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Overview of Fatty Liver Hemorrhagic Syndrome in Poultry

By Steven Leeson, PhD, University of Guelph

Fatty liver hemorrhagic syndrome (FLHS) was first described in the 1950s as excessive fat in the liver of prolific laying hens, associated with varying degrees of hemorrhage. The condition is almost universally confined to caged birds fed high-energy diets and is most often seen in white-egg layers in warm, summer months. The liver is usually enlarged, putty colored, and very friable, showing varying degrees of hemorrhage. The abdominal cavity often contains large amounts of oily, unsaturated fat. Affected birds often have pale combs, likely as a consequence of reduced egg production. The ovary is usually active, at least in the early stages of FLHS, and the metabolic and physical stress associated with oviposition may be factors that induce the final fatal hemorrhage.

Because FLHS seems to occur only when birds are in a positive energy balance, body weight monitoring is a good diagnostic tool, as is knowledge of daily feed intake and environmental temperature. Through force-feeding techniques, it has been shown that FLHS is caused by a surfeit of energy rather than an excess of any particular nutrients such as fat or carbohydrate. The condition can be induced experimentally in layers and even male birds by administration of estrogen. This supports the concept that FLHS occurs more frequently in high-producing birds that presumably are producing more estrogen from very active ovaries. Injecting immature pullets with testosterone also causes increased feed intake and liver fat accumulation, although without any major incidence of fatty liver.

FLHS is easy to recognize at necropsy because of the liver hemorrhage and the fact that the liver is enlarged and engorged with fat. 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, is not always specific to FLHS. Normal layers that are fed appreciable quantities of yellow corn or high levels of xanthophyll pigments will also have a yellow-colored liver but without associated hemorrhages. A number of specific diet ingredients can induce liver hemorrhage but without concomitant accumulation of excess fat. Likewise, feeding rancid fat can cause liver hemorrhage, again without fat accumulation. In birds with FLHS, the liver dry matter is characteristically at least 40% fat. The degree of FLHS can be described as a poultry liver hemorrhage score, which is usually based on a scale of 1–5, in which 1 = no hemorrhage; 2 = 1–5 hemorrhages; 3 = 6–15 hemorrhages; 4 = 16–25 hemorrhages; and 5 = >25 hemorrhages, as well as a massive, usually fatal, hemorrhage. There is some evidence that fatty liver disorder also impairs calcium metabolism in the bird, and hence skeletal integrity and eggshell quality. Layers with FLHS have increased blood levels of estrogen, osteocalcin, and leptin-like protein. There seems to be concomitant upregulation in bone turnover, which is a very significant occurrence for a laying hen that already relies on significant daily flux of calcium in and out of the skeleton.

Attempts have been made to prevent or treat the condition through dietary modification. Substituting carbohydrate with supplemental fat, while not increasing the energy content of the diet, seems to be beneficial. Presumably such modification means that the liver needs to synthesize less fat for yolk. Replacement of corn with other cereals, such as wheat and barley, is often beneficial. However, this substitution may involve reducing the dietary energy level or necessitate using additional fat to maintain isoenergetic conditions, two factors known to influence FLHS. FLHS has reportedly been reduced through the use of various byproduct feeds such as distiller’s grains, fish meal, and alfalfa meal. Although such mode of action is unclear, unintentional supplementation of selenium may be involved. There are reports of layers having greater incidence of fatty liver when fed chelated trace minerals versus conventional inorganic minerals. However, the use of organic minerals in layer diets is increasing, and FLHS is not usually reported. There are also reports of association with Mycoplasma infection.

FLHS is best prevented by not allowing an excessive positive energy balance in older birds. Body weight can be monitored and, when potential problems are seen, remedial action taken to limit energy intake through the use of lower energy diets and/or change in feed management. A wide energy:protein ratio in the diet will aggravate FLHS. When a farm has a history of FLHS, the diet should contain at least 0.3 ppm selenium, ideally as organic selenium, up to 100 IU vitamin E/kg diet, and appropriate levels of an antioxidant such as ethoxyquin. These various additives collectively help to limit the occurrence of tissue rancidity, and hence hemorrhage of the excess fat in the liver.