Fatty Liver Syndrome

   Fatty liver syndrome was first described in the 1950s as excessive fat in the liver associated with varying degress of hemorrhage. The condition is almost universally confined to caged birds fed high-energy diets, and is most often seen in summer months. The liver is usually enlarged, yellow or putty colored, and very friable. The abdominal cavity contains large amounts of fat. Fatty liver syndrome without excessive body fat is thought to be associated with mycotoxins (eg, aflatoxins) in feed. The affected birds may also have pale combs. The ovary is usually active and the metabolic and physical stress associated with oviposition may be factors that induce the fatal hemorrhage, although mortality generally is <5%. Because fatty liver syndrome seems to occur only when birds are in a positive energy balance, the monitoring of body weight is a good diagnostic tool.
Through force-feeding techniques, it has been shown that fatty liver syndrome is caused by an oversupply of energy rather than by any specific nutrient, such as fat or carbohydrate. The condition can be induced experimentally in layers and even male birds by the administration of estrogen, reinforcing the concept that it occurs more frequently in high-producing birds that presumably are producing estrogen from very active ovaries.
The condition is easy to recognize at necropsy due to the liver hemorrhage and also the fact that the liver is often enlarged and engorged with fat( 40-70%). This makes the liver friable, and it is difficult to remove each lobe in one piece. The pale yellow color of the liver, while characteristic, but, that can happen because of appreciable quantities of yellow corn in feed and/or dietary xanthophylls rather than fatty liver syndrome. In many studies, the degree of fatty liver syndrome is described via a liver hemorrhage score, which is usually based on a scale from 1-5, in which 1 = no hemorrhage, 2 = 1-5 hemorrhages, 3 = 6-15 hemorrhages, 4 = 16-25 hemorrhages, and 5 = >25 hemorrhages, including a massive(usually fatal) hemorrhage.

Attempts have been made to prevent or treat the condition through diet modification. Substituting carbohydrate with supplemental fat, without increasing the energy content of the diet, seems to be beneficial. Replacement of corn with other cereals, such as wheat and barley, oat keeping balance of energy ( even by adding fat)is often beneficial. Although the mode of action is unclear, unintentional supplementation of selenium may be involved.

Best way to ward off this problem is to monitor body weight  and limit energy intake in diet and/or change in feed management. A wide energy:protein ratio in the diet will aggravate fatty liver syndrome. On farms with history of fatty liver syndrome, the diet should be supplemented with 0.3 ppm selenium, up to 100 IU vitamin E/kg diet, and appropriate levels of an antioxidant such as ethoxyquin.
Reference :- Merck Veterinary Manual
 
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