DIGNOSIS TREATMENT & CONTROL OF NUTRITIONAL DEFICIENCY DISORDERS IN POULTRY

DIGNOSIS TREATMENT & CONTROL OF NUTRITIONAL DEFICIENCY DISORDERS IN POULTRY

DR. SURINDER KHANNA, POULTRY CONSULTANT

Feeding of poultry on a commercial scale represents a major cost input. Any lack, suboptimal lever or imbalance of nutrients in the feed could result in serious economic losses. Poultry feeds are formulated by incorporating various ingredients including vitamins and minerals to achieve optimum production, depending on the type and strain of birds. Therefore, the incidence of nutritional disorders is remarkably reduced, if not eliminated.
Nutritional deficiency disorders are likely to occur due to errors in mixing, imbalance of nutrients, loss of potency of vitamins, adequate storage or handling of raw ingredients and prepared feeds or interaction of various nutrients in the finished feed. The most common source of these disorders is in the home mixing of poultry feed without adequate knowledge of poultry nutrition and an lack of adequate mixing facilities.
With few exceptions, all ages of poultry are susceptible to nutrient deficiency and the condition is usually confined to an individual flock. Under commercial conditions suboptimal intake of vitamins may result in poor performance of the flock without showing clinical signs of deficiency. It is probably that such effects could occur where continuing changes in genotype are made with emphasis on production performance. Optimum intake of vitamins is important for maintenance of health and reproduction. Disorders due to single nutrient deficiency are rare and difficult to recognize in the field. The utilization of various ingredients depends upon the presence of other e.g. vitamins and miners. However for the sake of simplicity and completeness, each disorder is described separately.
Utilization of vitamins depends upon

1. The availability of vitamins from feed ingredients and their digestibility
2. The quantity of vitamins present in the feed ingredients
3. The quality and composition of feed ingredients, e.g. fat and vitamin E in the feed.
4. The presence of antagonists in the feed e.g. Amprosol and vitamin B1 avidin and biotin, linseed and B6
5. The presence of contaminants such as mycotoxins in the feed.
6. The destruction of vitamins through processing e.g. pelleting and prolonged storage
7. The inter current disease interfering with the absorption e.g. coccidiosis
8. The genetic variation
9. Vitamin A deficiency 
   Vitamin A deficiency is characte5rised by poor growth, weakness, in coordination. Ruffled feathers drop in production and hatchability and lesions in the digestive tract and eyes.

Cause: Low levels of vitamin A in the feed. oxidation of vitamin A in the feed, errors in mixing and inter current disease, e.g. coccidiosis , worm infestation

Clinical signs: The deficiency symptoms in chickens depend upon the vitamin A content and the duration of feeding on deficient feed. Due to the reserves of vitamin A in liver, signs and lesions in mature birds may take 2-5 months to develop. In mature flocks, drop in egg production, low hatchability and increased incidence of blood spots in eggs is common. In severe cases, conjunctiva and cornea are dry, there is loss of yellow pigmentation from shanks and skin, combs and wattles are pale and dry. Affected birds appear weak, ataxic, have ruffled feathers and continue to loss condition.
Vitamin A deficiency symptoms in young chickens may appear within 2-3 weeks, especially if the chickens are hatched from eggs produced by dams fed low vitamin A in the diet. The symptoms observed are lachryamation conjunctivitis, accumulation of cheesy material in the conjunctival sac and hyperkeratosis of corneal epithelium, resulting in blindness. A serous discharge is also seen from the nostril. Affected chickens grow poorly, are ataxic and susceptible to other infections.

Postmortem findings: The lesions seen on autopsy are keratinized pharyngeal epithelium and small white pustules in the mouth, pharynx and oesophagus. These pustules may become infected in long standing cases. The kidneys are pale, the ubules and ureters are distended with varying amounts of urates. The urate deposits may be found on other visceral organs. There is loss of cilia and the columnar epithelium is replaced by stratified squamous keratinizing epithelium in the respiratory tract and the mucous glands.

Diagnosis: The flock history, including typical signs and autopsy findings, is adequate to make a presumptive diagnosis and to commence treatment. There inadequate signs exist, the diagnosis should be confirmed as follows:

1. Determine vitamin A level in the fed.
2. Determine serum vitamin A levels of affected chickens. The normal serum vitamin A level is 100-150 i.u./ml.
3. Histopathology
4. Feed suspected feed to day old chickens and observe the symptoms and lesions.
5. Therapeutic response.

