Enterotoxemia is caused by Clostridium perfringens type D bacteria. It occurs commonly in young lambs and kids and is characterized by diarrhea, depression, and nervous signs. The bacteria produces alpha and epsilon toxins that damage the intestinal epithelium, causing necrosis and toxemia. Clinical signs include fever, abdominal pain, diarrhea, and neurological signs such as tremors and convulsions. Treatment involves antibiotics, antitoxin serum, supportive therapy, and prevention through gradual diet changes and vaccination.

1. ENTEROTOXEMIA
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2. ENTEROTOXEMIA CAUSED BY
CLOSTRIDIUM PERFERINGENS
TYPE D (PULPY KIDNEY,
OVEREATING DISEASE)
SUBMITTED TO: DR ARSHAD ZAHOOR SB
SUMITTED BY: TASBEEH ULLAH JAN
C/NO : 30
DVM 7TH SEMESTER
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3. ENTEROTOXEMIA
• Occurs in sheep and goat
• Cause by Cl.perfringens
• Cl.perferingens  gram + ve , soil borne,
• Spore forming highly resistant to environment and heat
• Natural inhibitor of GIT.
• Anaerobic bacteria
• Enterotoxaemia keep in mind food poisoning
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4. DEFINATION:
• Overeating, milk colic, pulpy kidney disease, food poisoning (enterocolitis)
• Enteric disease of ruminants specially in young lambs/kids characterized
by
• Diarrhea
• Depression (Depression is serious)
• Nervous signs
• Death
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5. PERFRINGENS
• Related to enteric disease
• Poultry  enteritis
• Sheep/goat  enterotoxemia
• Cl.welchii old name of cl.perfringens
• Types of perfringens
• A
• B
• C
• D
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6. WHY DIFFERENT BACTERIA TYPES
DUE TO EXOTOXIN
A → Alpha toxin
B → alpha + beta toxin
C → alpha + beta
D→ alpha + epsilon
E → alpha + beta +iota
Drug of choice against cl.perfringens  penicillin
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7. EPIDEMIOLOGY
• World wide distribution
• Prevalence rate 1-3% common practice of vaccination against this disease
has reduced but its still a common disease.
• Most common in lambs also important disease of calves and goat,
• Its rarely in adult cattle, deer, camel
• and possibly horses.
• The case fatality rate approximately 100% .
• Disease of young lamb/lids when they are give
• a) high CHO
• b) lush grasses
• c) Over weaned
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8. ETIOLOGY
• Cause by Cl.perfringens (Type D)
• Non motile, bacillus, anaerobic, gram +ve bacteria
• Classified in 5 toxino types (A,B,C,D,E)
1. Alpha (CPA)
2. Beta (CPB)
3. Epsilon (ETX)
4. Iota (ITX)
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9. • Enterotoxaemia type D  produce alpha + epsilon toxin
• Epsilon toxin is only produced By type D  effect the permeability of
membrane.
• Types D  specific to young less than 3 weeks of age.
• Can also effect older goat/cow/calves but less frequent.
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10. PATHOGENESIS
• BACTERIA present in the form of spores increase CHO, milk intake 
bacteria is already present in body but its waiting for CHO (food is a
medium for the growth of bacteria) spore germinate to Cl. In favorable
condition ( to the original shape Cl. Pref).
• Normally Cl. Needs wound but here it needs load 106 organism per gram
• Already in body + bail from feed  reach level ferment the CHO 
produce gas cause distention of the tissue ( sacrolytic  gas production) 
interfere the blood supplies  provide anorexic type environment for the
bacteria  bail produce enterotoxin destruct the GIT by damaging the
intestinal epithelium causing necrotizing enteritis  so loss of fluids +
electrolytes lead to food poisoning on  now cross the intestinal
epithelium enter to the blood stream  cause toxemia or blood poisoning
causes vascular damage to the brain also
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11. PATHOGENESIS
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12. Necrotizing enteritis Vascular damage to brain
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13. CLINICAL SIGNS
• GENERAL:
I. Fever (usually normal but during fever attack 104-105 F ̊ can be there.
II. Severely depressed + anorexic
III. Abdominal pain
IV. Diarrhea
V. Dysentery (sometimes presence of intestinal epith; (blood tinched))
VI. Anemia + dehydration
DIARRHEA
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14. CLINAL SIGNS
• Nervous signs:
I. Deep shallow respiration
II. Champing jaw
III. Teeth grinding
IV. Pressing head
V. Circular movement
VI. Muscular tremors
VII.Convulsions
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15. • Sudden death
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16. CLINICAL PATHOLOGY
• Pulpy kidney
• Gram stained purple color
• Brain
• intestine
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17. DIAGNOSIS
• LABS tests
• Gram staining to detect gram +ve
• Toxin detection
• PCR
• Blood test  hyperglycemia
• Urine test  glycosurea (increases sugar)
• ELISA  to detect antibodies
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18. D.DX
• GOATS
a) Salmonellosis
b) collibacillosis
c) Coocidiosis
• sheep
I. Acute pasteurellosis
II. Rumen overload
• LEAD POSIONING
• RABIES
• PREGNANCY TOXEMIA
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19. TREATMENT
• Antibiotic (broad spectrum)
• Penicillin 10-20000 IU/ kg b,wt
• Tetracycline 10-15-20 mg/kg
• Sulphademadine 100-200mg/kg followed by 50- 100 mg/kg
• Ceftiofur sodium 1.1 mg/kg
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20. • ANTITOXIN:
• 1) ATS (antitoxin serum) epsilon ATS 200 iu /kg
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21. • ANTI BLOTTING LIKE
• Polyoxy ethylne oliec acid triglycerine (blotaryle) star pharma
• Milk of magnesia
• mucines
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22. • SUUPORTIVE THERAPY
• Thiamine vitamin B1
• Fluids + electrolytes
• Dexamethasone 0.04 mg/kg
• Probiotics
• Scorax 10ml/kg
• Selmore 
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23. PREVENTION
• Prevent overeating
• Increases time ( more time feed a day) decreases quantity
• Gradually change the feed
• Do not use grains as CHO in young age.
• Antitoxin
• vaccination
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