Entertoxaemia

AFFECTIONS OF CLOSTRIDIUM PERFRINGENS

  • A – Icterus and Haemolytic anaemia
  • B – Lamb dysentery
  • C – Struck
  • D – Pulpy Kidney
  • E – Calves and Lambs .

CI. perfringens type ‘A’

  • Enterotoxaemia occurs in lamb and calves
  • Haemolytic anaemia, Haemoglobinuria and Icterus - acute syndrome

CI. perfringens type ‘B’

Lamb dysentery

  • Lamb – Less than 3 weeks
  • Also occurs in calves and foals
  • Haemorrhagic enteritis with ulceration
  • Beta toxin
  • Acute – Abdominal pain, depression and reluctance to suckle
  • Peracute -death without symptoms

Microscopic lesions : Haemorrhagic enteritis and ulceration.

CI. Perfringens type 'C' Enterotoxaemia

‘Struck’

  • Adult Sheep – Haemorrhagic enteritis and ulceration of Jejunum and duodenum
  • Peritionitis with large volume of clear yellow fluid accumulation
  • Another form -CI. Perfringens type 'C' – Haemorrhagic enterotoxaemia
  • Affects lambs, calves and piglets within a few days of birth and  fatal

Clostridium perfringens type D ‘ Enterotoxaemia’

Synonym: “Puply Kidney disease”, “Over eating disease”

Definition

  • Acute toxaemia of fattening lambs and sheep which receive ample milk and high concentration of diet characterized by brief nervous symptoms and sudden death with development of pulpy kidney

Incidence

  • It is occurs throughout the world including India

Susceptibility

  • It is an important disease of goats, sheep (fattening lambs) and less commonly in adult sheep
  • Enterotoxaemia has also been reported in calves

Pathogenesis and clinical signs

  • Organism is a normal inhabitant of alimentary tract and the toxin produced are removed by normal movement of ingesta
  • When excessive starch food is fed, the bacteria proliferate and liberate toxin.Hence the name “Over eating disease”
  • Atony of intestine & Stasis of ingests also favours growth of organisms
  • The epsilon toxin produced will be abosrbed immediately by intestinal mucosa resulting in toxaemia
  • Smaller quantities of alpha and theta fractions
  • Toxins reaches the brain causing opisthotonus, convulsion and coma.
  • Toxaemia (Few hours - clonic convulsions)
  • Hyperglycaemia and glycosuria are also observed

Gross lesions

  • Petechial or ecchymotic haemorrhages of epicardium, endocardium, serous surface of intestine, abdominal muscles, diaphragm and hydropericardium
  • Catarrhal or haemorrhagic gastroenteritis
  • Kidneys – swollen and pulpy – “Puply Kidney disease”
  • Reaching the brain causing symmetrical encephalomalacia

Microscopic lesions

  • Kidney: Cloudy swelling and necrosis of epithelium of proximal convuluted tubules
  • Liver and spleen- Congested
  • Brain: Lysis and liquefaction of the white matter, while the grey matter is oedematous.
  • Hyperglycaemia due to increased glycogenolysis of liver glycogen

Diagnosis

  • Symptoms.
  • Glycosuria is a supporting symptom - Urinalysis for glucose
  • Biological test
    • Intestional contents of the affected lambs contain large number of Clostridium organisms. The filtered intestinal contents containing toxin is highly fatal to mice when given intravenously and dies within few minutes to 4 hrs
    • Neutralization test: When the filtrate mixed with known Cl.perfringens type D antitoxin, after incubation, when gives intravenously to swiss mice does not cause its death as the toxins gets inactivated
Last modified: Wednesday, 21 March 2012, 7:40 AM