Nutritional Relationship with Necrotic Enteritis Victoria Drouet Pratt, D.V.M., M.A.M. Candidate ! The University of Georgia! Poultry Diagnostic Research Center!
Jefo Poultry Tour, August 2016!
Necrotic Enteritis The Disease
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Clostridium perfringens types A and C !
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Gram positive, spore forming anaerobe!
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Normal inhabitant of the intestines; ceca!
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Egg shells fragments, chick papers, and chick fluff!
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In 2000, estimated to cause $2B worldwide; treatment, loss in production and plant condemns (Timbermont, 2011)!
Normal Clostridium Behavior ✤
Feed on “left overs” from the small intestine; undigestible fiber !
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Clostridium produces its own digestive enzymes!
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Retroperistalsis occurs, but Clostridium are regulated, sent back home!
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Regulators are Lactobacillus that produce antimicrobials and antibacterial peptides produced by intestine (defensins)!
Which Bucket?
Necrotic Enteritis Target Population
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Birds 14 days to 6 months of age!
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Broilers: 2-5 weeks of age!
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Turkeys: (commonly toms) 4-10 weeks of age!
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Commercial layers: 12-16 weeks of age!
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Breeder adults: over 30 weeks of age!
Necrotic Enteritis The Disease
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Clostridium perfringens lacks genetic machinery to produce essential AA. ! Use exotoxins and endotoxins to acquire nutrients from host.! Ability to produce 17 or more toxic exoproteins; classified as types A-E. Immunological difference among the types.!
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Clostridium perfringens Type A: Alpha and Net B!
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Clostridium perfringens Type C: Alpha and Beta !
Toxigenic Effects
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Net B Toxin! Pore former! Holes to cellular membrane! Ion influx (Ca, Na, Cl)!
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Alpha Toxin! Phospholipase-C Sphingomyelinase ! Enterocyte, RBC, and Heterophil!
NE Histopathology
Turkish Towel
Dark livers
Focal areas of necrosis
Necrotic Enteritis Predisposing Factors
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Dietary Ingredients!
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Immune Status!
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Coccidiosis!
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Farm Management!
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Seasonal!
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Antibiotic use Status!
Dietary Factors !
Feed particle size!
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Small Grains/NSP!
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Protein Content!
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Protein Source!
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Fat Quality !
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Calcium Content!
Particle Size !
Feed with mixed large and small size particles, predispose to more NE than feed with uniform particle sizes (Timermont, 2011)!
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Fine particle diets, remain relatively unchanged size in the gizzard and in the gastrointestinal tract (Gabriel, 2003)! Remaining fine feed provides available substrate for Clostridium perfringens growth! Feeding program change; 18doa is ideal (starter-grower)!
Small Grains ! ! !
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Cereals/ Small Grains ! Wheat, barley, rye, and oats! High levels indigestible, water soluble, non starch polysaccharides (NSP)! Change the intestinal viscosity, pH, and bacterial counts compared to maize fed diets (Shakouri, 2008)! Increased viscosity can increase feed retention time, allowing for additional substrate for Clostridium perfringens.!
Small Grains Nonstarch Polysaccharides! Increase Viscosity! Increase Mucous! Decreased Peristalsis! Decreased Digestion! Clostridium �� Environment!!
Protein Content !
Protein rich diets results in a high concentration of proteins in lower GI tract! !
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Unused protein can serve as growth media for Clostridium! In the small intestine, the unused proteins are broken down into nitrogenous compounds (ammonia and amines); increases intestinal pH!
Both protein changes allow for proliferation of Clostridium perfringens (Pavia, 2013)!
Protein Source !
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Animal Protein Meals: Fishmeal and Meat and Bone Meal! Fishmeal may change the cecal microbiota due to its high nutrient availability (Wu, 2014)! Damage to the mucosal epithelium; releasing serum and other nutrients, allowing additional growth factors for Clostridium! Animal fat increases C. perfringens counts compared with vegetable oil (Knarreborg, 2002)!
Fat Quality !
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Biogenic amines can cause lower intestinal pH; overwhelm fermentative capacity of the cecum (Hoerr, 1998)! Rancid fat produces toxic peroxides, damages intestinal integrity (Cabel, 1988)! Do poor quality fat products contain increased C. perfringens spores??!
Calcium Content !
High calcium diets (0.9%) verses lower calcium diets (0.6%) had negative effect on mortality associated with NE. (Paiva, 2013)!
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No changes seen in bone ash or bone fractures with 0.6% Ca!
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Diets greater than 0.75% calcium inclusion, linear effect with NE!
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Both Alpha and NetB toxins depend on Ca for full activity!
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Net B pore forming in enterocytes, influx of ions, then osmotic lysis!
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More Ca in the environment, more apoptosis; more NE?!
Necrotic Enteritis Predisposing Factors
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Dietary Ingredients!
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Immune Status!
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Coccidiosis!
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Farm Management!
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Seasonal!
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Antibiotic use Status!
Coccidiosis !
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Often 2 or more different types of Eimeria spp. present! Damage to the intestinal mucosa causes inflammation, then mucous production.! Leakage of plasma proteins; rich in amino acids, growth factors, and vitamins ❤️ Clostridium! Intestinal damage causes decreased digestion of feed; additional nutrients for Clostridium!
Intestinal Environment Alterations Management!
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Feed outages! Cold Stress! Litter Conditions! Changes in feed! Stress; Stocking density, air quality, lights…!
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Diseases! ! ! ! !
Coccidiosis! IBDV! CAV! Marek’s!
Summary ! 
There does appear to be a correlation between feed ingredients and the incidence of Necrotic Enteritis-high calcium, high protein, high cereal inclusion, high animal protein inclusion!
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Monitor trends within your operation!
! Veterinarians and Nutritionists to closely monitor feed ingredient and diet changes with an increase in field cases!
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Acknowledgments !
Dr. Chuck Hofacre!
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Dr. Steve Roney !
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Dr. Steve Collett!
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Dr. Margie Lee!