Title: enteritis

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

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

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

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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

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)

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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
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.