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Enteritis in Poultry
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Gizzard Pancreas Duodenum (E. acervulina) Jejunum (E. maxima) Meckel’s
diverticulum Normal poultry digestive tract. Important structures are duodenum, jejunum and ceca. Cp normally lives in ceca NOT duodenum. Coccidia species identified to show mucosal damage to respective intestinal region. Ceca (E. tenella)
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Poultry Digestion Feed passes from mouth to cloaca
Normal reflux from posterior gut Bile commonly in gizzard, bile duct empties in jujenum Cecal contents reflux Cp normally in anaerobic ceca With altered upper intestine Cp can survive and produce pro-toxins Normal poultry intestinal function involves reflux back and forth. Reflux demonstrated by bile empties into jujenum but often found in gizzard. Cecal contents normally refluxed back into intestine. Cp can leave ceca and migrate proximally to upper intestine. Increase in Cp counts in ceca increases chances for Cp colonization in duodenum. Altered duodenal environment necessary for Cp colonization.
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Enteritis in Poultry E. acervulina Cp E. tenella DAMAGE MULTIPLY
Damage to proximal intestine, like E. acervulina, may create anaerobic conditions in the upper intestine. Cp may replicate in the upper intestine near ample trypsin available from the pancreas. Trypsin may cleave pro-toxin Cp metabolic by-product producing intestine damaging toxin. Damage to cecal lining, like E. tenella, may allow proliferation of Cp above normal levels. Cp MULTIPLY READ THE SLIDE! Damage in the duodenum/jejunum needed for Cp colonization in upper gut. E. acervulina may be source of damage to upper intestine. Damage in the ceca allows Cp to multiply. E. tenella may be source of damage to ceca. E. tenella
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What is Enteritis? Disease of small intestine that destroys the gut wall Can be caused by Clostridium Perfringens Produces powerful toxins, which: Damage intestinal mucosa Impair nutrient absorption Can lead to blood loss, toxemia, and death Primarily occurs in broilers 2-6 weeks old and replacement pullets under stress Threatens birds world wide Can spread to subsequent flocks
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Enteritis in Poultry Disease of multiple etiology
A variety of diseases are associated with enteritis Can be chronic or acute Inflammation of the intestines Economic effects can be devastating
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Enteritis in Poultry Conditions commonly associated: Coccidiosis
Ulcerative enteritis Necrotic enteritis Malabsorption syndrome Stunting syndrome Dysbacteriosis Spiking mortality Mycotoxicosis Infections - viral, bacterial, protozoa Nutrient deficiencies Immune responses
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Enteritis in Poultry The problem with enteritis: Often misdiagnosed
Challenge related Causative organisms can occur naturally Can be sub-clinical while eroding performance Etiology is mostly multi-factorial Outbreaks cause severe economic losses Prevention and control is the key
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Enteritis in Poultry Factors contributing to the impact of enteritis:
Management/Control Environment Genetics Nutrients Presence of infectious agents such as: Viruses Bacteria Mycotoxins Protozoa (coccidiosis) Parasites (nematodes)
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The Enteritis Cycle Toxins Release Clostridium Perfringens Intestinal
Damage
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Enteritis in Poultry Types of bacterial enteritis:
Clostridial enteritis Necrotic enteritis Dysbacteriosis Ulcerative enteritis
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Enteritis Economics Costs of disease Also losses when
Costs: 20,000 birds/house Also losses when mortalities not detected Mortality $321.00 Extra Feed $327.60 Weight losses $230.00 Total $878.60/ house +Carcass quality/down grading/ and processing DETAIL Norton, R. A. and Hess, J. B., Auburn University.