Treatment: Administer 3-5 times the recommended levels of vitamin A either through water or feed. The recovery is rapid and the symptoms completely disappear within a few days.

Control

1. Use stabilized vitamin A in poultry feed.
2. Add adequate levels of antioxidants in feed
3. Regularly assay fed for vitamin A content.
4. Provide adequate storage for fed and feed ingredients.
5. Vitamin D deficiency
   Vitamin D deficiency in poultry is characterized by faulty utilization of calcium and phosphorous, resulting in skeletal abnormalities and adverse effect on eggshell quality
   
   Cause
6. Lack or inadequate amounts of Vitamin D. particularly D3 in poultry feed, especially in confinement rearing.
7. Sulphur drugs in the feed may interfere with Vitamin D adsorption.
8. Vitamin D2 is sensitive to oxidation and catalyzed by minerals.

Clinical signs: Chickens in rapid growing phase exhibit signs of retarded growth and rickets within 2 weeks of being fed on low levels of Vitamin D in the feed. The beak, claws and bones become soft; the chickens walk with unsteady gait or tend to sit on their hocks. As the deficiency progresses, morbidity reaches 100%. Chickens appear dull, with ruffled feathers and progressive loss of weight. In untreated flocks, mortality may reach 100%. Recovered chickens may show bent legs. In hens it may take up to 3 months before any signs appear. There is an increase in thin shelled eggs, followed by a decrease in egg production and hatchability. Occasionally a hen may appear paralyzed but recovers soon after laying a shell –less egg. The affected hen tends to sit like a penguin and the symptoms progress into softening of beak, claws and long bones. The sternum may be bent and ribs turned inwards.

Postmortem findings: In chickens, soft long bones, bending of the ribs at their junction with the spinal column and poor calcification at the epiphyses of tibia and femur are seen on autopsy. The epiphyses of long bones and parathyroid glands are enlarged.
In laying hens, bones are soft and break easily; well defined knobs appear at the costochondral junction and the sternum may show lacteal bending.

Diagnosis

1. Where symptoms and lesions are well defined, presumptive diagnosis of Vitamin D deficiency should be mae.
2. Presumptive diagnosis should be confirmed as follows.
3. Determine bone ash from both normal and affected chickens.
4. Assay suspected feed for Vitamin D content.
5. Administer Vitamin D to affected chickens and observe the response.
6. Reproduce clinical disease by feeding suspected feed to day old chickens.

Treatment: In advanced cases, injection of a single dose of Vitamin D3is likely to produce a better response than generous levels of Vitamin D in the feed. Suggested dose for young chickens is 50 iu /kg body weight and double this level for hens. Following injection, adequate levels of Vitamin D should be maintained in the feed. Injections may be given either by intramuscular or subcutaneous route.

Control: Add adequate levels of Vitamin D, in the diet and assay a feed sample for its Vitamin D, content at regular intervals.
The requirement of Vitamin D, in the feed is related to the source of phosphorous, amount of calcium, calcium and phosphorous ratio, and exposure of chickens to sunlight.
Excessive levels of Vitamin D, given for long period will cause renal damage, due to dystrophic calcification of kidney tubules, aorta and arteries.

3. Vitamin E deficiency
   Vitamin E deficiency in chickens is characterized by encephalomalacia, exudative diathesis, muscular dystrophy. Low fertility and hatchability.
   
   Cause: Oxidation of fatty acids in the diet, errors in mixing, inadequate levels of Vitamin E in the feed, use of propionic acid as grain preservative may lower the Vitamin E content of the grain and inadequate selenium levels in the feed.
   
   Symptoms and Postmortem findings: In older birds no clinical signs are observed, except for low hatchability and embryo deaths at 4 th day of incubation, prolonged deficiency may cause testicular degeneration in males resulting in infertility.
4. Encephalomalacia:characterized by ataxia, backward or downward retraction of the head, increased inco-ordination or forced movement, rapid contraction and relaxation of the legs and finally complete prostration and death. The signs usually appear between second and fourth day of chicks’ life.On autopsy, the cerebellum in severe cases shows petechial hemorrhages and necrosis on the surface, which appears brownish in colour. The meninges are also edematous.
   2. Exudative diathesis: E.D of chickens are characterized by edema of subcutaneous tissues associated with abnormal permeability of capillary walls, Affected chickens grow poorly, appeared ruffled and develop a soft swelling behind the crop. On autopsy, greenish blue, viscous fluid may be seen below the skin. It is some times tinged with blood. Distension of the pericardium in some chickens may be seen. There may be hemorrhage in muscles and fatty tissues. 
   3. Muscular dystrophy: In chickens this condition is apparent when vitamin E deficiency is accompanied by deficiency of sulphur amino acids and the lesions of breast and thigh muscles may be seen as early as 4 weeks of age. The lesions appears as light coloured streaks consists of dystrophic fibres among the normal fibres. 
   4. Immune response: Vitamin E deficiency in chickens increases susceptibility to infections and may inhibit the immune response following vaccination. 
   
