The mycotoxin deoxynivalenol predisposes for the development of Clostridium perfringens-induced necrotic enteritis in broiler chickens

PLoS One. 2014 Sep 30;9(9):e108775. doi: 10.1371/journal.pone.0108775. eCollection 2014.

Abstract

Both mycotoxin contamination of feed and Clostridium perfringens-induced necrotic enteritis have an increasing global economic impact on poultry production. Especially the Fusarium mycotoxin deoxynivalenol (DON) is a common feed contaminant. This study aimed at examining the predisposing effect of DON on the development of necrotic enteritis in broiler chickens. An experimental Clostridium perfringens infection study revealed that DON, at a contamination level of 3,000 to 4,000 µg/kg feed, increased the percentage of birds with subclinical necrotic enteritis from 20±2.6% to 47±3.0% (P<0.001). DON significantly reduced the transepithelial electrical resistance in duodenal segments (P<0.001) and decreased duodenal villus height (P = 0.014) indicating intestinal barrier disruption and intestinal epithelial damage, respectively. This may lead to an increased permeability of the intestinal epithelium and decreased absorption of dietary proteins. Protein analysis of duodenal content indeed showed that DON contamination resulted in a significant increase in total protein concentration (P = 0.023). Furthermore, DON had no effect on in vitro growth, alpha toxin production and netB toxin transcription of Clostridium perfringens. In conclusion, feed contamination with DON at concentrations below the European maximum guidance level of 5,000 µg/kg feed, is a predisposing factor for the development of necrotic enteritis in broilers. These results are associated with a negative effect of DON on the intestinal barrier function and increased intestinal protein availability, which may stimulate growth and toxin production of Clostridium perfringens.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Chickens
  • Clostridium perfringens / growth & development
  • Clostridium perfringens / metabolism*
  • Duodenum / metabolism
  • Enteritis / etiology*
  • Enteritis / microbiology
  • Enteritis / veterinary
  • Intestinal Mucosa / drug effects
  • Intestinal Mucosa / metabolism
  • Necrosis / pathology
  • Poultry Diseases / etiology*
  • Poultry Diseases / microbiology
  • Protein Transport / drug effects
  • Trichothecenes / toxicity*

Substances

  • Trichothecenes
  • deoxynivalenol

Grants and funding

This work received the financial support from Biomin GmbH, Herzogenburg, Austria. Co-author Sabine Hessenberger is employed by Biomin GmbH. The funder provided support in the form of salary for author Sabine Hessenberger and provided the deoxynivalenol for in vivo experiments for free, but did not have any additional role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript. The specific role of this author is articulated in the ‘author contributions’ section.