Understanding Enteritis

8/3/2019 Understanding Enteritis

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Enteritis in Poultry


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Duodenum(E. acervulina)

Gizzard

Jejunum(E. maxima)

Meckels

diverticulum

Ceca(E. tenella)

Pancreas


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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

Poultry Digestion


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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 cecallining, like E. tenella, may allow proliferation

of Cp above normal levels.

Cp

E. acervulina

E. tenella

DAMAGE

MULTIPLY


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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 andreplacement pullets under stress

Threatens birds world wide

Can spread to subsequent flocks

What is Enteritis?


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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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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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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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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

ToxinsRelease

IntestinalDamageClostridiumPerfringens


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Types of bacterial enteritis:

Clostridial enteritis

Necrotic enteritis

Dysbacteriosis

Ulcerative enteritis



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Necrotic Enteritis can have a significantly

negative economic impact Economic losses can escalate within a flock,

along with subsequent flocks

A preventative strategy can minimizeeconomic losses, thus resulting in maximum

profitability

Enteritis

Economic Losses


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The role of enteritis

influencing nutrient utilization:

Ingestion

Digestion

Absorption

Transport

Storage

Mobilization

Metabolism

Reference: Ruff & Allen 1990; Baker 1993



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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, poorhygiene and digestion, immune

suppression and other factors



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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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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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Controlling Enteritis Clean and disinfect buildings

Maintain dry litter

Ensure proper ventilationAvoid 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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Productivity Enhancer

Use a productivity enhancer witheffective MIC against Clostridium

perfringens

This provides a combination ofprevention and performance

Controlling Enteritis



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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

Enteritis in PoultryControlling Enteritis


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Caused by Clostridium colinum

Ulcerative enteritis in small intestine

Small yellow foci with hemorrhagicborders

Often liver lesions

Congested enlarged spleen

Reference: Berkoff, 1997

Ulcerative Enteritis


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Caused by Clostridium perfringens Type A or C

Lesions usually confinedtothe smallintestine, primarily jejunum and ileum

Severe necrosis of intestinal mucosa

Distention due to gas production Swollen livers with necrotic foci

Necrotic Enteritis


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Cannot normally survive in the small intestine

since it is an aerobic environment

Changes can lead to an anaerobic environment inthe 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

Necrotic Enteritis


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Forced by the economic and genetic

demands, the composition of broilerfeeds have changed.

This could result in dysbacteriosis

where birds quit eating and growing.Many broiler producers are faced with

this problem

Dysbacteriosis


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Droppings

loose threadlike and sticky

Water/Feed

lower feed intake with water consumption

normally staying constant

Consequences

reduced growth and uniformity

Dysbacteriosis


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In the cecum:

Co-exist naturally

In the small intestine:

Proliferate and release harmful toxins

Destroys gut wall

Thickened and inflamed walls

Clostridium

Perfringens


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Mortality:

Death loss: 3%/week

Mortality age: 4 weeksBird 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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Raw Materials

Wheat/low quality corn

Fishmeal

Bakery byproducts

Enzymes

Rape seed

Fusaria sp.

Nutritional

Influences

Documents

Understanding Enteritis