Deficiency diseases-pregnancy toxaemia in sheep , Biology

Pregnancy toxaemia in sheep (twin lamb disease, sleeping ewes disease, pregnancy ketosis).

Pregnancy toxaemia is a multifactor disorder of energy metabolism affecting sheep during late gestation. The disease is characterized by anorexia, neurological dysfunctions, recumbency and death. Pregnancy toxaemia also occurs in goats during late pregnancy.

Aetiology: In sheep, the disease commonly occurs in the last 6 weeks of pregnancy due to inadequate nutrition usually when energy content in the diet is low and insufficient to meet the increasing energy demand during the half of the gestation.Short period of food deprivation, management practices such as crutching, shearing or drenching and change in feed and environment during late pregnancy predispose onset of pregnancy toxaemia.Very well fed ewes may have depressed appetite in late pregnancy due to reduction in rumen volume by the pressure of growing foetus and intra abdominal fat. This can induce excessive adipose mobilization and fatty liver (hepatic lipidosis) and the pregnancy toxaemia. Lack of exercise in such ewes is an important predisposing factor. Excessively thin ewes with poor body condition score (BCS < 2.0) can also suffer from pregnancy toxaemia. Toxaemia may less commonly be associated with transport stress and housing of unaccustomed sheep in late pregnancy. Secondary pregnancy toxaemia occurs concurrently with diseases such as foot-rot and foot-abscess that influence food intake. The ewes carrying triplet or twin lambs and in the 3rd parity are at higher risk. Breed associated susceptibility is also suggested. However, susceptibility in individual sheep depends upon difference in rates of hepatic glucogenesis.

Clinical findings: Foremost signs of pregnancy toxaemia are separation from group, refusal to eat, altered mental state and apparent blindness, which is manifested by an alert appearance but disinclination to move. The disease is more severe, if onset is earlier than day 140 of gestation. The ewes will stand unmoved when approached; and if forced to move, they may hit into the objects and press head against obstacle. As the disease progresses ewes show aimless walking, muscle twitching or tremors of head muscles causing twitching of lips, champing of the jaws and salivation. The muscle tremors spread to other body parts and the sheep falls with tonic-clonic convulsions. Periods between convulsions are marked by head pressing and assumption of ‘star gazing posture’ and incoordination and falling. The breath smells ketotic. Ewes remain recumbent and in a state of profound depression or coma for 6-8 days. There may be foetid diarrhoea prior to death.

Laboratory findings of hypoglycaemia, ketonaemia and ketonuria suggest ketosis. However, hypoglycaemia is not a consistent finding and can be more useful diagnostic test during the early stages of the disease. Concentration of glucose in CSF is more accurate than blood glucose in diagnosis of the disease. Elevated level of ß-hydrobutyrate in serum is also a better indicator. The condition should be differentiated from hypocalcaemia, hypomagnesaemia, pariparturient diseases of central nervous system, lead poisoning, pulpy kidney disease, listeriosis and rabies. Hypocalcaemia occurs within 12 hr of the stress, and considerable proportion of flock  is affected. Laboratory and clinical findings can be used for differential diagnosis.

Treatment and Prevention: Animals respond favourably when treated at an early stage. However, recovery is poor if sheep are recumbent. Administration of intravenous 50% dextrose solution may hasten the death in such cases. Replacement therapy with glucose (60-100 ml 50% dextrose solution intravenously) followed by intravenous drip of balanced salt solution with 5% dextrose is successful. Intramuscular Zinc protamine insulin at dose rate of 20-40 units alternate day for 3 days, and 50-100 ml of calcium borogluconate solution subcutaneously are used for supportive therapy. Oral doses of propylene glycol or glycerine (110g/day) are given to support parenteral glucose therapy in early stage. Oral calcium (12.5g calcium lactate) and potassium (7.5 g potassium chloride), and subcutaneous insulin injection (0.4 unit/kg per day) enhance survival rate.Preventive measures include nutritional management during gestation. Grains should be included in ration to meet the energy demand during the last 6 weeks of gestation. Cereal grains containing 10% protein can be given at the rate of 0.25 kg daily and enhanced to 1 kg daily in the last 2 weeks. Sudden change in type of feed should be avoided and well-fed ewes should be put to sufficient exercise.

Posted Date: 9/19/2012 3:41:19 AM | Location : United States

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