<i>Clostridium perfringens</i>
            Beta-Toxin Forms Potential-Dependent, Cation-Selective Channels in Lipid Bilayers

Shatursky, Oleg Ya.; Bayles, Robert; Rogers, Marianne; Jost, B. Helen; Songer, J. Glenn; Tweten, Rodney K.

doi:10.1128/iai.68.10.5546-5551.2000

Cited by 80 publications

(87 citation statements)

References 27 publications

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“…CPB forms ϳ12-Å channels that are selective for monovalent cations (90). The toxin shows specificity for only a few cultured cell lines, possibly due to the limited distribution of a still unidentified receptor.…”

Section: Plasmid-encoded Toxinsmentioning

confidence: 99%

Toxin Plasmids of Clostridium perfringens

Adams

Bannam

et al. 2013

Microbiol Mol Biol Rev

231

282

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SUMMARY In both humans and animals, Clostridium perfringens is an important cause of histotoxic infections and diseases originating in the intestines, such as enteritis and enterotoxemia. The virulence of this Gram-positive, anaerobic bacterium is heavily dependent upon its prolific toxin-producing ability. Many of the ∼16 toxins produced by C. perfringens are encoded by large plasmids that range in size from ∼45 kb to ∼140 kb. These plasmid-encoded toxins are often closely associated with mobile elements. A C. perfringens strain can carry up to three different toxin plasmids, with a single plasmid carrying up to three distinct toxin genes. Molecular Koch's postulate analyses have established the importance of several plasmid-encoded toxins when C. perfringens disease strains cause enteritis or enterotoxemias. Many toxin plasmids are closely related, suggesting a common evolutionary origin. In particular, most toxin plasmids and some antibiotic resistance plasmids of C. perfringens share an ∼35-kb region containing a Tn 916 -related conjugation locus named tcp (transfer of clostridial plasmids). This tcp locus can mediate highly efficient conjugative transfer of these toxin or resistance plasmids. For example, conjugative transfer of a toxin plasmid from an infecting strain to C. perfringens normal intestinal flora strains may help to amplify and prolong an infection. Therefore, the presence of toxin genes on conjugative plasmids, particularly in association with insertion sequences that may mobilize these toxin genes, likely provides C. perfringens with considerable virulence plasticity and adaptability when it causes diseases originating in the gastrointestinal tract.

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Section: Plasmid-encoded Toxinsmentioning

confidence: 99%

Toxin Plasmids of Clostridium perfringens

Adams

Bannam

et al. 2013

Microbiol Mol Biol Rev

231

282

View full text Add to dashboard Cite

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“…Moreover, the beta toxin can form a multimeric complex on human umbilical vein endothelial cells, suggesting that it can oligomerize, typical for pore-forming toxins (Steinthorsdottir et al, 2000). Shatursky et al (2000) showed that the beta toxin forms sodium and potassium selective channels in lipid bilayers.…”

Section: Perfringens Virulence Factorsmentioning

confidence: 99%

Clostridium perfringensin poultry: an emerging threat for animal and public health

et al. 2004

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The incidence of Clostridium perfringens-associated necrotic enteritis in poultry has increased in countries that stopped using antibiotic growth promoters. Necrotic enteritis and the subclinical form of C. perfringens infection in poultry are caused by C. perfringens type A, producing the alpha toxin, and to a lesser extent type C, producing both alpha toxin and beta toxin. Some strains of C. perfringens type A produce an enterotoxin at the moment of sporulation and are responsible for foodborne disease in humans. The mechanisms of colonization of the avian small intestinal tract and the factors involved in toxin production are largely unknown. It is generally accepted, however, that predisposing factors are required for these bacteria to colonize and cause disease in poultry. The best known predisposing factor is mucosal damage, caused by coccidiosis. Diets with high levels of indigestible, water-soluble non-starch polysaccharides, known to increase the viscosity of the intestinal contents, also predispose to necrotic enteritis. Standardized models are being developed for the reproduction of colonization of poultry by C. perfringens and the C. perfringens-associated necrotic enteritis. One such model is a combined infection with Eimeria species and C. perfringens. Few tools and strategies are available for prevention and control of C. perfringens in poultry. Vaccination against the pathogen and the use of probiotic and prebiotic products has been suggested, but are not available for practical use in the field at the present time. The most cost-effective control will probably be achieved by balancing the composition of the feed.

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“…Ασκεί την παθογόνο της δράση σχηματί ζοντας πόρους με ολιγομερισμό της κυτταρικής μεμ βράνης. Οι πόροι αυτοί προκαλούν μεταβολή της δια περατότητας της κυτταρικής μεμβράνης, με αποτέλε σμα την εκροή ιόντων καλίου και την εισροή ιόντων JOURNAL OF THE HELLENIC VETERINARY MEDICAL SOCIETY 2010,61(3) ΠΕΡΙΟΔΙΚΟ ΤΗΣ ΕΛΛΗΝΙΚΗΣ ΚΤΗΝΙΑΤΡΙΚΗΣ ΕΤΑΙΡΕΙΑΣ 2010,61(3) νατρίου, ασβεστίου και χλωρίου, οδηγώντας στη διόγ κωση και τελικά στη λΰση του κυττάρου (Shatursky et al 2000, Nagahama et al 2003. Στον άνθρωπο, τα ενδοθηλιακά κύτταρα φαίνεται να αποτελούν τα κύτ-ταρα-στόχος, χωρίς ωστόσο να εκδηλώνει αιμολυτική δράση (Steinthorsdottir et al 2000).…”

