It is also known as acetonemia in bovines or pregnancy toxaemia in sheep and is associated with ketonemia, ketonuria and low blood glucose.
Etiology: The disease occurs in high producing animals at peak of lactation and is caused due to defective glucose metabolism in the body or dysfunction of adrenal gland. The disease occurs if there is excess of butyrate in the feeds or by feeding of ketogenic feeds. If animals are fed poor quality fodder deficient in propionate and protein, they suffer from the disease. It also occurs in well fed animals due to feeding of excessive protein as there is more production of butyrate in rumen by protein metabolism. During early stage of lactation, low energy intake or inadequate exercise also results in disease. Deficiency of cobalt is also related to the disease as it is helpful in metabolism of propionic acid in TC A cycle.
Pathogenesis: There is low level of glucose due to which liver glycogen level is also reduced and ketone bodies are increased in circulation. These ketone bodies are excreted in all the secretions and excretions of body.
Clinical signs: In bovines, the disease occurs in wasting and nervous form. In wasting form the animal shows gradual loss of appetite and milk yield and does not consume grains. In nervous form, the animal shows false chewing movements, excess salivation, hyperesthesia, blindness, trembling, abnormal movements, and kicking like mule. They also reveal tremors and tetany, and these symptoms usually present for 1-2 h and they reoccur after 10-12h.
Ewes show the symptoms similar to nervous form of disease and they prefer to remain in isolation, reluctant to move and presses its head against inanimate objects. Constipation, drowsiness, muscle tremors, salivation, twitching of lips and champing of jaws are also noticed along with ketotic smell from body secretions and excretions.
Diagnosis: It is detected by symptoms and confirmed by urine examination for presence of ketone bodies by Rothera's test. The level of ketone bodies is also increased in blood and milk. Blood glucose and calcium levels are reduced while eosinophilia, lymphocytosis and neutropenia also occur.
The disease should be differentiated from milk fever which shows flaccid paralysis and is seen within 24-72h of parturition; abomasal displacement which reveals ruminal stasis and loss of body weight is not very prominent; pyelonephritis is associated with presence of casts and cells; TRP shows shift to left and pain in sternal region; and metritis shows escape of pus from uterus and loss of body weight is not prominent.
Treatment: Use of 50% glucose solution @ 500 ml intravenously is very effective. The cases can also be treated with 225 g propylene glycol or glycerol twice daily for 2 days followed by 110 g once daily for 2 days. Glucogenic substances like sodium propionate given @ 110-220 g dose daily orally and calcium and sodium lactate given 1 kg initially followed by 500 g daily for 7 days prevent occurrence of the disease. Adrenocorticoides like dexamethasone used @ 15-25 mg intramuscularly also enhances gluconeogenesis. Along with the glucocorticoid or glucose, insulin may also be given which helps in proper utilization of the glucose inside the body. The occurrence of disease can be prevented by proper feeding of animals and giving exercise. Diets should have proper balance of cobalt, phosphorus and iodine.