Effects of a blend of chestnut and quebracho tannins on gut health and performance of broiler chickens.

Antimicrobial restrictions prompted the search for cost and biologically effective alternatives to replace antimicrobial growth promoters (AGPs) in food-producing animals. In addition, the efficacy of this alternatives needs to be contrasted in field/commercial trials under different challenge conditions. However only a few studies describing the impact of tannins or others AGP-alternatives in commercial poultry production conditions are actually available. The aim of the present work is to study how the inclusion of a blend of chestnut and quebracho tannins can affect broiler productive performance and health under commercial conditions. Three experiments with different approaches were conducted: (1) a trial comparing the effects of both additives (tannins vs AGP) on different commercial farms at the same time; (2) the follow-up of one farm during an entire productive year; and (3) an experimental trial using a C. perfringens challenge model in broiler chickens. Although productive results from field trials were similar among treatments, evaluations of gut health indicators showed improvements in the tannins treated flocks. Frequency and severity of intestinal gross lesions were reduced in jejunum (42% vs 23%; p<0.05-1.37 vs. 0.73; p<0.01, respectively) and ileum (25% vs. 10%; p<0.0.5-1.05 vs. 0.58; p<0.01) in tannins treated birds. Results from 16S studies, show that cecal microbiota diversity was not differentially affected by AGPs or tannins, but changes in the relative abundance of certain taxa were described, including Lactobacillus and Bifidobacterium groups. Results from experimental C. perfringens necrotic enteritis showed that tannins treated birds had reduced incidence of gross lesions in jejunum (43.75 vs. 74.19%; p<0.01) and ileum (18.75% vs. 45.16%; p<0.05) compared with control. These results suggest that AGPs can be replaced by tannins feed additives, and contribute in the implementation of antimicrobial-free programs in broilers without affecting health or performance.

Effects of Clostridium perfringens iota toxin in the small intestine of mice.

Iota toxin is a binary toxin solely produced by Clostridium perfringens type E strains, and is structurally related to CDT from C. difficile and CST from C. spiroforme. As type E causes hemorrhagic enteritis in cattle, it is usually assumed that associated diseases are mediated by iota toxin, although evidence in this regard has not been provided. In the present report, iota toxin intestinal effects were evaluated in vivo using a mouse model. Histological damage was observed in ileal loops treated with purified iota toxin after 4 h of incubation. Luminal iota toxin induced fluid accumulation in the small intestine in a dose dependent manner, as determined by the enteropooling and the intestinal loop assays. None of these changes were observed in the large intestine. These results suggest that C. perfringens iota toxin alters intestinal permeability, predominantly by inducing necrosis and degenerative changes in the mucosal epithelium of the small intestine, as well as changes in intestinal motility. The obtained results suggest a central role for iota toxin in the pathogenesis of C. perfringens type E hemorrhagic enteritis, and contribute to remark the importance of clostridial binary toxins in digestive diseases.

Clostridium perfringens type E virulence traits involved in gut colonization.

Clostridium perfringens type E disease in ruminants has been characterized by hemorrhagic enteritis or sudden death. Although type E isolates are defined by the production of alpha and iota toxin, little is known about the pathogenesis of C. perfringens type E infections. Thus far, the role of iota toxin as a virulence factor is unknown. In this report, iota toxin showed positive effects on adherence and colonization of C. perfringens type E while having negative effect on the adherence of type A cells. In-vitro and in-vivo models suggest that toxinotype E would be particularly adapted to exploit the changes induced by iota toxin in the surface of epithelial cells. In addition, type E strains produce metabolites that affected the growth of potential intra-specific competitors. These results suggest that the alteration of the enterocyte morphology induced by iota toxin concomitantly with the specific increase of type E cell adhesion and the strong intra-specific growth inhibition of other strains could be competitive traits inherent to type E isolates that improve its fitness within the bovine gut environment.