   Diagnosis: The flock history with typical autopsy findings is suggestive of Vitamin E deficiency. The presumptive diagnosis may be confirmed by any or all of the following methods:
5. Demonstrate lesions in affected muscles by histopathology.
6. Demonstration of elevated levels of serum glutamic oxalacetic transaminase activity in affected chickens as compared to normal.
7. Administration of Vitamin E to affected chickens will result in complete recovery.
8. Determine Vitamin E content of the feed.
9. Feed suspected feed to day old chickens to reproduce symptoms and lesions.

Treatment: Administration of Vitamin E via drinking water or by injection gives a rapid recovery. This should then be followed by adequate levels of Vitamin E in the feed.
Advanced cases of encephalomalacia may not respond to treatment.

Control

1. Avoid excess fat in the diet and addition of rancid fats in the diet.
2. Supply adequate levels of Vitamin E in the diet Add antioxidants in feed to prevent rancidity and provide adequate selenium levels in the fed.
3. Provide adequate levels of sulphur containing amino acids in the diet.
4. Vitamin K deficiency
   Vitamin K deficiency in chickens is characterized by prolonged bleeding time or death due to bleeding from a minor injury.
   
   Cause
5. Inadequate levels of Vitamin K in feed.
6. Loss of Vitamin K potency in feed during storage
7. Presence of sulphur drugs in feed or water will interfere with Vitamin K metabolic activity
8. Prolonged administration of bactericidal chemicals which may destroy intestinal bacteria responsible for Vitamin K synthesis
9. Poor absorption from the intestine due to disease or dietary factors.
10. Low Vitamin K in fertile eggs to meet the needs of day old chickens.

Clinical signs: Young chickens are relatively more susceptible than old hens. Symptoms of Vitamin K deficiency in young chickens are seen especially when they are hatched from eggs produced by hens fed low Vitamin K in the feed. Following debeaking, chickens bleed, more than normal, resulting in ingestion of blood, causing pasted vents. In some cases blood loss may result in anemia.
In older hens hemorrhages may appear on various parts of the body and sudden death may occur through internal bleeding. Bruising occurs readily in broiler chickens.

Postmortem findings: The lesions found on autopsy include hemorrhages in various organs, including subcutaneous tissues, muscles and internal organs,. Chickens which died following debeaking may show bloodstained crop contents or digested blood in the intestines.

Diagnosis: Flock history, clinical signs and autopsy findings are usually adequate for presumptive diagnosis. Definite diagnosis is based on the determination of bleeding and prothrombin time of affected chickens, compared to the normal chickens.

Treatment: Within 48-72 hours of Postmortem findings
Administration, blood clotting time returns to normal

Control: Supply adequate levels of vitamin K in the feed and administer antibiotics and sulpha drugs with great care.

5. Thiamine deficiency (B1)
   Vitamin B1 deficiency in chickens is characterized by extreme anorexia, polyneuritis and death
   
   Cause: Inadequate levels of Vitamin B1 in the feed and high carbohydrate-based feed, low in Vitamin B1
   
   Clinical signs: The onsets of symptoms are sudden in chickens and gradual in hens. When, fed Vitamin B1 deficient feed, with suboptimal levels of Vitamin B1 in the feed, anorexia is followed by loss of weight, ruffled feathers, leg weakness and unsteady gait. These signs then progress to wards paralysis, beginning with flexors of the toes and working upwards, affecting the extensor muscles of the legs, wings and neck. In severe cases the chicken sits on its flexed legs and draws back the head in a “star gazing” position. Finally the chicken is unable to stand walk or feed, and affected chickens invariably die without treatment.
   
   Postmortem findings: Atrophy of the genital organs occurs and is more marked in the male than the female. There may be slight atrophy of the heart, wit h the right side dilated, and noticeable atrophy of stomach and intestines.
   
