enteritis

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Enteritis in Poultry
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Gizzard
Pancreas
Duodenum (E. acervulina)
Jejunum (E. maxima)
Meckels diverticulum
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

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Enteritis in Poultry
DAMAGE
E. acervulina
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
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
Intestinal Damage
Clostridium Perfringens
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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
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"
Wall of Protection
Line of Treatment
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 BreaksThe Enteritis Cycle
Clostr. Perf. control Surmax/ Maxus
Elancoban Monteban Maxiban Tylan
Cocci control Monteban Elancoban Maxiban
Toxins Release
X
X
Intestinal Damage
Clostridium perfringens
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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
• 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 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.
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Nutritional Influences

• Raw Materials
• Wheat/low quality corn
• Fishmeal
• Bakery byproducts
• Enzymes
• Rape seed
• Fusaria sp.