Responses of broiler chickens orally challenged with Clostridium perfringens isolated from field cases of necrotic enteritis

Olkowski, A. A.; Wojnarowicz, Chris; Chirino‐Trejo, Manuel; Drew, M. D.

doi:10.1016/j.rvsc.2005.10.006

Cited by 101 publications

(103 citation statements)

References 26 publications

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“…The incidence of Clostridium sp. in poultry gut samples was high, but similar to that reported by authors from other countries such as Johansson et al (2004), Olkowski et al (2006) etc. These high incidences were not surprising if the spread of microorganisms in environment, diet, water, litter, slaughtering, etc were considered.…”

Section: Discussionsupporting

confidence: 90%

“…The alpha-toxin producing C perfringens is a phospholipase C sphingomyelinase that hydrolyzes phospholipids, and as a consequence induces the production of inflammatory mediators (Titball, 1993). This potentially leads the blood vessel contraction and myocardial dysfunction, and as a consequence acute death (Olkowski et al 2006). Therefore, C perfringens, using this toxin, causes necrotic enteritis (NE) in chickens, which can lead to increased mortality, impaired feed conversion, and retarded growth rate (Lovland and Kaldhusdal, 1999;Petit et al 1999;Kaldhusdal et al 2001).…”

Section: Introductionmentioning

confidence: 99%

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Detection of Clostridium sp. and its Relation to Different Ages and Gastrointestinal Segments as Measured by Molecular Analysis of 16S rRNA Genes

Mirhosseini

Seidavi

Saifeddine

et al. 2010

Braz. arch. biol. technol.

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Detection of Clostridium sp. and its Relation to Different Ages and Gastrointestinal Segments as Measured by Molecular Analysis of 16S rRNA Genes

Mirhosseini

Seidavi

Saifeddine

et al. 2010

Braz. arch. biol. technol.

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“…Furthermore, the combination of a lack of gross NE with the presence of histologic abnormalities found in all affected birds resembled the results of experiments in which broilers were orally challenged with C. perfringens. These experiments resulted in an intestinal disorder described as a subclinical form of NE (Olkowski et al, 2006).…”

Section: Discussionmentioning

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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“…6). Each of the bird of experimental groups was drenched with 3 ml of broth that contained 1x10 8 CFU (Olkowski et al, 2006).…”

Section: Determination Of Cfu/mlmentioning

confidence: 99%

“…This experiment was performed with 40% and 20% increase level of maize and another group was given normal feed. Birds of group A were fed with 400gm maize/kg (40% increase of carbohydrate than normal) of normal feed from day 14 to day 20 and challenged on day 21 with 1x10 8 CFU/3ml of inoculums for consecutive 5 days long term exposure trail (Olkowski et al, 2006). The carbohydrate diet was also fed up to 28 days of age of the birds.…”

Section: Experimental Designmentioning

confidence: 99%

Effect of Carbohydrate Rich Diet on Experimental Pathology of Necrotic Enteritis in Broilers

Rahman

Kabir

Sultana

et al. 2014

Bangl. J. Vet. Med.

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The present research work was designed to know the effect of carbohydrate rich diet on the experimental pathology of necrotic enteritis in broilers. For experimental purpose, 15 birds of 14 days of age were grouped into 3 (A, B and C). Birds of group A were fed with 400gm maize/kg (40% increase) and group B were fed with 200gm maize/kg (20% increase) of normal feed from day 14 to day 27 and challenged from day 21 to 25 days with 1x10 8 CFU/3ml of inoculums of Cl. perfringens consecutive 5 days. Group C was kept in control without additional maize. Birds of all groups were observed up to 27 days of age. The clinical signs diarrhea, ruffled feather were common in both group A and B, and less feed intake in group A than group B. There was no mortality in any groups. Birds of all groups were sacrificed at the day 28. Necrosis and hemorrhage in intestine, enlarged liver, and hemorrhage in the base of heart were found in group A (+++). In impression smear of intestines, the average 10-12 bacteria were found in group A and 8-10 bacteria were found in group B in higher magnification (100X). In histopathology, severe infiltration of inflammatory cells including heterophils and lymphocytes and sloughing off mucosal epithelium that changed by pink color cytoplasm with pyknotic nuclei were observed in group A (+++) while group B showed infiltration of inflammatory cells and sloughing off mucosal epithelium (++). The birds of group C were normal in all respects. Anaerobic bacteria counted from intestinal content of group A was 2.8x10 7 CFU/ml, group B was 2.2x10 7 CFU/ml and group C was 1.0x10 7 CFU/ml. From the findings, it may be said that carbohydrate rich diet is a predisposing factor for necrotic enteritis in broilers.

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Responses of broiler chickens orally challenged with Clostridium perfringens isolated from field cases of necrotic enteritis

Cited by 101 publications

References 26 publications

Detection of Clostridium sp. and its Relation to Different Ages and Gastrointestinal Segments as Measured by Molecular Analysis of 16S rRNA Genes

Detection of Clostridium sp. and its Relation to Different Ages and Gastrointestinal Segments as Measured by Molecular Analysis of 16S rRNA Genes

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

Effect of Carbohydrate Rich Diet on Experimental Pathology of Necrotic Enteritis in Broilers

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