Deoxynivalenol predisposes for the development of necrotic enteritis in broilers

Deoxynivalenol predisposes for the development of necrotic enteritis in broilers

Gunther Antonissen1,2, Filip Van Immerseel1, Frank Pasmans1, Richard Ducatelle1, Freddy Haesebrouck1, Leen Timbermont1, Marc Verlinden1, Jeroen Dewulf3, Mia Eeckhout4, Sarah De Saeger5, Evelyne Delezie6, An Martel1, Siska Croubels2

1) Department of Pathology, Bacteriology and Poultry Diseases, Faculty of Veterinary Medicine, Ghent University, Salisburylaan 133, 9820 Merelbeke, Belgium 2) Department of Pharmacology, Toxicology and Biochemistry, Faculty of Veterinary Medicine, Ghent University, Salisburylaan 133, 9820 Merelbeke, Belgium 3) Department of Reproduction, Obstetrics and Herd Health, Faculty of Veterinary Medicine, Ghent University, Salisburylaan 133, 9820 Merelbeke 4) Department of Food Science and Technology, Faculty of Biosciences and Landscape Architecture, Ghent University, Schoonmeerstraat 52, 9000 Ghent, Belgium 5) Department of Bio-analysis, Faculty of Pharmaceutical Sciences, Ghent University, Harelbekestraat 72, 9000 Ghent, Belgium 6) Institute for Agricultural and Fisheries Research (ILVO) Animal Sciences Unit, Scheldeweg 68, 9090 Melle, Belgium
E-mail: [email protected]

Subclinical necrotic enteritis (NE) contributes to important economic losses in the broiler industry. The pathology is caused by netB producing strains of Clostridium perfringens, a Gram-positive, anaerobic bacterium that is present in a restraint quantity in the normal intestinal flora and requires a substantial amount of free amino acids in order to proliferate. The Fusarium mycotoxin deoxynivalenol (DON) has a maximum guidance level set at 5000 µg/kg feed (2006/576/EC) and may affect the intestinal epithelial integrity, subsequently inducing protein leakage into the intestinal lumen (Girish and Smith, 2008). The objective of this study was to examine whether DON at contamination levels below the maximum recommended concentration in poultry feed is a predisposing factor for NE in broilers.
The experiment leans on a highly reproducible in vivo infection model mimicking subclinical NE (Gholamiandehkordi et al., 2007). A total of 360 one-day-old Ross 308 broilers from a commercial hatchery were randomly divided into four groups of three replicates with 30 birds per replica. All birds were fed a starter diet during the first eight days of the experiment, subsequently a grower diet for eight days, followed by a finisher diet during the remaining days. Throughout the entire experiment, group 1 and 4 received a blank diet while group 2 and 3 received an experimentally contaminated diet with DON. All birds in group 1 and 2 were challenged orally with one ml of a culture of C. perfringens strain 56 containing approximately 4 x 108 cfu/ml for four consecutive days starting at day 17. The remaining groups received sterile medium orally. The contamination level of DON and other mycotoxins was assayed using a validated multi-mycotoxin LC-MS/MS method (Monbaliu et al., 2010).
The blank feed contained DON at 75 ± 22 µg/kg (starter), 83 ± 24 µg/kg (grower) and 100 ± 29 µg/kg (finisher). The contaminated feed contained DON at 3761 ± 1100 µg/kg (starter), 4281 ± 1300 µg/kg (grower) and 4384 ± 1300 µg/kg (finisher).
At 1, 2 or 3 days after the final challenge with C. perfringens, chickens were euthanized and scored macroscopically for intestinal NE lesions. Chickens that received DON and C. perfringens had significantly (alpha=0.05, P<0.001) more lesions than chickens that received only C. perfringens, with 46.6% and 19.5% of chickens positive for NE lesions, respectively. In non-inoculated groups no NE lesions were present.
Feeding DON contaminated feed in concentrations lower than the maximum guidance contamination level of 5000 µg/kg to broilers is a predisposing factor for the development of NE.

References
Gholamiandehkordi, A.R.; Timbermont, L.; Lanckriet, A.; Van Den Broeck, W.; Pedersen, K.; Dewulf, J.; Pasmans, F.; Haesebrouck, F.; Ducatelle, R.; Van Immerseel F., 2007. Quantification of gut lesions in a subclinical necrotic enteritis model. Avian Pathology 36, 375-382.
Girish, C.K.; Smith, T.K., 2008. Impact of feed-borne mycotoxins on avian cell-mediated and humoral immune responses. World Mycotoxin Journal, 1, 105-121.
Monbaliu S.; Van Poucke C.; Detavernier C.; Dumoulin F.; Van de Velde F.; Schoeters E.; Van Dyck S.; Averkieva A.; Van Peteghem C.; De Saeger S., 2010. Occurence of mycotoxins in feed as analyzed by a multi-mycotoxin LC-MS/MS method. Journal of Agricultural and Food Chemistry 58, 66-71.

Acknowledgements
This work was financially supported by BIOMIN GmbH, Austria.