Response of Ligated Rabbit Ileal Loop to <i>Clostridium perfringens</i> Type C Strains and Their Toxic Filtrates

Yamagishi, Toshio; Gyobu, Yotaku; Sakamoto, Kenichi; Ishisaka, S; Saito, Kazue; Morinaga, Shinichi; Katsuda, Shogo; Umei, Tamiko; Konishi, Kenichi

doi:10.1111/j.1348-0421.1987.tb03147.x

Cited by 8 publications

(10 citation statements)

References 27 publications

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“…ETX does not induce morphological damage to the small intestine of sheep under experimental or natural conditions (2,6,26), suggesting that ETX is probably not directly responsible for the intestinal mucosal damage occurring during type B infections. Experimental data for the intestinal effects of purified CPB are not available, although type C culture supernatants containing CPB reportedly induced fluid accumulation and damage to the intestine of rabbits (30). Similar histological findings are described for the intestines of young and adult sheep with type B-and C-mediated diseases (18,24).…”

Section: Vol 75 2007 C Perfringens Type B Toxigenic Characteristicsupporting

confidence: 51%

Both Epsilon-Toxin and Beta-Toxin Are Important for the Lethal Properties of Clostridium perfringens Type B Isolates in the Mouse Intravenous Injection Model

et al. 2007

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Clostridium perfringens is capable of producing up to 15 toxins, including alpha-toxin (CPA), beta-toxin (CPB), epsilon-toxin (ETX), enterotoxin, beta2-toxin (CPB2), and perfringolysin O. Type B isolates, which must produce CPA, CPB, and ETX, are associated with animal illnesses characterized by sudden death or acute neurological signs, with or without intestinal damage. Type B pathogenesis in ruminants is poorly understood, with some animals showing lesions and clinical signs similar to those caused by either type C or type D infections. It is unknown whether host or environmental conditions are dominant for determining the outcome of type B disease or if disease outcomes are determined by variable characteristics of type B isolates. To help clarify this issue, 19 type B isolates were evaluated for toxin production during late-log-phase growth via quantitative Western blotting and by biological activity assays. Most type B isolates produced CPB levels similar to those produced by type C isolates in vitro and have the potential to produce genotype C-like disease. The lethality of type B isolate supernatants administered intravenously to mice was evaluated with or without prior trypsin treatment, and monoclonal antibody neutralization studies also were performed. Correlation analyses comparing toxin levels in type B supernatants versus lethality and neutralization studies both found that the main contributor to lethality without pretreatment with trypsin was CPB, whereas neutralization studies indicated that CPB and ETX were both important after trypsin pretreatment. At least part of the CPB produced by type B isolates remained active after trypsin treatment. However, the overall lethalities of most supernatants were lower after trypsin pretreatment. Also, there was a significant association between ETX, CPB2, and CPA production in vitro among type B isolates. However, our results suggest that both CPB and ETX are likely the most important contributors to the pathogenesis of C. perfringens type B infections in domestic animals.

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Section: Vol 75 2007 C Perfringens Type B Toxigenic Characteristicsupporting

confidence: 51%

Both Epsilon-Toxin and Beta-Toxin Are Important for the Lethal Properties of Clostridium perfringens Type B Isolates in the Mouse Intravenous Injection Model

et al. 2007

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“…Production and detection of beta-, epsilon-and iotatoxins. Production and detection were carried out by methods described previously (1,9,14). Twenty percent cooked meat broth supplemented with fructose at a concentration of 1%, 0.5% and 0% was used for the production of beta-, epsilon-and iota-toxins, respectively.…”

Section: Methodsmentioning

confidence: 99%

Polymerase Chain Reaction Test for Differentiation of Five Toxin Types of Clostridium perfringens

Yamagishi

Sugitani

Tanishima

et al. 1997

Microbiology and Immunology

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In order to avoid the use of experimental animals, the polymerase chain reaction (PCR) method was applied to differentiate Clostridium perfringens into five toxin types. Twenty-two out of 23 strains tested produced the toxin(s) corresponding to the toxin gene(s) identified by PCR, and vice versa. Consequently, the gene typing was consistent with conventional typing by animal tests. Twenty-five strains were identified as types different from original ones by the PCR method as well as a toxin neutralization test. These findings suggest that the PCR method, which is easy and timesaving, is applicable to identify the toxin types of C. perfringens as an alternative to animal tests, and that beta-, epsilon-and iota-toxin genes might be lost by long-term preservation. The reasons why the strains lost the genes are discussed.

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“…Isolates of Clostridium perfringens type B and C are responsible for fatal diseases ranging from necrotizing enterocolitis to enterotoxemia in humans and livestock [ 1 – 3 ]. Delta-toxin is a basic protein (32-kDa) produced by certain strains of C .…”

Section: Introductionmentioning

confidence: 99%

Clostridium perfringens Delta-Toxin Induces Rapid Cell Necrosis

et al. 2016

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Clostridium perfringens delta-toxin is a β-pore-forming toxin and a putative pathogenic agent of C. perfringens types B and C. However, the mechanism of cytotoxicity of delta-toxin remains unclear. Here, we investigated the mechanisms of cell death induced by delta-toxin in five cell lines (A549, A431, MDCK, Vero, and Caco-2). All cell lines were susceptible to delta-toxin. The toxin caused rapid ATP depletion and swelling of the cells. Delta-toxin bound and formed oligomers predominantly in plasma membrane lipid rafts. Destruction of the lipid rafts with methyl β-cyclodextrin inhibited delta-toxin-induced cytotoxicity and ATP depletion. Delta-toxin caused the release of carboxyfluorescein from sphingomyelin-cholesterol liposomes and formed oligomers; toxin binding to the liposomes declined with decreasing cholesterol content in the liposomes. Flow cytometric assays with annexin V and propidium iodide revealed that delta-toxin treatment induced an elevation in the population of annexin V-negative and propidium iodide-positive cells. Delta-toxin did not cause the fragmentation of DNA or caspase-3 activation. Furthermore, delta-toxin caused damage to mitochondrial membrane permeability and cytochrome c release. In the present study, we demonstrate that delta-toxin produces cytotoxic activity through necrosis.

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Response of Ligated Rabbit Ileal Loop to Clostridium perfringens Type C Strains and Their Toxic Filtrates

Cited by 8 publications

References 27 publications

Both Epsilon-Toxin and Beta-Toxin Are Important for the Lethal Properties of Clostridium perfringens Type B Isolates in the Mouse Intravenous Injection Model

Both Epsilon-Toxin and Beta-Toxin Are Important for the Lethal Properties of Clostridium perfringens Type B Isolates in the Mouse Intravenous Injection Model

Polymerase Chain Reaction Test for Differentiation of Five Toxin Types of Clostridium perfringens

Clostridium perfringens Delta-Toxin Induces Rapid Cell Necrosis

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