Necrotic enteritis in poultry

necrotic enteritis in poultry

Introduction

Necrotic enteritis in poultry is caused by Clostridium perfringens and serotypes responsible for our Type A and B . Mostly young broilers are affected, but sometimes laying hens ( birds of 4 weeks of age or older) are affected. High-protein feed, intestinal obstruction, and coccidiosis infections create an environment for the growth and infection of C. perfringes in poultry.

Causative Agent:

  • Caused by Clostridium perfringens, a gram-positive, obligate anaerobe.
  • Grows on blood agar at 37°C (98.6°F), producing a distinct double zone of hemolysis.

Types Involved:

  • C. perfringens Types A and C are most commonly linked to necrotic enteritis in poultry.
  • Bacteria produce toxins that damage the small intestine and liver.

Environmental Presence:

  • Ubiquitous in soil, dust, feces, feed, and used poultry litter.
  • Naturally inhabits the intestines of healthy birds without necessarily causing disease.

Triggers & Predisposing Factors:

  • The disease develops when the intestinal balance is disrupted or mucosal damage occurs.
  • Common triggers include:
    • Intestinal disturbances: Coccidiosis, mycotoxicosis, salmonellosis, ascaridiasis.
    • Dietary factors: High levels of animal by-products (e.g., fish meal), wheat, barley, oats, or rye.
    • Slow intestinal transit: Promotes bacterial overgrowth and toxin production.

Pathogenesis

  1. ColonizationC. perfringens overgrows in the small intestine, aided by gut disruptions (e.g., coccidiosis, diet changes).
  2. Toxin Production: Key toxins like NetB (pore-forming) and alpha toxin (membrane-damaging) are released.
  3. Mucosal Damage: Toxins destroy intestinal epithelial cells, causing necrosis, ulceration, and hemorrhage.
  4. Inflammation: Immune response worsens tissue injury, impairing nutrient absorption.
  5. Systemic Spread: Severe cases lead to bacteremia, septicemia, and death.

Disease Duration & Mortality:

  • Outbreaks last 5–14 days in an affected flock.
  • Mortality ranges from 2% to 50%, depending on severity.

Clinical findings

  • Primary Clinical Sign:

    • The sudden increase in flock mortality is often the first and only noticeable symptom.
  • Additional Symptoms:

  • Affected birds may show:
  • Lethargy and depression.
  • Ruffled feathers.
  • Diarrhea
  • loss of appetite
  • unwillingness to move
  • Gross Lesions:
  • Primarily found in the small intestine (jejunum and ileum).
    • Characteristic findings:
  • Intestines may appear ballooned, fragile, and distended with foul-smelling, brown fluid.
  • The mucosa is covered with a tan-to-yellow pseudomembrane(Turkish Towel appearance), which sometimes takes on a diphtheritic-like appearance.
  • The coloration, ranging from light orange to deep brown, is likely due to fresh or oxidized blood mixed with bile staining.
  • In severe cases, epithelial sloughing may occur, with lesions either localized or extending throughout the intestine.

Diagnosis

Presumptive Diagnosis

  • Clinical signs: diarrhea, depression.
  • Gross lesions: thickened, necrotic small intestine.

Confirmation

  • Microscopy: Gram-positive rods in mucosal scrapings.
  • Histology: Coagulative necrosis, bacterial rods in debris.
  • Bacterial Isolation: C. perfringens with double-zone hemolysis on blood agar.
  • Note: Use selective media for accurate identification.

Differential Diagnosis

  • Coccidiosis: Eimeria brunetti causes less severe lesions.
  • Ulcerative Enteritis: C. colinum causes focal lesions and hepatic necrosis.

Treatment for Necrotic Enteritis

Antibiotics for Treatment (Administered in Drinking Water):

  • Amoxicillin
  • Ampicillin
  • Chloramphenicol
  • Ciprofloxacin
  • Doxycycline
  • Neomycin
  • Erythromycin
  • Furazolidone

Antibiotics for Reducing Fecal Shedding (Administered in Feed):

  • Lincomycin
  • Tylosin
  • Bacitracin
  • Furazolidone

Prevention and Control

1. Prevent Coccidiosis 

  • Control Eimeria acervulina and Eimeria maxima infections.
  • Use coccidiosis vaccines (modified live or recombinant).
  • Historically managed with anticoccidial feed additives (virginiamycin, bacitracin, lincomycin, ionophores).

2. Dietary Management

  • Avoid excessive animal by-products, wheat, barley, rye, and fish meal.
  • Add enzymes to improve digestion if feeding wheat, barley, or rye.

3. Probiotics & Competitive Cultures

  • Supplement feed with probiotics to prevent C. perfringens overgrowth.

FAQ’s

What is Necrotic Enteritis (NE)?

  • Bacterial infection by Clostridium perfringens, causes intestinal necrosis, inflammation, and mortality.

2. What causes NE?

  • Overgrowth of C. perfringens due to high-protein diets, gut damage (e.g., coccidiosis), poor sanitation, or stress.

3. What are the signs?

  • Acute: Sudden death, dark diarrhea.
  • Chronic: Poor growth, diarrhea.
  • Post-mortem: Thickened, necrotic intestines.

4. How is it diagnosed?

  • Clinical signs, post-mortem lesions, and lab tests for C. perfringens.

5. How is NE treated?

  • Antibiotics (e.g., bacitracin), probiotics, and addressing predisposing factors.

6. Can it be prevented?

  • Yes, via biosecurity, balanced diets, coccidiosis control, and feed additives (probiotics, prebiotics).

7. Is NE zoonotic?

  • No, but C. perfringens can cause human foodborne illness.

 

About the Author

Hamza Sajid

I’m Hamza Sajid, the passionate creator behind vethsm.com. As an animal lover and enthusiast, I’ve dedicated this space to celebrating the wonderful world of pets and large animals. From heartwarming pet care tips to fascinating insights about majestic large animals, my goal is to educate, inspire, and connect with fellow animal lovers. Whether you’re a proud pet parent or simply curious about the animal kingdom, you’ve come to the right place.

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