Section: τοξίνη -βunclassified

“…Τέλος, σύμφωνα με τους Shatursky et al (2000), η τοξίνη -β εκδηλώνει δράση κυρίως νευροτοξίνης δρώντας στις προγαγγλιακές ίνες ή σε στοιχεία του αυτόνομου νευρικού συστήματος και λιγότερο δράση κυτταρολυσίνης. Η μεταβολή της διαπερατότητας της κυτταρικής μεμβράνης και η διευκόλυνση της ροής των μονοσθενών ιόντων προκαλούν ταχύτατη και μη αναστρέψιμη εκπόλωση του κυττάρου, με αποτέλεσμα τη βλάβη του νευρώνα (Shatursky et al 2000).…”

Section: τοξίνη -βunclassified

“…Η μεταβολή της διαπερατότητας της κυτταρικής μεμβράνης και η διευκόλυνση της ροής των μονοσθενών ιόντων προκαλούν ταχύτατη και μη αναστρέψιμη εκπόλωση του κυττάρου, με αποτέλεσμα τη βλάβη του νευρώνα (Shatursky et al 2000).…”

Section: τοξίνη -βunclassified

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Update on the toxins of Clostridium perfringens and their actions

Tsiouris

Georgopoulou

Petridou

2017

J Hellenic Vet Med Soc

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Clostridia appeared as a distinct class, approximately 2.7 billion years ago, before the initial formation of oxygen. Clostridium perfringens is widely distributed throughout the environment due to its ability to form spores. Furthermore, it is a member of intestinal microbiota in animals and human. In 2002, the complete genome of C perfringens strain 13 was published. Genomic analysis has revealed that C. perfringens lacks the genetic machinery to produce 13 essential amino acids and it obtains these in vivo via the action of its toxins. Toxins of C perfringens can be divided into major, minor and enterotoxin. C perfringens strains are classified into five toxinotypes (A, B, C, D and E), based on the production of four major toxins. Alpha toxin is the best and most studied major toxin of C perfringens and it was the first bacterial toxin established to possess enzymatic activity. It has haemolytic, necrotic and cytolytic activity, it can lyse platelets and leukocytes and it can damage fibroblasts and muscle cell membranes. Expression of epa gene, which is responsible for the production of alpha toxin by C perfringens, is down-regulated in the normal healthy gut, but it is upregulated to initiate enteric disease in response to an environmental signal. C perfringens appears to be regulated in a quorum sensing manner, using oligopeptides, AI-2 or both, to regulate expression of the epa gene, and thus the synthesis of alpha toxin. Beta toxin is recognized as an important agent in necrotic enteritis of humans and it is the second most lethal C. perfringens toxin following epsilon toxin. Beta toxin is a membrane spanning protein that oligomerizes to form channels in susceptible cells or it primarily acts as a neurotoxin. Epsilon toxin is the most potent of the C. perfringens toxins and the third most potent neurotoxin from the Clostridium spp., following botulinum and tetanus toxins. Epsilon toxin of C perfringens type D causes enterotoxaemia and pulpy kidneys disease of lambs. Iota toxin causes disruption of the actin cytoskeleton and cell barrier integrity and it is the less toxic of the major toxins of C perfringens. Although C perfringens enterotoxin is not classified as one of the major toxins of C perfringens, it is the third most common cause of food poisoning in industrialized nations. It is not secreted by the cells of growing bacteria, but it is released only with the sporulation of C perfringens. Not all strains of C perfringens carry the epe gene, which is responsible for the production of enterotoxin. Theta toxin is a pore-forming cytolysin that can lyse red blood cells. It is produced by all types of C perfringens. Together with alpha-toxin, theta-toxin modulates the host inflammatory response. ß2 toxin is a pore forming toxin which is involved in necrotic enteritis of swine and horse, in haemorragic enteritis of bovine in diarrhea cases of dogs and along with enterotoxin in diarrhea cases of humans. Recently, -NetB, a novel toxin that is associated with broiler necrotic enteritis, has been described. The mechanism of its action seems to involve the formation of small hydrophilic pores. Other toxins of C. perfringens include λ-toxin, ô-toxin, μ-toxin, v-toxin, κ-toxin, a-clostripain like protease and neuraminidase/sialidase. These toxins can act as enzymes, while many of them can act synergically or supplementally with major pore forming toxins. Potentially, C. perfringens might produce more toxins, which have not been identified. Finally, the actions of C. perfringens toxins, major or minor, in some diseases have not been figured out.

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Clostridium perfringens Beta-Toxin Forms Potential-Dependent, Cation-Selective Channels in Lipid Bilayers

Cited by 80 publications

References 27 publications

Toxin Plasmids of Clostridium perfringens

Toxin Plasmids of Clostridium perfringens

Clostridium perfringensin poultry: an emerging threat for animal and public health

Update on the toxins of Clostridium perfringens and their actions

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