Enteropathogenic and enterotoxaemia producing clostrida

• Clostridia which produces both localized and generalized effects due to replication and elaboratation of toxins leading to enterotoxaemia and enteropathy.
• Clostridium perfringens types A to E produce a number of potent, immunologically distinct exotoxins which cause the local and systemic effects encountered in enterotoxamias.
• Clostridium perfringens types B, C and D are important in domestic animals.
• Factors which predispose to clostridial proliferation in the intestine include:
• Inappropriate husbandry methods,
• Sudden dietary changes and
• Local environmental influences.

Usual habitat:

• Clostridium perfringens is found in soil, in faeces, and in the intestinal tracts of animals and man.

Types of Clusfridiurn perfringens and their major toxins:

​

​

Note: Alpha toxin causes haemolysis and tissue necrosis , and Beta toxin causes haemorrhagic enteritis and ulcers in the intestines

Lamb dysentery

• Lamb dysentery, caused by C. perfringens type B.
• Morbidity in flock outbreaks can be up to 30% with high mortality rates. Affected lambs, usually in the first week of life, may show abdominal distension, pain and bloodstained faeces.
• Many die suddenly without premonitory signs.
• The high susceptibility of this age group can be attributed to the absence of microbial competition and low proteolytic activity in the neonatal intestine .
• In the absence of proteolytic activity, the (3 toxin retains its potency and produces disease.
• At postmortem, extensive haemorrhagic enteritis with areas of ulceration in the small intestine is present.
• Increased capillary permeability induced by the toxin results in fluid accumulation in the peritoneal cavity and in the pericardial sac.

Factors which predispose to the development of enterotoxaemias associated with Clostridium perfringens in sheep:

A. Low proteolytic activity in the neonatal intestine:

• Presence of trypsin inhibitors in colostrum
• Low level of pancreatic secretion

B. Incomplete establishment of normal intestinal flora in neonates.

C. Dietary influences in older animals:

• Abrupt change to a rich diet
• Grazing on energy-rich diet
• Intestinal hypomotility, a consequence of overeating.

Pulpy kidney disease

• This disease occurs in sheep worldwide , caused by C. perfringens type D.
• The condition is also described as 'over-eating disease' because gorging on a high grain diet or on succulent pasture predisposes to its development.
• Ingestion of excessive quantities of food leads to 'carry-over' of partially digested food from the rumen into the intestine.
• The high starch content in the partially digested food is a suitable substrate for rapid clostridial proliferation.
• Sustained production of Epsilone toxin, which exists as a prototoxin and requires activation by proteolytic enzymes, leads to toxaemia and the development of clinical signs.

Clinical signs:

• Thriving lambs from 3 to 10 weeks of age are commonly affected.
• The course of the disease is usually short and lambs are often found dead. Clinical signs include dullness, opisthotonos, convulsions and terminaI coma.

• Central nervous system signs such as blindness and head pressing may be present in subacute disease.
• Bloating may be evident in the later stages of illness.
• Hyperglycaemia and glycosuria are constant features of the disease.
• Affected adult sheep, which have survived for several days, may exhibit diarrhoea and staggering.
• In acute disease, the only postmortem findings may be scattered hyperaemic areas in the intestines and fluid accumulation in the pericardial sac.
• Rapid kidney autolysis which leads to pulpy cortical softening is a typical postmortem finding.
• Focal symmetrical encephalomalacia, a manifestation of the subacute effects of E toxin on the vasculature, is characterized by symmetrical haemorrhagic lesions in the basal ganglia and midbrain.

STRUCK

• It is caused by C. perfringens type C causes 'struck', an acute enterotoxaemia in adult sheep.
• The disease, which occurs in sheep at pasture, manifests as sudden death, although some animals may be found in terminal convulsions.
• The Beta toxin plays the major role in the pathogenesis of the disease.
• Postmortem findings include jejunal ulceration, patchy hyperaemia in the small intestine and accumulation of fluid in the peritoneal cavity along with congestion of peritoneal vessels and petechial haemorrhages.

Diagnostic procedures:

• Sudden deaths in groups of unvaccinated animals on farms where outbreaks of clostridial enterotoxaemias have previously been recorded may suggest the involvement of C, perfringens types B, C or D.
• In recently-dead animals, postmortem findings may be of value. The presence of focal symmetrical encephalomalacia is indicative of C. perfringens type D.
• Direct smears from the mucosa or contents of the small intestine of recently-dead animals, which contain large numbers of thick Gram-positive rods, are consistent with clostridial enterotoxaemia.
• Glycosuria is a constant finding in pulpy kidney disease.
• Toxin neutralization tests using mouse and guinea-pig inoculation can definitively identify the toxins of C. perfringens present in the intestinal contents of recently-dead animals
• ELISA can be used as an alternative to in vivo assays for demonstrating toxin in intestinal contents.

Treatment and control

• Hyperimmune serum.
• Antibiotic therapy because of acute nature of disease.
• Vaccination is the principal control method:
• Ewes should be vaccinated with toxoid 6 weeks before lambing to ensure passive protection for lambs up to 8 weeks of age.
• Ewes being vaccinated for the first time should be given two doses of vaccine one month apart.
• Annual revaccination is recommended.
• For the prevention of pulpy kidney disease, lambs should be vaccinated with toxoid before they are two months old and a booster injection should be given one month later.
• Sudden dietary changes and other factors predisposing to enterotoxaemia should be avoided

​