDI is determined by the severity of infectious-toxic, diarrheal and abdominal syndromes. Severe CDI is characterized by manifestations of colitis, accompanied by severe leukocytosis, a decrease in albumin levels and an increase in serum creatinine levels. Development of fulminant forms, pseudomembranous colitis, toxic megacolon, intestinal perforation, sepsis is possible. The risk factors include in-hospital stay; recent use of antibiotics (within the previous 12 weeks, especially the use of fluoroquinolones, cephalosporins of III–IV generations, carbapenems and clindamycin), PPI and H2-histamine blockers; presence of inflammatory bowel diseases (ulcerative colitis, Crohn’s disease), immunodeficiency states, including iatrogenic; recent endoscopic examinations, surgical interventions on the gastrointestinal tract, tube feeding, enemas; possible contact with a family member who recently had a C..difficile infection. The «gold standard» for confirming the CDI diagnosis is the identification of the causative agent and/or toxins of C. difficile in the stool using specific laboratory research methods. Vancomycin or metronidazole are recommended as first-line therapy.

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Bentley, David W. "Clostridium difficile -Associated Disease in Long-Term Care Facilities." Infection Control & Hospital Epidemiology 11, no. 8 (August 1990): 434–38. http://dx.doi.org/10.1086/646204.

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Clostridium difficile is a major cause of gastrointestinal infections. In 1978, Bartlett and colleagues identified C difficile and its toxin as the cause of the antibiotic-associated pseudomembranous colitis (PMC). Within a few years, there was the development of a diagnostic assay, a description of a clinical and pathological spectrum of the disease, a definition of risk factors and characterization of the two toxins that account for the pathological event. Additional information regarding the microbiology, pathogenesis, clinical manifestations, diagnosis and treatment has rapidly developed. These features are beyond the scope of this report, and the reader is referred to several recent reviews.

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Pothoulakis, Charalabos, Ignazio Castagliuolo, and J. Thomas LaMont. "Nerves and Intestinal Mast Cells Modulate Responses to Enterotoxins." Physiology 13, no. 2 (April 1998): 58–63. http://dx.doi.org/10.1152/physiologyonline.1998.13.2.58.

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Experiments in intact animals exposed to enterotoxins demonstrate that neurons and immune cells of the lamina propria regulate toxin-induced diarrhea and tissue damage. Clostridium difficile toxins cause profound diarrhea and acute inflammation by activating a complex cascade initiated by toxin binding to enterocyte receptors.

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Rupnik, Maja, and Sandra Janezic. "An Update on Clostridium difficile Toxinotyping." Journal of Clinical Microbiology 54, no. 1 (October 28, 2015): 13–18. http://dx.doi.org/10.1128/jcm.02083-15.

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Toxinotyping is a PCR-restriction fragment length polymorphism (RFLP)-based method for differentiation ofClostridium difficilestrains according to the changes in the pathogenicity locus (PaLoc), a region coding for toxins A and B. Toxinotypes are a heterogenous group of strains that are important in the development of molecular diagnostic tests and vaccines and are a good basis forC. difficilephylogenetic studies. Here we describe an overview of the 34 currently known toxinotypes (I to XXXIV) and some changes in nomenclature.

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Karlsson, Sture, Bruno Dupuy, Kakoli Mukherjee, Elisabeth Norin, Lars G. Burman, and Thomas Åkerlund. "Expression of Clostridium difficile Toxins A and B and Their Sigma Factor TcdD Is Controlled by Temperature." Infection and Immunity 71, no. 4 (April 2003): 1784–93. http://dx.doi.org/10.1128/iai.71.4.1784-1793.2003.