   Diagnosis: The flock history and the characteristic signs are usually enough to confirm a diagnosis to recommend flock treatment. Diagnosis may be confirmed by therapeutic response, assay of suspected feed for Vitamin B1 contents and reproduction of clinical signs in young chickens by feeding suspected feed.
   
   Treatment: Upon administration of Vitamin B1 to affected chickens, recovery from nervous signs takes place in a matter of a few hours. Supplementation with improved feed will further hasten recover. Recommended dose rate for young chickens is 5-10mg per day and older chickens 10-50 mg/day.
6. Riboflavin deficiency (B2)

Vitamin B2 deficiency in chickens is characterized by slow growth ataxia, emaciation curled toe paralysis and, in hens, low egg production and hatchability.

Cause: Inadequate levels of Vitamin B2 in the feed. Riboflavin is sensitive to light and pH, hence may be destroyed and result in deficiency.

Clinical signs: Symptoms of Vitamin B2 deficiency in chickens during the first 4 weeks of age includes poor growth, weakness, loss of weight, poor feathering and dirrhoea. In severe cases, paralysis develops and the chickens sit and tend to walk on their hocks. The toes of one or both feet are curled down and inward. If the condition is allowed to progress, chickens lie with their legs sprawled out and death occurs through starvation, dehydration and smothering. In hens, the oly manifestation is reduced egg production and hatchability. The embryo dies towards the end of the second week of incubation. The embryos heave defective downs, referred to as “clubbed” This is also evident in some hatched chicks!

Postmortem findings: There is marked swelling and softening of sciatic and brachial nerves in young chickens. Histologically there are degenerative changes in the myelin sheaths of the main peripheral nerve trunks. Schwann cell proliferation, myelin changes, gliosis and chromatolysis occur in the spinal cord. Degeneration of neuro-muscular end plate and muscle tissue is often seen.

Diagnosis: In low grade deficiency, symptoms are not specific enough to make a presumptive diagnosis. However, the presence of “clubbed” down in day old chickens and curled toe paralysis is considered diagnostic of Vitamin B2 deficiency. The presumptive diagnosis may be confirmed as follows:

1. Histopathology of nerve tissues
2. Therapeutic response to the administration of Vitamin B2 to the affected chickens.
3. Assay the suspected feed for Vitamin B2 content.

Treatment: All sub clinical cases should be given additional levels of Vitamin B2 and adequately supplemented diet following recovery. Where the deficiency is long standing, no recovery is expected. Suggested oral dose of Vitamin B2 is 5 mg per chicken and 15 mg per hen per day.

Control: Add sufficient Vitamin B2 in poultry feeds. Monitor Vitamin B2 content of feeds by routine assays.

7. Pantothenic acid deficiency
   Pantothenic acid deficiency in chickens is characterized by retarded growth. Rough plumage, lesions around the mouth and embryonic mortality.
   
   Cause: Low pantothenic acid in breeder feed
   Inadequate levels in chick starter feed
   
   Clinical signs: In young chickens pantothenic acid deficiency produces symptoms of poor growth, rough and brittle plumage, dermatitis, perosis and excessive mortality. Definite crusty scab-like lesions appear in the corners of the mouth and the eyes and in small cracks between the toes and bottom of the feet. The eyelids may be scaled together with viscous discharge from the eyes.
   Depending upon the degree of pantothenic acid deficiency, egg production and hatchability is reduced. Embryos show feather malformation, shortening of the lower beak and hydrocephalus.

cracks between the toes and bottom of the feet
Postmortem findings: On necropsy, a pus-like substance can be found in the mouth and grayish-white exudates in the proventriculus. The liver and kidneys are enlarged and spleen atrophied.

Diagnosis: Symptoms and lesions are fairly conclusive, however biotin deficiency needs to be eliminated. The presumptive diagnosis can be confirmed as follows:

1. Administration of pantothenic acid to the affected chickens should eliminate the symptoms.
2. Determine the pantothenic acid content in the suspect feed.

Treatment: Upon oral administration or by injection of pantothenic acid, recovery is complete. This should then be followed by adequate levels of pantothenic acid in the feed. Suggested dose rate is 10-20mg/chick/day

Control: Maintain adequate levels of pantothenic acid in the feed and regularly check feed for its contents.

