Fat cow syndrome, Biology

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Fat cow syndrome

Fat cow syndrome, also known as fatty infiltration of liver, is a highly fatal disease in high yielding dairy animals that occurs a few days before or after parturition.

Etiology: There is excess mobilization of fat from the body depots to liver due to lack of nutrition or excess demand of energy just after parturition. Usually fat from subcutaneous tissue is mobilized and deposited in liver, muscles or kidney. The disease is more common in high yielding dairy cows in early lactation period. It occurs because the energy requirement in high yielding animals is not met by the diet. The affected animals usually die and mortality rate is up to 90%.

Pathogenesis: In normal animals, little amount of fat is deposited in the liver during later stages of pregnancy but at the calving, its amount is greatly increased. However, within few weeks of parturition, the level of fat in liver becomes normal. When there is excess demand of energy, subcutaneous fat is mobilized and free fatty acids are released. It results in increased hepatic lipogenesis and accumulation of lipids in enlarged hepatocytes. The liver glycogen is depleted and lipoproteins are not transported properly from the liver.

Clinical signs: The disease is usually seen within few days of calving or may occur few days before calving. They suffer from loss of appetite and may reveal symptoms of parturient paresis, indigestion or abomasal displacement but do not respond to the treatment of these conditions. Later on they become anorectic and recumbent and show symptoms of ketosis, but glucose treatment also does not help. They reveal ketonuria, gradual weight loss, normal temperature, pulse and heart rates, nervous symptoms like muscular tremors and staring look. Such animals die within one week and before death, they reveal coma and tachycardia.

On the postmortem examination, liver is enlarged, has pale yellow colour and greasy appearance. There is fatty infiltration in the liver.

Diagnosis: It is diagnosed by symptoms and confirmed by blood examination. Activity of liver specific enzymes, bilirubin concentration, and â hydroxybutyrate level are increased while cholesterol, albumin and magnesium levels are decreased. In such animals, ketonuria, leukopenia, neutropenia and lymphopenia are also noticed.

Examination of liver biopsy to record fatty infiltration of liver also helps in its diagnosis.The disease should be differentiated from left abomasal displacement, post- parturient paresis and downer 's cow syndrome. In left abomasal displacement, auscultation of left abdomen reveals tinkling sounds, whereas, cases of post-parturient paresis respond to calcium therapy. In downer's cow syndrome, animals are bright and alert and cannot put weight on hind legs.

Treatment: The affected animals should be treated immediately otherwise they will die. Glucose and electrolyte solution intravenously along with 200-300 units of insulin twice daily subcutaneously and 20 mg dexamethasone on alternate days can be given. This treatment should be continued for about 1 week. In severe cases, 25 g choline chloride can be given 4-times a day by subcutaneous route. Propylene glycol given through oral route also helps in recovery. Occurrence of disease can be prevented by avoiding fat deposition in last trimester of pregnancy and providing proper nutrition to the animals just before and after calving.


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