Transcript enteritis
Enteritis in Poultry Gizzard Pancreas Duodenum (E. acervulina) Jejunum (E. maxima) Meckel’s diverticulum Ceca (E. tenella) 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 Enteritis in Poultry DAMAGE Damage to proximal E. acervulina intestine, like E. acervulina, Cp 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 MULTIPLY intestine damaging toxin. Damage to cecal lining, like E. tenella, may allow proliferation E. tenella of Cp above normal levels. 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 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 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 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 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) The Enteritis Cycle Toxins Release Clostridium Perfringens Intestinal Damage Enteritis in Poultry Types of bacterial enteritis: Clostridial enteritis Necrotic enteritis Dysbacteriosis Ulcerative enteritis Enteritis Economics Costs of disease Costs: 20,000 birds/house Mortality Extra Feed Weight losses $321.00 $327.60 $230.00 Total $878.60/ house +Carcass quality/down grading/ and processing Also losses when mortalities not detected DETAIL Norton, R. A. and Hess, J. B., Auburn University. 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 Enteritis in Poultry The role of enteritis influencing nutrient utilization: • • • • • • • Ingestion Digestion Absorption Transport Storage Mobilization Metabolism Reference: Ruff & Allen 1990; Baker 1993 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 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 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 The Elanco Commitment • • • • • • Consistent scoring guide EHTS MIC - Studies Ongoing efficacy studies Global impact assessment Product Portfolio "Building the Wall of Protection" Maxus Clostridium Enteritis Challenge Feed Composition/ Genetics 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. 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 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 Elanco Breaks The Enteritis Cycle Clostr. Perf. control Surmax/ Maxus Elancoban Monteban Maxiban Tylan Cocci control Toxins Release X X Clostridium Intestinal perfringens Damage Monteban Elancoban Maxiban 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 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 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 Dysbacteriosis • Also known as – Clostridial enteritis – SIBO (small intestinal bacterial overgrowth) – "summer gut" – "hit the wall" – "flushing" – "feed passage" 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 Dysbacteriosis • Droppings – loose threadlike and sticky • Water/Feed – lower feed intake with water consumption normally staying constant • Consequences – reduced growth and uniformity Clostridium Perfringens In the cecum: Co-exist naturally In the small intestine: Proliferate and release harmful toxins Destroys gut wall Thickened and inflamed walls Mortality: Death loss: 3%/week 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: 2.20 (+.20 worse) Weight loss: .25 lbs./bird Extra feed: .84 lbs./bird Feed cost: $195/ton Production cost: 23¢/lb. Nutritional Influences • • • • • • • Raw Materials Wheat/low quality corn Fishmeal Bakery byproducts Enzymes Rape seed Fusaria sp.