8. Nicotinic acid deficiency (niacin)
   Nicotinic acid deficiency in chickens is characterized by inflammation of athe buccal cavity, poor feathering, enlarged hocks, flightness and diarrhea.
   
   Cause: Nicotinic acid biologically unavailable, insufficient absorption, xcess of lysine, argentine and glycine in the feed and stress condition requiring high levels.
   
   Clinical signs: Niacin deficiency symptoms are only seen in young chickens and include poor feathering, growth depression inflammation of the buccal cavity including the tongue, diarrhea and flightiness in some flocks. The hock joint is enlarged without the displacement of the Achilles tendon.
   
   Postmortem findings: The lesions seen on autopsy are varying degrees of inflammation of the mouth cavity, tongue, pharynx and oesophagus. The tip of the tongue may appear black in some chickens.
   
   Diagnosis: Presumptive diagnosis of nicotinic acid deficiency is made on symptoms and lesions on autopsy.
   Definite diagnosis can be made based upon the therapeutic response.
   
   Treatment: Recovery of the affected chickens takes place upon supplementing the feed wit h normal niacin requirement of the chicken. Pure nicotinic acid can be used at does rate of 40-50 mg per chicken.
   
   Control: For young chickens, supply well balanced feed with adequate levels of niacin.
9. Pyridoxine deficiency (B6)
   Pyridoxine deficiency in chickens is characterized by loss of appetite, poor
   growth, and drop in production, low hatchability and nervous signs.
   
   Cause: High protein feed with low Vitamin B6 content and inadequate levels of Vitamin B6 in the feed
   
   Clinical signs: Pyridoxine deficiency in chickens results in general weakness, poor growth, ruffled feathers and loss of appetite. Affected chickens squat with the wings slightly spread and the head resting on the ground. In advanced cases, trembling and vibration of the tip of the tail occurs. The movements are stiff and jerky and chickens run aimlessly with their heads lowered and droopy wings. Finally, there are convulsions during which chickens fall on their sides or back and die.
   In hens, loss of appetite, reduced feed intake, loss of weight, drop in egg production and hatchability are the only symptoms followed by death.
   
   Postmortem findings: No specific lesions are seen on autopsy examination
   
   Diagnosis: Flock history and symptoms should suggest the Pyridoxine deficiency and it may be confirmed by therapeutic response.
   
   Treatment: Administration of deficiency will result in complete recovery of affected chickens.
   
   Control: Since the deficiency symptoms in chickens appear within a few days of being fed Pyridoxine deficiency feed , it is essential that adequate levels of Vitamin B6 maintained in well balanced feed.
10. Biotin deficiency
    Biotin deficiency in chickens is characterized by dermatitis of the mandible and feet. Reduced growth rate, and lowered hatchability.
    
    Cause: Administration of antibiotics to chickens may kill those bacteria which synthesize biotin in the gut, presence of biotin antagonists and binders in feed and inadequate levels of biotin in the feed.
    
    Clinical signs: Symptoms of biotin deficiency include unthrift ness, poor growth, brittle feathers, scaly dry skin and excessive mortality in young chickens. In severe cases lesions of dermatitis appear on the corners of the mouth, feet and legs. The lesions on feet progress to develop into fissures. The eyelids are stuck together. Embryo mortality occurs during the first week and during the last 3 days of incubation. Embryo lesions include syndactyly, shortening and bending of bones, crooked tibia and parrot beaks.
    
    Postmortem findings: No specific lesions are found on autopsy
    
    Diagnosis: Flock history and external lesions are suggestive of biotin deficiency, but pantothenic acid deficiency needs to be eliminated
    
    Treatment: Administration of biotin via drinking water, followed by adequate levels in the feed provides complete recovery.
    
    Control: Supply adequate levels of biotin in chicken feed and avoid excessive use of antibiotics. Eliminate biotin antagonists where possible. Assay feed samples to determine the levels of biotin at frequent intervals.
11. Folic acid deficiency
    Folic acid deficiency in chickens is characterized by poor growth, poor feathering, anemia, perosis and loss of feather pigmentation.
    
    Cause: Inadequate levels of folic acid in the chicken feed. Solvent extracted Soya bean meal is low in folic acid content. Stability of folic acid is poor particularly through the pelleting process.
    
    Clinical signs: Folic acid deficiency symptoms in young chickens cause poor growth, poor feathering, anemia and feather depigmentation in colored breeds. The anemia results from decreased red blood cell count and low haemoglobin values.
    