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Enteritis Economic Losses
Necrotic Enteritis can have a significantly negative economic impact Economic losses can escalate within a flock, along with subsequent flocks A preventative strategy can minimize economic losses, thus resulting in maximum profitability
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Enteritis in Poultry The role of enteritis
influencing nutrient utilization: Ingestion Digestion Absorption Transport Storage Mobilization Metabolism Reference: Ruff & Allen 1990; Baker 1993
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Enteritis in Poultry Bacterial enteritis:
Subclinical infection of small intestine Caused by mainly Gram positive bacteria Most bacteria exist naturally in cecum and small intestine Triggered by intestinal lesions, poor hygiene and digestion, immune suppression and other factors
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Enteritis in Poultry Predisposing factors of bacterial enteritis:
Increased gut viscosity caused by wheat, barley, rye and fiber diets Some performance enhancers and chemical anticoccidials ineffective against Clostridium perfringens Stress, crowding, ventilation, wet litter Immune suppression Diseases, infections and coccidiosis Poor hygiene/sanitation
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Enteritis in Poultry Clinical Symptoms of Bacterial enteritis:
Depression Loss of appetite Diarrhea Dark feces Blood in feces can be present Increased water consumption Wet litter Mortalities
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The Elanco Commitment Consistent scoring guide EHTS MIC - Studies
Ongoing efficacy studies Global impact assessment Product Portfolio
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"Building the Wall of Protection"
Line of Treatment Maxus Clostridium Enteritis Challenge Feed Composition/ Genetics
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And The Research Goes On …..
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Enteritis in Poultry Controlling Enteritis
Clean and disinfect buildings Maintain dry litter Ensure proper ventilation Avoid overcrowding Reduce immunosuppresive stress and disease Evaluate nutritional and fiber content of feed Control coccidiosis by using stable programs and ionophores vs. chemicals Use preventative as well as controlling medication with effective MIC against Clostr. Perfr.
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Enteritis in Poultry Controlling Enteritis Productivity Enhancer
Use a productivity enhancer with effective MIC against Clostridium perfringens This provides a combination of prevention and performance
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Enteritis in Poultry Controlling Enteritis
Develop preventative coccidiosis control program Create stability and immune stimulation 2-3 programs/year Manage cocci vs. eradication Use primarily ionophore vs. chemicals Specifically select appropriate ionophore
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Elanco Breaks The Enteritis Cycle
Clostr. Perf. control Surmax/ Maxus Elancoban Monteban Maxiban Tylan Cocci control Monteban Elancoban Maxiban Toxins Release X X Clostridium perfringens Intestinal Damage
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Ulcerative Enteritis Caused by Clostridium colinum
Ulcerative enteritis in small intestine Small yellow foci with hemorrhagic borders Often liver lesions Congested enlarged spleen Reference: Berkoff, 1997
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Necrotic Enteritis Caused by Clostridium perfringens Type A or C
Lesions usually confined to the small intestine, primarily jejunum and ileum Severe necrosis of intestinal mucosa Distention due to gas production Swollen livers with necrotic foci
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Necrotic Enteritis Cannot normally survive in the small intestine since it is an aerobic environment Changes can lead to an anaerobic environment in the small intestine Migration from the cecae and proliferation of CP in the small inestine is associated with protoxin elaboration Trypsin will release the toxin from the pro-toxin and initiate necrotic enteritis
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Dysbacteriosis Also known as Clostridial enteritis
SIBO (small intestinal bacterial overgrowth) "summer gut" "hit the wall" "flushing" "feed passage"
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Dysbacteriosis Forced by the economic and genetic demands, the composition of broiler feeds have changed. This could result in dysbacteriosis where birds quit eating and growing. Many broiler producers are faced with this problem
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Dysbacteriosis Droppings Water/Feed Consequences
loose threadlike and sticky Water/Feed lower feed intake with water consumption normally staying constant Consequences reduced growth and uniformity
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Clostridium Perfringens
In the cecum: Co-exist naturally In the small intestine: Proliferate and release harmful toxins Destroys gut wall Thickened and inflamed walls
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Mortality: Death loss: 3%/week Morbidity: Sick birds: 20%
Mortality age: 4 weeks Bird cost: 19¢/bird Feed cost: 34.5¢/bird Mortality cost: 53.5¢/bird Morbidity: Sick birds: 20% 50-day target weight: 5 lbs./bird FCR: (+.20 worse) Weight loss: .25 lbs./bird Extra feed: .84 lbs./bird Feed cost: $195/ton Production cost: 23¢/lb.
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Nutritional Influences
Raw Materials Wheat/low quality corn Fishmeal Bakery byproducts Enzymes Rape seed Fusaria sp.
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