Enterotoxemia
• Introduction
• Enterotoxemia, also known as "overeating disease" or "pulpy
kidney disease," is a fatal disease in ruminants caused by
toxins produced by Clostridium perfringens bacteria. It
primarily affects calves, lambs, goats, and other livestock
consuming high-energy diets.
• Etiology (Cause)
• Causative Agent: Clostridium perfringens (Types C and D)
• Toxin Production:
• Type C: Produces Beta toxin, leading to hemorrhagic enteritis.
• Type D: Produces Epsilon toxin, affecting the nervous system and
kidneys.
• Triggering Factors:
• Sudden increase in carbohydrate-rich diets (grain, lush pasture,
milk).
• Rapid bacterial multiplication in the gut, releasing toxins.
• Clinical Signs
• Acute Form:
• Sudden death (often without visible signs).
• Nervous signs (convulsions, head pressing, opisthotonus).
• Frothing at the mouth, difficulty breathing.
• Subacute/Chronic Form:
• Diarrhea (often bloody in Type C cases).
• Abdominal pain, bloating.
• Lethargy, weakness, and loss of appetite.
• Diagnosis
• Clinical History: Sudden death in well-fed animals.
• Post-Mortem Findings:
• Pulpy, swollen kidneys (Type D).
• Hemorrhagic intestines (Type C).
• Pericardial effusion (fluid around the heart).
• Treatment
• Antibiotics (limited success): Penicillin, tetracyclines.
• Anti-Toxin Serum: Effective if administered early.
• Supportive Therapy:
• IV fluids for dehydration.
• Probiotics to restore gut flora.
• Activated charcoal to absorb toxins
•Vaccination:
•Clostridial vaccines (toxoid) given to pregnant animals before parturition.
•Booster doses for young animals.
•Dietary Management:
•Gradual introduction of high-energy feeds.
•Ensure adequate fiber intake.
•Hygiene & Biosecurity:
•Proper sanitation in feeding areas.
•Avoid overfeeding with grains and rich pastures.

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  • 1.
  • 2.
    • Introduction • Enterotoxemia,also known as "overeating disease" or "pulpy kidney disease," is a fatal disease in ruminants caused by toxins produced by Clostridium perfringens bacteria. It primarily affects calves, lambs, goats, and other livestock consuming high-energy diets.
  • 3.
    • Etiology (Cause) •Causative Agent: Clostridium perfringens (Types C and D) • Toxin Production: • Type C: Produces Beta toxin, leading to hemorrhagic enteritis. • Type D: Produces Epsilon toxin, affecting the nervous system and kidneys. • Triggering Factors: • Sudden increase in carbohydrate-rich diets (grain, lush pasture, milk). • Rapid bacterial multiplication in the gut, releasing toxins.
  • 4.
    • Clinical Signs •Acute Form: • Sudden death (often without visible signs). • Nervous signs (convulsions, head pressing, opisthotonus). • Frothing at the mouth, difficulty breathing. • Subacute/Chronic Form: • Diarrhea (often bloody in Type C cases). • Abdominal pain, bloating. • Lethargy, weakness, and loss of appetite.
  • 5.
    • Diagnosis • ClinicalHistory: Sudden death in well-fed animals. • Post-Mortem Findings: • Pulpy, swollen kidneys (Type D). • Hemorrhagic intestines (Type C). • Pericardial effusion (fluid around the heart).
  • 6.
    • Treatment • Antibiotics(limited success): Penicillin, tetracyclines. • Anti-Toxin Serum: Effective if administered early. • Supportive Therapy: • IV fluids for dehydration. • Probiotics to restore gut flora. • Activated charcoal to absorb toxins
  • 7.
    •Vaccination: •Clostridial vaccines (toxoid)given to pregnant animals before parturition. •Booster doses for young animals. •Dietary Management: •Gradual introduction of high-energy feeds. •Ensure adequate fiber intake. •Hygiene & Biosecurity: •Proper sanitation in feeding areas. •Avoid overfeeding with grains and rich pastures.