    Postmortem findings: No specific lesions are seen on autopsy
    
    Diagnosis: Presence of depigmentation of feathers is suggestive of the folic acid deficiency in chickens. Therapeutic response may be used to confirm the suspected folic acid deficiency.
    
    Treatment: Addition of folic acid in the diet results in complete recovery of the affected chickens. A single injection produces good recovery from anemia; oral administration is much less effective.
    
    Control: Provide adequate levels of folic acid in the feed.Assay feed samples at frequent intervals to determine the folic acid levels in the feed.
12. Choline deficiency
    Choline deficiency in chickens is characterized by poor growth and perosis
    
    Cause: Inadequate choline levels in the feed and lack of choline synthesis by the chicken.
    
    Clinical signs: In young chickens poor growth and perosis is common in choline deficiency. There is also flattening of tibio tarsal joint due to the rotation of the metatarsus. If the process continues, the articular cartilage is deformed and Achilles tendon slips off the condyles.
    
    Postmortem findings: Other than perosis, no lesions are seen in young chickens, Enlarged fatty livers may be seen in pullets and hens.
    
    Diagnosis: 1. Flock history and symptoms are suggestive of choline deficiency. The diagnosis may be confirmed by therapeutic response.
    
    Treatment: Response to treatment is good, provided the conditions have not progressed too far. Choline can be given either through feed or water
    
    Control: Maintain adequate levels of choline in the feed given to young chickens.
13. Vitamin B12 deficiency (Cobalamine)
    The Vitamin B12 deficiency signs are rarely in chickens raised on the litter.
    The signs of a Vitamin B12 deficiency include slow growth, lowered feed conversion, increased mortality and reduced hatchability. Perosis may only occur when the diet is also deficient in choline and methionine . Peak embryonic mortality occurs at 17th day of incubation, characterized by myoatrophy of the legs. Some embryos may show haemorhages and perosis. Response to treatment is good, usually within one week.

Selenium deficiency
Selenium deficiency in chickens is characterized by myopathy and exudative diathesis in young chickens.

Cause:

1. Low Se content of the soil, resulting in lower levels in feed and forages.
2. The sulphate inhibits intake of Se from the soil, therefore muscular dystrophy often follows application of sulphate fertilizers.
3. Se is of low biological value in many feedstuffs
4. Cereal fats may go rancid during storage
5. Addition of certain drugs in the diet may interfere with Se utilization
6. The action of Se is also prevented by high protein, arsenic or linseed oil in feed.
7. Se in a premix may become unstable on storage
8. Individual chick variation in susceptibility
9. Se requirement varies with the unsaturated fat content of the diet
10. Low vit. E or sulphur amino acid in the diet requires higher levels of Se.

Clinical signs: The signs and lesions of a selenium deficiency in chickens include:

1. Congenital white muscle disease. This is found in chickens 3-4 days after hatching; the lesions are confined to the gizzrd muscle.
2. Haemorrhagic syndrome. Haemorrhagic syndrome Is characterized by increased blood clotting time , accompanied by haemorrhages on the serosal surface of the gizzard. It is seen during the first seven days of the chicks life.
3. Exudative diathesis. The condition is seen in the field outbreaks from 3-6 weeks of age, bu may occur as early as 5 days of age. It is a similar condition as described under Vitamin E. However, in selenium deficiency dystrophy of gizzard and pectoral muscle may occur at the same time.
4. White Muscle disease. Occurs in older birds from 2 months onwards. Muscle lesions are present anywhere on skeletal muscles and gizzard. When leg muscles are involved there may be complete paralysis. Affected birds are listless, have depressed appetite, loss of weight lowered egg production and poor feathering. White areas of muscle atrophy may be seen easily in long standing cases. Severity of lesions depends upon the degree of the deficiency and its duration. Lesions in pectoral muscles are vacuolation. Hyaline degeneration of sarcoplasm, hypertrophy and atrophy of muscle fibers; interstitial fibrosis and fatty infiltration may also be seen. Skeletal muscles show coagulative necrosis of muscle fiber with fragmentation, lysis of necrotic fibers and calcification, sarcolemmal neclei proliferation and regeneration. The pancreas loses zymogen granules, there is loss of zonation, invasion by fibroblasts and macrophages and acinar atrophy.

Diagnosis: Clinical Diagnosis is based upon flock history , clinical signs and
autopsy findings.

