Fatty Liver Haemorrhagic Syndrome in Commercial Laying Hens
Fatty liver hemorrhagic syndrome (FLHS) is a metabolic disorder of layer birds. This condition occurs worldwide and affects all the species of birds. It is characterized by sudden death of birds, heavy fat deposition around the liver along with haemorrhages. Hepatomegaly is most in important features and prone to bleeding lead to death of birds. Fatty liver hemorrhagic syndrome is “the major cause of mortality in laying hens. This condition occurs due to high energy diet and low protein and lack of exercise. It occurs most often in warm, summer months.
Fatty liver syndrome is a dyslipidemia of lipid metabolism, which occurs frequently in caged laying hens, especially during laying peak period. The disease can lead to reduced performance of laying hens, reduced egg production, egg quality, shortened egg production peak or no peak. Fatty liver may also cause sporadic deaths in laying hens. Under normal circumstances, the mortality rate does not exceed 6%, but sometimes more than 20%.
When fatty liver syndrome occurs in the flock, in most cases egg production rate is about 70%-85% and it is hard to reach laying peak. Chronic loss of appetite, depression, soft belly abdomen, less moving activities, pale and even yellow cockscomb and flesh are easy to see. When crowded, driving and catching, hens often occur liver rupture, crest suddenly white, head stretched out or bent back, fell to spasm and died. Some hens showed the symptoms of choline deficiency.
Etiology
Excessive energy diet
Lack of exercise
Hereditary
Excessive estrogen
Clinical Findings
Affected birds shows overweight, pale comb, lethargic, laying of egg is slow, excessive fat deposition around the abdomen. Most of the case bird found dead. In blood serum analysis affected bird increased blood levels of estrogen, osteocalcin, and leptin-like protein.
Necropsy lesions
Necropsy reveals that hepatomegaly, liver pale and engorged with fat. Abdomen shows varying degree of blood clots. The damaged liver also lost structural integrity lead to prone for rupture and hemorrhage. The abdominal cavity also having huge amount of unsaturated fat. The ovary become 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. Affected birds often have pale combs, either due to reduced egg production or blood loss.
Histopathology
Microscopic examination of liver tissue shows liver cells (hepatocytes) that are grossly distended with fat. There may be hemorrhages present. Fat within the hepatocytes are seen as clear spaces (vacuoles) within the cytoplasm of the hepatocytes. The accumulation of fat within the liver weakens the integrity of blood vessels, leading to hemorrhage .
Pathological changes: Liver enlargement, bleeding points on the surface, deposition of a large amount of fat, fragile, yellow brown; when cutting there will be fat droplets attached to the knife and it is easy to see intra-abdominal large blood clot. Abdomen, subcutaneous, kidneys, bottom of heart, intestine, stomach muscle also see a large amount of fat deposition. The birth canal also accumulates a lot of fat, laying eggs must be forced to squeeze and enlarge liver, leading to rupture of the liver and internal bleeding. Fat tissue shows pink colour due to capillaries congestion. Some chickens have pericardial hydrops. Muscular stomach due to congestion and swelling of blood vessels, the surface may have exudate, muscle and intestine sometimes have dark brown liquid, and sometimes the beak also exudates liquid. Duodenal content appears as pale and creamy.
Diagnosis:
Sign : Fatty liver hemorrhagic syndrome is easy to recognize at necropsy because of the liver hemorrhage and because 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, although characteristic, is not always specific to FLHS. Normal layers 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:
• 1 = no hemorrhage
• 2 = 1–5 hemorrhages
• 3 = 6–15 hemorrhages
• 4 = 16–25 hemorrhages
• 5 = >25 hemorrhages, as well as a massive, usually fatal, hemorrhage
Fatty liver disorder also impairs calcium metabolism in the bird, thus affecting skeletal integrity and eggshell quality.
Treatment Options:
- Supplementing feed with 6 % oat hulls
• High protein feed (up to 20% protein).
• Adding Choline chloride, Vitamin E, Vitamin B12 and Inositol to their feed.
• Feeding biotin rich foods for proper fat metabolism
• fish meal
• alfalfa meal
• Increase exercise and free ranging
• Limit fatty foods
• The use of L-Tryptophan in the diet can decrease the syndrome
Prevention and control
- To reduce diet density to avoid birds gaining excess weight. Limit energy intake through the use of a lower energy diet and/or changing feed management.
• Replacing dietary carbohydrates with supplemental fat has been shown to reduce the incidence of FLHS as long as the energy level of the diet is not increased
• Supplemental fat depresses synthesis of new fatty acids, so the liver has to produce less fat for the yolk. This reduces the metabolic burden on the liver.
• Use of crumbled or pelleted feed results in greater feed and energy intake than mash feed. Avoid crumb and pellets in flocks susceptible to FLHS.
• Layer diets should contain adequate levels of Vitamin E (50-100I/kg) and selenium (0.3ppm) to ensure adequate levels of antioxidants to prevent tissue rancidity.
• Supplementation with lipotropic agents such as choline (500mg/ kg), methionine (0.1%), and Vitamin B12 help to mobilize fat from the liver, and support recovery in affected hens.
• Calcium deficiency has been associated with FLHS. This can be addressed with the addition of large-particle calcium and Vitamin D to the ration.