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ABSTRACT Growth temperature was found to control the expression of toxins A and B in Clostridium difficile VPI 10463, with a maximum at 37°C and low levels at 22 and 42°C in both peptone yeast (PY) and defined media. The up-regulation of toxin A and B mRNA and protein levels upon temperature upshift from 22 to 37°C followed the same kinetics, showing that temperature control occurred at the level of transcription. Experiments with Clostridium perfringens using gusA as a reporter gene demonstrated that both toxin gene promoters were temperature controlled and that their high activity at 37°C was dependent on the alternative sigma factor TcdD. Furthermore, tcdD was found to be autoinduced at 37°C. Glucose down-regulated all these responses in the C. perfringens constructs, similar to its impact on toxin production in C. difficile PY broth cultures. C. difficile proteins induced at 37°C and thus coregulated with the toxins by temperature were demonstrated by two-dimensional sodium dodecyl sulfate-polyacrylamide gel electrophoresis and identified as enzymes involved in butyric acid production and as electron carriers in oxidation-reduction reactions. The regulation of toxin production in C. difficile by temperature is a novel finding apparently reflecting an adaptation of the expression of its virulence to mammalian hosts.

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Stojanović, Predrag, Nevena Stojanović, Branislava Kocic, Dobrila Stanković-Đorđević, Tatjana Babić, and Kristina Stojanović. "Asymptomatic carriers of clostridium difficile in serbian population." Open Medicine 7, no. 6 (December 1, 2012): 769–74. http://dx.doi.org/10.2478/s11536-012-0067-z.

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AbstractThe aim of the research was to determine the intestinal carriers of C. difficile in different human population groups in Serbia. The research enrolled 877 persons with formed stools: (newborn children in maternity hospitals for up to two weeks old) (23), group A; children aged from two weeks to two years (121), group B; children aged two to 10 years (54), group C, healthy individuals aged 10 and over (516), group D; patients hospitalized for at least 48 hours (100), group E; staff of the Clinical Center in Nis, Serbia, (63), group F. The toxins A and B of C. difficile were detected by ELISA-ridascreen Clostridium difficile Toxin A/B (R — Biopharm AG, Darmstadt, Germany). The toxin A of C. difficile was detected using ColorPAC Toxin A test (BectonDickinson, New Jersey, USA). Out of the total number of persons (877), the carriers of certain types of toxin-producing strains of C. difficile were distributed as: 6.04% (A−/B−), 1.83% (A+/B+) and 0.11% (A−/B+). In most groups (5/6), the dominance of non-toxigenic (A−/B−) isolates was established, with the rate of carriers 1.75 – 30.43% depending on the group. Toxigenic isolates were prevalent only in the group F in relation to non — toxigenic (7.94% versus 4.76% of persons). In other groups, the carriers of toxigenic strains ranged from 0.00 – 17.45%. The presence of asymptomatic intestinal carriers of C. difficile in the human population, indicate the possible reservoirs and sources of infection.

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Sharma, Madhu, Uma Chaudhary, Aparna *, Sarita Yadav, and Aakanksha *. "Detection of Clostridium difficile toxins A & B." Journal of Gastrointestinal Infections 3, no. 1 (2013): 64–65. http://dx.doi.org/10.5005/jogi-3-1-64.

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Young, V. B., and P. C. Hanna. "Overlapping Roles for Toxins in Clostridium difficile Infection." Journal of Infectious Diseases 209, no. 1 (August 27, 2013): 9–11. http://dx.doi.org/10.1093/infdis/jit461.

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Murray-Leisure, Katherine A., and Eden A. Suguitan. "Detection of Clostridium difficile Toxins A and B." American Journal of Clinical Pathology 88, no. 3 (September 1, 1987): 394. http://dx.doi.org/10.1093/ajcp/88.3.394a.

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Khardori, N. M. "Treatment with Monoclonal Antibodies against Clostridium difficile Toxins." Yearbook of Medicine 2010 (January 2010): 106–8. http://dx.doi.org/10.1016/s0084-3873(10)79679-6.

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Polage, Christopher R., David L. Chin, Jhansi L. Leslie, Jevon Tang, Stuart H. Cohen, and Jay V. Solnick. "Outcomes in patients tested for Clostridium difficile toxins." Diagnostic Microbiology and Infectious Disease 74, no. 4 (December 2012): 369–73. http://dx.doi.org/10.1016/j.diagmicrobio.2012.08.019.

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Chandrasekaran, Ramyavardhanee, and D. Borden Lacy. "The role of toxins in Clostridium difficile infection." FEMS Microbiology Reviews 41, no. 6 (October 18, 2017): 723–50. http://dx.doi.org/10.1093/femsre/fux048.

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Journal articles on the topic 'Clostridium difficile toxins'

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