1. Histopathology of affected tissues is useful in confirming Clinical Diagnosis.
2. Serum oxal-acetic-transaminase level is increased during myopathy.
3. Administration of selenium produces good clinical response in affected chickens.
4. Analysis of feed for S content.

Treatment: Addition of selenium via drinking water or feed for affected flocks should provide good recovery.
Control

1. Addition of adequate level of vit. E and selenium in the feed
2. Keep unsaturated fatty acids to a low level in the feed.
3. Avoid oxidation of the feed ingredients by the addition of antoxidants.

Calcium and phosphorus deficiency
Calcium and phosphorus are required for bone and eggs hell formation as well as in the maintenance of acid base balance. Calcium is important for normal clotting of blood, and phosphorus in the metabolism or carbohydrates and fats. The utilization of both Ca and P is dependent upon the presence of Vit. D. Deficiency in any of the three will result in rickets in chicks, reduced egg production and poor shell quality. In laying hens calcium deficiency tends to deplete the calcium content of the bone , which becomes so thin that spontaneous fracture may occur. A condition described as cage layer fatigue is discussed separately.Continuing deficiency results in poor appetite, retarded growth, weakness and death. Calcium deficiency increases the susceptibility to haemorrhages.

Manganese Deficiency

Manganese deficiency in chickens results in poor growth, loss of production and perosis. Affected chicks are weak and exhibit nervous signs, characterized by a star gazing posture. Mamgamese deficiency in young chickens results in shortening and thickening of the leg bones. The twisting of tibia and malformation of tibiometatarsal joint results in displacement of the gastrocnemius tendon from its condyles. The resulting perosis makes it difficult for the chicken to walk. Manganese deficiency causes a drop in egg production, low hatchability and increases the incidence of this shelled eggs. Manganese deficiency
In embryos results in chondrodystrophy and embryo deaths occur on 20-21st day of incubation.

3. Sodium and chlorine deficiency (salt)
   Sodium deficiency in chicks results in failure to grow, develop soft bones, corneal keratinization, gonodal inactivity, adrenal hypertrophy, impaired food utilization and decrease in plasma and special fluid volumes.
   A lack of salt in the diet of laying hens results in decreased egg production, egg size, loss of weight and cannibalism.
   Chlorine deficient chickens, when frightened, show nervous signs characterized by falling forward with their feet stretched out behind them and lay paralysed for several minutes. Other signs include poor growth dehydration, hemoconcentration and death.

4.Potassium deficiency Potassium is an intracellular element and the requirement of this element is high in chickens. It is necessary for heart function, to increase membrane permeability and bone formation
Signs of a deficiency include muscle weakness, poor intestinal tone, and weakness of cardiac and respiratory muscles.

Zinc deficiency
A deficiency of zinc in chickens causes retarded growth, poor feathering enlarged hocks, scaling of the skin especially on the feet, shortening and thickening of leg bones. An increase in calcium content in the ration will enhance the severity of Zinc deficiency. In severe cases of Zinc deficiency, embryos have no spinal column beyond a few vertebrae, no body walls and no legs.

5.Magnesium deficiency
Magnesium deficiency to young chickens results in poor growth and high mortality. The chickens are lethargic and when disturbed may exhibit nervous signs, including convulsions. Deficiency of Magnesium in laying hens causes a drop in egg production, Egg size and weight of shell. The increase in calcium levels in the feed will accentuate the magnesium deficiency.

6. Cage layer fatigue
   Cage layer fatigue in hens is characterized by withdrawal of calcium phosphate fro bones, resulting in lameness and paralysis.
   
   Cause: The exact cause cage layer fatigue is not totally established, however, the condition appears to occur in high producing hens in cages under the following circumstances:
7. Poultry feed low in calcium and high in phosphorus
8. High energy feed resulting in low feed intake
9. High environmental temperature resulting in low feed intake
10. Feed formulated to meet out the calcium requirement of average production

Clinical signs: Sign Of cage layer fatigue are exclusively seen in layers housed in cages. The flock has reached or passed peak production and egg size is its maximum. The rate of lay in the affected hens is above the average egg production of the flock. The hens appear normal but are unable to stand up and are reluctant to reach feed and water. In the affected hens egg production may remain normal, with little or no deterioration of shell quality. Permanent paralysis may result due to excessive pressure, resulting from fracture of spinal vertebrae, causing pressure on the spinal column. Death occurs in the absence of corrective measures.

