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Selected Publication:

Publication type: Journal Article
Document type: Full Paper

Year: 2013

Author(s): Metzler-Zebeli, BU; Lange, JC; Zijlstra, RT; Gänzle, MG

Title: Dietary non-starch polysaccharides alter the abundance of pathogenic clostridia in pigs.

Source: Livest Sci (152), 1 31-35.



Authors Vetmeduni Vienna:

Metzler-Zebeli Barbara


Abstract:
Some non-starch polysaccharides (NSP) promote the intestinal abundance of pathogenic Escherichia coli in pigs. However, their impact on pathogenic clostridia in the porcine intestinal tract is unknown. The present study aimed to determine the abundance of pathogens belonging to Clostridium clusters I and XI in faeces of growing pigs fed four semi-purified diets containing 5% of purified NSP differing in viscosity and fermentability (low-fermentable low-viscous cellulose; low-fermentable high-viscous carboxymethylcellulose; high-fermentable low-viscous oat beta-glucan; and high-fermentable high-viscous oat beta-glucan). For quantification of clostridial pathogens, toxin genes were determined using quantitative PCR. Clostridium perfringens alpha-toxin was detected in faeces of pigs fed low-fermentable cellulose and carboxymethylcellulose diets but was generally below detection limit for the two high-fermentable oat beta-glucans. Clostridium botulinum toxin C2 was higher (P < 0.05) by 0.7 to 0.9 log units in faeces of pigs fed the low-fermentable low-viscous cellulose diet than of pigs fed the other three diets. Clostridium difficile toxin B and Clostridium sordellii phospholipase C were not detected in pig faeces indicating that pigs were not colonized by these clostridial species belonging to Clostridium cluster XI. In conclusion, high-fermentable beta-glucans decreased the faecal abundance of C perfringens and, together with low-fermentable high-viscous CMC, that of C botulinum in growing pigs when compared to low-fermentable low-viscous CEL. Besides fermentability, structural characteristics and indirect effects of NSP on nutrient flow into the large intestine may have played a role for the abundance of pathogenic clostridial species. (c) 2013 Elsevier B.V. All rights reserved.


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