Immunohistochemical Localization of <i>Clostridium perfringens</i> β2-Toxin in the Gastrointestinal Tract of Horses

Bacciarini, L. N.; Boerlin, Patrick; Straub, R.; Frey, Joachim; Gröne, Andrea

doi:10.1354/vp.40-4-376

Cited by 59 publications

(47 citation statements)

References 26 publications

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“…Recently, the newly discovered beta 2 toxin has been associated with porcine, equine and bovine gastro-enteritis Bacciarini et al, 2003;Waters et al, 2003). This toxin has also been demonstrated in avian C. perfringens type A strains , but its exact role in pathogenesis needs to be further elucidated.…”

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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Section: Perfringens Virulence Factorsmentioning

confidence: 99%

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

et al. 2004

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“…Beta2 toxin, encoded by cpb2, which is another toxin produced by many C. perfringens isolates (Gibert et al, 1997), has been associated with NE in horses (Bacciarini et al, 2003), ruminants (Lebrun et al, 2007), and pigs Waters et al, 2003). However, it has been suggested that beta2 toxin is not involved in NE in poultry (Gholamiandekhordi et al, 2006;Crespo et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

NetB-producing and beta2-producingClostridium perfringensassociated with subclinical necrotic enteritis in laying hens in the Netherlands

et al. 2012

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Since 2006 increasing numbers of laying hen flocks with decreased production have been reported in the Netherlands. At necropsy, birds from affected flocks showed multifocal areas of necrosis in the duodenum. Histologically the duodenum had moderate to marked villus atrophy and fusion with crypt hyperplasia and a mixed inflammatory infiltrate within the lamina propria underlying focal areas of degenerative epithelium. Multifocally, free within the intestinal lumen and associated with epithelial necrosis, were marked numbers of large rod-shaped bacteria. Anaerobic culturing and subsequent toxin typing revealed, in 19 out of 73 affected birds, the presence of Clostridium perfringens strains, either type A or type C harbouring the atypical allele of cpb2 and netB. Eighteen out of these 19 birds carried C. perfringens strains capable of producing beta2 toxin in vitro and all of these birds harboured C. perfringens strains capable of producing NetB toxin in vitro. In contrast, specific pathogen free (SPF) birds lacked gross or histological lesions in their duodenum, and C. perfringens type C was isolated from four out of 15 SPF birds tested. One of these isolates harboured the consensus three allele of cpb2 that produced beta2 toxin in vitro. None of the C. perfringens isolates originating from SPF birds harboured netB. These findings might indicate that the NetB toxin produced by C. perfringens is associated with subclinical necrotic enteritis in layers, whereas the involvement of beta2 toxin in subclinical necrotic enteritis, if any, might be variant dependent.

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“…Clostridium perfringens β-toxin is known to be the primary pathogenic factor of necrotic enteritis in type C strains that produce β-toxin. Necrotizing enteritis is believed to be due to the production of β-toxin by Clostridium perfringens type C. Clostridium perfringens β-toxin can also cause dermonecrosis and oedema in the dorsal skin of animals [16][17][18] . This paper describes the successful isolation and cloning of α-toxin and β-toxin genes from the strains NCTC64609 and C58-1 of Clostridium perfringens respectively.…”

Section: Discussionmentioning

confidence: 99%

Cloning of α-β fusion gene from Clostridium perfringens and its expression

Bai

Yan²,

Zhao

2006

WJG

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Immunohistochemical Localization of Clostridium perfringens β2-Toxin in the Gastrointestinal Tract of Horses

Cited by 59 publications

References 26 publications

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

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

NetB-producing and beta2-producingClostridium perfringensassociated with subclinical necrotic enteritis in laying hens in the Netherlands

Cloning of α-β fusion gene from Clostridium perfringens and its expression

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