Postmortem findings: The lesions are seen only in bones, particularly in leg bones, which are very thin and brittle. The ribs and sternum are deformed in prolonged cases or where the condition occur repeatedly in the same hen.

Diagnosis: Flock history, characteristic signs and postmortem findings are usually sufficient to recommend corrective measures.

Treatment: Remove affected hens from cages and feed on balanced feed. This will result in recovery in 2-3 weeks.
Allowing hens to run on the ground with normal feeding will result in recovery with in 2 weeks.
Supply additional calcium with feed.

Control: Formulate poultry feed to meet the requirement of maximum egg production. Calcium addition should be adjusted to the energy level and phosphorous levels in the feed and environmental condition.
Once or twice weekly an extra addition of calcium in the diet will help reduce the problem.

7. Rickets
   Rickets is characterized by poor mineralization of bones resulting in lameness, skeletal deformities and poor growth.
   
   Incidence: Rickets is rare in occurrence in commercial
   
   Susceptibility: Chickens under 4 weeks of age are most susceptible but the condition may occur at any time.
   
   Cause: Faulty mixing of the feed ingredients, inadequate level of mineral and vitamin D3 ­­in the feed, imbalance of calcium and phosphorus in the feed and inter current disease influencing the absorption of calcium and Vitamin D­3
   
   Clinical signs: Affected chickens show signs of ataxia and progressive lameness with a tendency to remain squatted. Severely affected chickens when forced to move appear walking in pain. As the condition progresses, feathers become ruffled, loss of condition, and dehydration become apparent. Morbidity in untreated flock may reach 100% and mortality up to 50% has been observed.
   
   Postmortem finding: On autopsy, apart from varying degree of emaciation, beak and bones are soft. Characteristically bones do not break with a snap. Bent keel bones, beading of ribs and thickening of the growth plate of long bones is commonly observed. Parathyroid gland may be enlarged.
   Flock history, clinical signs and lesions are usually enough for field diagnosis. To determine exact cause, determine the vitamin D­3 and calcium content of the diet, their potency and therapeutic response.
   
   Treatment: Administration of vitamin D3; 2-3 times the recommended level should be administered via drinking water. Additional calcium and phosphorus should be supplied ad lib for 5-7 days. Replace the suspected feed with the well known balanced and mix feed.
   
   Control: Ensure adequate supply of vitamin D3 and calcium and phosphorus in 2:1 ratio in the feed.
8. Visceral gout
   Visceral gout is characterized by deposition of uric acid and urates on different organs of the body. The mortality is not high but continuous.
   
   Cause: Excessive protein in the diet especially animal protein such as meat meal, deficiency of vitamin A, disease affecting kidneys and fungal toxins

Deposition of chalk like white substance
Symptoms and lesions: Swollen, mottled or brown colored kidneys, distended ureter due to accumulation of stick white colored substance. Deposition of chalk like white substance on various membrane and different organs of the body.

Treatment and control: Remove the cause first. Increase the water intake of the birds and give additional vitamin A. 4% molasses and diuretic in drinking water often help in this disease. Give balance feed to birds.

9. Fatty Liver Hemorrhagic syndrome (FLHS)
Cause: Not definitely known. Possible causes for the excessive accumulation of fat in the liver which weakens its cellular structure may include; excessive caloric intake (high energy rations); aflatoxin-induced liver damage; feed deficiency of lipotropic agents. Most frequent in overweight, high-producing caged hens and especially during hot weather periods.

Signs: 30 to 40% sudden drop in egg production; mortality increases moderately as birds die suddenly and without previous signs of disease. Some birds may show pafe combs and wattles.

Swollen liver           Hemorrhage in liver

Postmortem Lesions: Excessive fat in abdominal cavity. Liver and kidneys are enlarged, greasy, yellow and soft. Livers may have few or numerous petechial sub capsular hemorrhages, some times hematocysts. If these rupture, internal hemorrhage may be evident.

Diagnosis: Flock history, signs and lesions. Check feed ingredients for aflatoxins

Treatment: None specific. Addition of lipotropic agents 10-30 I.U may be helpful at times (1kgcholine, 10,000 I.U. vitamin E 12 mg vitam B 12 0.5kg inositol/tonne. Add also enough selenium to give 0.1-0-2 ppm feed) Reduce energy in ration by substituting ingredients.

DIGNOSIS,TREATMENT & CONTROL OF NUTRITIONAL DEFICIENCY DISORDERS IN POULTRY

Reference-On Request

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