• This allows the bird to eat more calcium without over-consuming the energy component of the feed.
• Avoid any form of stress. Heat stress is a particular concern as it can precipitate or accentuate the occurrence of FLHS.
• Feed intake should be monitored, along with increases in body weights and mortality, and decreases in egg production.
• Routine (at least every 30 days) body weight and uniformity checks can help reveal development of excess body weight.
• Less uniform flocks are more likely to contain relatively heavier birds with a greater risk of FLHS. Perform post-mortem examinations of mortality to assess the condition of the liver, and be alert to excess abdominal fat.
• Methionine, choline, inositol, Vitamin B12, biotin, L-trytophan, carnitine, and selenium are essential for proper liver function and fat metabolism.
Synthetic Choline in Poultry Diet
Choline, a lipotropic factor was first isolated by Strecker in 1962 from hog bile. Choline is commonly supplemented in poultry feed as Choline Chloride. Choline plays very important role in body of birds.
Since methyl group (CH3+) donor feed ingredients play an important role in prevention and management of Fatty Liver Syndrome, inclusion of such quality nutrients in poultry ration is a common practice. Choline is an important methyl group donor, but it has to be converted into betaine before it can donate methyl group. Also, the uptake and conversion of Choline is adversely affected due to gut infection, mal absorption, mitochondrial insufficiency & mycotoxins in the ration etc.
Fatty Liver Syndrome is a condition that generally affects fast growing broilers kept on high energy diets & caged layers since they do not get sufficient opportunity for free movement. Fatty Liver Syndrome is associated with deficiency of methyl group donors in feed, increased liponeogenesis due to deficiency of vitamin-B Complex, reverse mobilization of fat due to stress, high estrogen activity, mycotoxins etc.
Choline is must for birds in modern farming
- Birds provided with high energy diet for faster body weight, therefore to convert the energy into fatty acids require more methyl groups. (To convert them into phospholipids, the transportable form of lipids.)
• Layer birds remain under high estrogenic activity, which stimulates lipogenesis in the liver.
• Cage rearing of birds reduces physical activity, leading to availability of more energy for conversion into fatty acids. Whitehead & Randall (1982)
Requirement of choline though depends upon the type of bird (layers/broilers), availability of Folic acid, Vitamin B12 and methionine level in feed. Insufficiency of the aforesaid may increase the requirement.
Suggested practical requirement is furnished below:
• Commercial Broiler :
Choline mg/Kg. (Added) – 900.00
• Commercial Layers:
Choline mg/Kg. (Added)
(a) Chick mash – 600.00
(b) Grower mash – 250.00
(c) Layer mash – 500.00
Though, small quantity of Choline is synthesized by liver but is not sufficient hence, poultry diets are now a day supplemented with synthetic Choline to bridge the gap.
Limitations of synthetic Choline
• Being a quaternary base, poorly absorbed by G.I, tract
• Gets converted into Tri Methyl Amine (TMA) which is toxic
• Obnoxious smell is a practical concern in processing units & feed mills
• Corrosive nature hence, not a user friendly & damages machinery & equipments
• Interacts adversely with ionophores
• Hygroscopic, hence very unstable
• Interacts also with Vitamins
• Reacts with metal
Whitehead & Randall (1982)
Limitations of synthetic choline have forced the researchers to find out an alternative to replace synthetic choline in poultry diet.
Prevention and treatment of hen’s fatty liver syndrome:
- The scientific preparation of diet: excessive intake of energy feed is the main cause of fatty liver caused by excessive deposition of fat. Diet should be formulated based on the species and egg production rate, so that energy to production ratio can be controlled within a reasonable range. Reduce dietary metabolic energy intake, such as the increase of some fat rich in linoleic acid and reducing carbohydrate can reduce the incidence of this disease. The ratio of metabolic energy to protein in feed (ME / P) varies with temperature and egg laying rate. At high temperature, the ME / P decreased by 10%, at low temperature the number increased by 10%. When egg production rate is greater than 80%, egg ratio in the diet is 60 (16.5%); egg production rate is 65% to 80%, the ratio set as 54 (15%), laying rate is less than 40%,the ratio set as 51 (14%).
- Strengthen the feeding management, provide suitable living space, ambient temperature, reduce the stress of chicken, feed the flock with complete feed can prevent the occurrence of fatty liver syndrome. On the other hand, we should minimize or avoid the frequent activities of workers in breeding house, vibrations in houses, noise, ventilation and heat stress. Due to many factors affecting the occurrence of fatty liver, we must take a comprehensive approach to control.
- A reasonable addition of bile acids: bile acid as a fat metabolism to promote digestion and excretion of liquid can effectively prevent and cure hen fatty liver, improve egg laying performance, extend egg laying peaks, reduce the laying hens sporadic death. On the one hand, bile acids can promote the emulsification, digestion and absorption of fat in the feed and reduce the damage caused by fat deposition to the liver; on the other hand, bile acids serve as signal molecules to repair liver cells; finally, bile acids can promote liver detoxification and removal of those toxins. Bile acid can solve the problem of fatty liver as the above stated aspects.
Compiled & Shared by- Team, LITD (Livestock Institute of Training & Development)
Image-Courtesy-Google
Reference-On Request.
