Enteritis in Poultry

Gizzard Pancreas Duodenum (E. acervulina) Jejunum (E. maxima) Meckels 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 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

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

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.