Liver Disorders
Disease challenges by viruses, bacteria, parasites and toxic compounds are common in poultry. One of the most significant factor limiting efficiency and good performance is disease. Hence if disease is prevented or limited efficiency will automatically rise. Poultry production is subjected to intensive housing and management systems. This intensification has been accompanied by an increase in the incidence of diseases.

Healthy flocks normally results in good performance but raising a healthy flock depends upon a number of factors. These factors include management, nutrition, medication and vaccination program and most importantly on the proper development of the birds immune system.

Here we are giving a brief account of those diseases of bacterial or viral origin and that resulted due to metabolic impairment which affect the most important organ of poultry ie LIVER

Fatty Liver Syndrome
Hepatic pathology is a common problem observed by avian practitioners in many diseases. Some diseases are specific to liver, but often the liver is involved in disease processes that also affect a number of other organ systems.

Fatty Liver syndrome is one such condition, which has attracted the attention of poultry breeders and Veterinarians alike. Fatty liver syndrome was first described during 1950s as excessive fat in the liver associated with varying degrees of hemorrhage. This condition is mostly confined to caged birds fed high-energy diets, and often seen in summer months. The liver is usually enlarged, yellow in colours and very friable. The abdominal cavity contains large amounts of fat.

Fatty liver syndrome is an important metabolic disorder in laying flocks after they reach peak in egg production. Liver is the main site of lipid biosynthesis and is particularly very active in egg laying adult females. Yolk lipids and proteins are secreted as lipoproteins under the influence of estrogen in the liver. When hepatic lipogenesis exceeds the capacity of fat transport as lipoproteins, triacylglycerols commence to accumulate in the liver, leading to fatty liver syndrome. The type and level of certain fatty acids may play an important role in the occurrence of this disorder. Certain fatty acids (i.e. conjugated linoleic acids) inhibit the activity of this enzyme in the liver and cause lower levels of oleic acid, which have a significant role in the secretion of triacylglycerols from chicken hepatocytes compared to other fatty acids such as linoleic or palmatic acid.

Deficiency of linoleic acid may be associated with decreased metabolic efficiency, and interfere with the absorption of other nutrients including calcium. Paradoxically, lack of fatty acids can also result in fatty liver infiltration because essential fatty acids are needed for lipid metabolism. If fats become rancid, essential fatty acids may be destroyed, amino acid availability may be reduced and peroxidases may be produced that interfere with the activities of fat and water soluble vitamins (biotin).

It is also a biotin deficiency-related metabolic disease resulting in impaired hepatic gluconeogenesis and increased fat deposition. The problem is caused by low activity of the biotin dependent enzyme pyruvate carboxylase. Birds die from hypoglycemia and the clinical signs and death are related to hypoglycemia.
FLKS in laying hens occur as a result of feeding a low protein, high calorie ration to hens that are not laying enough eggs. In broilers this condition occurs suddenly, as an outbreak usually associated with some management, feed (perhaps fat level) or environmental change that affects feeding. Affected broilers are usually well grown. Clinical signs include weakness with uncoordinated behavior and head movement. The chicks may lie on their breast with their neck and legs extended. Mortality may vary from 5 to 35%. At PM the liver and kidneys are markedly enlarged, pale and fatty with abnormal deposits of fat in subcutaneous tissues, abdominal cavity, and visceral organs. The weights and sizes of the liver, kidney and heart increased, whereas the weight of the thymus decreased?. In addition, the liver appears fragile, rounded with light yellow or yellowish-brown colour. Birds with fatty liver syndrome have 40-70% fat in the liver on dry matter basis.
Metabolic Changes Associated with FLKS
Changes in metabolic measurements brought about by low-biotin diets associated with high and low incidences of fatty liver and kidney syndrome (FLKS):
Liver pyruvate carboxylase (pyruvate: CO2 ligase (ADP) activity will be low in birds affected with FLKS resulting in significantly lower plasma glucose concentrations. It is suggested that the cause of death in birds with FLKS is a low rate of gluconeogenesis during periods without feed, which results in lack of glucose to meet essential functions
Liver weights, blood lactate concentrations, plasma lactate dehydrogenase activities and C16:1: C18:0 fatty acid in liver, adipose tissue and plasma triglyceride will be increased in FLKS.
It may be concluded that FLKS occurs in birds with little or no hepatic gluconeogenesis capacity via pyruvate carboxylase as a result of dietary insufficiency of biotin. The initiation of the syndrome is probably associated with the inhibition of other pathways of gluconeogenesis.

FLKS is frequently confused with fatty liver-haemorrhagic syndrome (FLHS), but these two conditions are different: FLKS causes drop in egg production as hens become increasingly obese, but little increase in mortality, whereas FLHS causes increased mortality with little drop in egg production, since affected hens die from hypovolaemic shock because of liver haemorrhage. Usually hens that die are in full production. Some of the fat in the liver in FLHS may lead to increased fragility and rupture of the liver. This may be the result of high requirement for lipid in the egg yolk of hens in high production and hens that do not die also have fatty livers.

Fatty liver-haemorrhagic syndrome occurs in commercial layers in high production and is frequently the major cause of death in healthy flocks causing up to 5% mortality during the laying cycle. Haemorrhage occurs from ruptured livers. The liver in high production hens may be fragile because of large amount of lipid present to supply lipid for the developing ova. Rupture and death frequently occur during the increased abdominal pressure of egg laying. There has been extensive research into the cause and prevention of FLHS with higher incidence being reported in birds on a high-energy ration in hot weather that could increase the fat content of the liver. Analysis of the fatty acid composition of plasma phospholipids has indicated a difference between normal and FLHS-susceptible laying hens.

However the composition of dietary lipids may be more important than total dietary lipids. Rapeseed meal in the ration increases the incidence of FLHS because erucic acid or other toxic products affect the strength of the connective tissue in the liver.

Attempts have been made to prevent or treat the condition through diet 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. The syndrome has reportedly been reduced through the use of various byproduct feeds such as distiller's grains and fishmeal. Although the mode of action is unclear, unintentional supplementation of selenium may be involved. Fatty liver syndrome 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 fatty liver syndrome. On farms with history of fatty liver syndrome, the diet should be supplemented with selenium and vitamin E, appropriate levels of an antioxidants and liver stimulants.