Over Eating Disease or Pulpy kidney (Enterotoxemia Type D)

Over Eating Disease or Pulpy kidney (Enterotoxemia Type D) is caused by Clostridium perfringens type D. It is sometimes associated with sudden death in cattle due to proliferation of organism in the presence of high amount of carbohydrates in diet.

Etiology

C.perfringens isolates are categorized in to type A-E as based on their ability to produce alpha, beta, epsilon, and Iota toxins.
These toxins are important to exert their effect in developing pathogenesis.
It is caused by Clostridum perfringens Type – D produces alpha and epsilon toxin.
Clostridium perfringen is a Gram-positive, spore-forming, anaerobic bacteria.

Enterotoxemia Types (causing bacteria types) (A, B, C, D and E)

Epidemiology

Prevalence of Infection

The disease prevails mostly in sheep and goats reared on young grass routes and shoots.
The disease has been widely recorded from many countries.

Predisposing factors

Upset in gut flora.
Sudden changes to a rich diet.
Continuous feeding of concentrates.
Presence of excess dietary starch in the small intestine.
Enterotoxemia may also seem to occur spontaneously due to sudden or dramatic changes in weather or other stressors.

Source of infection

Infected materials, fomites, excess rich diets containing organism, soil infection and environmental infection etc.

Transmission

By contact, ingestion of excess diet and inhalation.

Host Affected

All age group of sheep affected except new born.
Lambs 3 weeks to 10 weeks old, suckling lambs and lactating ewes are commonly affected.

Pathogenesis

Degenerative necrosis in the central nervous system is typical and focal encephalomyelitis is a chronic neurological manifestations of non fatal disease.
In normal course ingested organism are destroyed in large numbers in the rumen and abomasum, where in the organism multiply and produce toxin.
Toxaemia does not occur because the movement of ingesta keeps the bacterial population and toxin content down to a low level.
Sometimes if stocked produce toxaemia.
Passage of large quantities of starch granules in to the duodenum when a sheep overeat grain diet or/are change suddenly from a ration consisting largely of roughage to an consisting mainly of grain.
Heavy milk feeding.
Slowing of intestinal movement permit the accumulation of toxin and intestinal stasis predisposes the disease.
The epsilon toxin of the C. perfringens type D increases the permeability of the intestinal mucosa to this and other toxins, thereby facilitating its own absorption.
A receptor for epsilon toxin has been identified on vascular endothelial cells.
Clinical signs and pathology develops due to widespread vascular damage and increase in vascular permeability
Acute: in brain, degeneration of vascular endothelium, Perivascular and intracellular edema, and microscopic foci of necorsis in the basal ganglia, thalamus, internal capsule, substantia nigra, subcortical white matter, and cerebellum. vascular endothelial damage leads accumulation of prolin rich fluid effusions in heart, brain and lung.
Post mortem autolysis of kidney tissue rapidly and is the characteristic of pulpy kidney.
Pronounced hyperglycemia due to mobilization of hepatic glycogen due to mobilization of hepatic glycogen, severe haemoconcentration and elevation of blood concentration of pyruvate, lactate, alpha-ketoglutarate.In goats, ( in contrast to sheep) develop haemorrhagic enterocolitis.
A degree of natural immunity may be attained by non lethal exposure to the toxin, as a proportion of lambs and calves appear to be exposed to subclinical but antigenic levels of C. perfringens toxin so that they become immune mechanism.
The extent of in co-ordination and convulsion is directly related to the severity of lesions.
Peritoneal and pericardial effusions typical in sheep.
Glycosuria is characteristic.

Clinical Signs

Toxin facilitates its own absorption, toxaemia with no enteritis, dullness, retraction of the head, opisthotonus, convulsions and sudden death.

Lambs

Course of the illness is very short (Less than 2 hours and never more than 12 hours).
Many lambs found dead with no signs.
dullness , depression, yawning, facial movements and loss of interest in feed.
Acute: severe chronic convulsion is higher with frothing at the mouth and rapid death.
Cases survive for a few hours show a green , pasty diarrhoea, staggering, recumbency, ophisthotonous, and severe, clonic convulsion.
With normal temperature and increase in the case of severe convulsion.
Death due to convulsion after a period of coma.

Sheep

Adult sheep survive for a long periods upto 24 hours Lagging behind the flock staggering and knuckling Champing of the jaw, salivation, rapid shallow, irregular respiration.
There may be bloat in the terminal stages Irritation-convulsion , muscle tremor, grinding of teeth and salivation.

Calves

Similar to that of adult sheep
Nervous signs predominating
Peracute cases found dead no, no struggling.
Acute: common-sudden onset of bellowing , mania, convulsion persists until death 1-2 hours later
Subacute: many recover do not drink guiet and docile and appear to be blind. Eyes preservation reflex persists.
They may continue to be in this state for 2-3days and recover quickly and completely.
In an outbreak of the disease in calves all three forms of the disease may be seen.

Goats

Diarrhoea is a prominent signs.
Peracute: young kids-convulsions, after initial attack of fever 40.5 degree centigrade Severe abdominal pain, Dysentry and Death in 4-36 hours.
Acute: more common in adults, there is usually no fever, abdominal pain, diarrhoea, prominent with death or recovery in 2-4days.
Chronic: goat may be ill for several weeks, anorexia, intermittent severe diarrhoea, dysentry with epithelial shreds in the feces. Chronic wasting, anemia, eventual emaciation, in chronic cases.

Necropsy Findings

Pericardial and peritoneal effusion is typical in sheep, acute lysis, hyperaemic, toxin damaged tissues and pulpy kidney.
Goats: Catarrahal, fibrinous haemorrhageic enterocolitis.
In chronic cases, Pulpy kidney absent.

Diagnosis

Based on clinical signs, and post mortem examinations.
Bacteriological examination by culture, (isolation and identification).
Definitive diagnosis can be made in the laboratory.
Affected sheep is positive for glycosuria.

Sample Collection

Intestinal contents should be preserved by adding 1 ml of chloroform to 10 ml of contents which have been collected in glass within 12 hours of death.

Differential Diagnosis

Coccidiosis
Salmonellosis
Rumen impaction

Prevention

Inactivated culture of anaerobically grown clostridium welchi type D organism. the prototoxin is converted into toxin by trypsinization. The toxin is rendered non-toxic by formalisation. This is then adjusted with alum hydroxide gel. It is give S/c route 2ml to sheep and goats.
Primary vaccine at 4 months age and above and repeated annually. It gives cross protection between type C and type B. IVPM Vaccine The vaccine is prepared from a highly toxigenic strain of Clostridium perfringens type D grown in anaerobic fluid medium, activated by trypsin, rendered sterile and atoxic by the addition of formalin and precipitated by addition of alum.
It is used for active immunisation of lambs and sheep against enterotoxaemia. pregnant ewes can also be safely vaccinated and the second injection is being given about 3 weeks before lambing.
Lambs above 3 months of age can be be safely vaccinated.
Two injection at an interval of 3-4 weeks are recommended.
The first injection may be so timed that the second one becomes due about a fortnight before the outbreak is anticipated to occur.
Regular vaccination once in 6 months is recommended. Adult sheep 5ml, and lambs 2-3 ml S/C. The immunity is expected to last for 6 months.

Control

Type – D toxoid
Antiserum after birth is given