Vitamin Deficiencies

Vitamin deficiencies are most commonly due to inadvertent omission of a vitamin premix from the birds’ diet. Multiple signs are therefore seen, although in general, problems with deficiencies of the B vitamins appear first. Because there are some stores of the fat-soluble vitamins in the body, it often takes longer for these deficiencies to affect the bird.

Treatment and prevention rely on an adequate dietary supply, usually protected by gelatin micro-encapsulation, that also contains an antioxidant. Vitamin destruction in feeds is a factor of time, temperature, and humidity. For most feeds, vitamin efficiency is little affected over 2-mo storage within mixed feed.

Vitamin A Deficiency

Adult birds, depending on liver storage, could be fed a vitamin A-deficient diet for 2-5 mo before signs of deficiency develop. As the deficiency progresses, birds become emaciated and weak with ruffled feathers, egg production drops, hatchability decreases, and embryonic mortality with incubated eggs increases. As egg production declines, there will likely be atretic follicles in the ovary, some of which show signs of hemorrhage. A watery discharge from the eyes may also be noted. As the deficiency continues, milky white, cheesy material accumulates in the eyes, making it impossible for the birds to see (xerophthalmia). The eye, in many cases, may be destroyed.

The first lesion usually noted in adult birds is in the mucous glands of the alimentary tract. The normal epithelium of the glands is replaced by a stratified squamous, keratinized layer, which blocks the ducts of the mucous glands, resulting in distention and necrosis. Small, white pustules may be found in the nasal passages, mouth, esophagus, and pharynx, and may extend into the crop. Breakdown of the mucous membrane may allow pathogenic microorganisms to invade these tissues and cause secondary infections.

Depending on the quantity of vitamin A passed on from the breeder hen, day-old chicks reared on a vitamin A-deficient diet may show signs from one week to 7 week( chicks with a good reserve of vitamin A ). Gross signs in chicks include anorexia, growth retardation, drowsiness, weakness, in-coordination, emaciation, and ruffled feathers. If the deficiency is severe, the chicks may exhibit an ataxia similar to that noted with a vitamin E deficiency , no gross lesions are found in the brain of vitamin A-deficient chicks as compared with degeneration of the Purkinje cells in the cerebellum of vitamin E-deficient chicks. The yellow pigment in the shanks and beaks is usually lost, and the comb and wattles are pale. A cheesy material may be noted in the eyes, but xerophthalmia is seldom seen because chicks usually die before the eyes become affected. Infection may play a role in many of the deaths noted with acute vitamin A deficiency.

Young chicks with a chronic vitamin A deficiency may also show pustules in the mucous membrane of the esophagus that can extend down the respiratory tract. Kidneys may be pale and the tubules distended due to the uric acid deposits. In extreme cases, the ureters may be filled with urates. Blood levels of uric acid can rise from a normal of ~5 mg to as high as 40 mg/100 mL of blood. Vitamin A deficiency does not interfere with uric acid metabolism but does prevent normal excretion of uric acid from the kidney. Histologic findings include atrophy of the cytoplasm and a loss of the cilia in the columnar, ciliated epithelium.

The livers of ataxic vitamin A-deficient chicks contain little or no vitamin A.

Vitamin D3 Deficiency

Abnormal development of the bones is discussed under calcium and phosphorus deficiencies ( Calcium and Phosphorus Imbalances) and manganese deficiency ( Manganese Deficiency). Vitamin D3 is required for the normal absorption and metabolism of calcium and phosphorus. A deficiency can result in rickets in young growing chickens or in osteoporosis and poor eggshell quality in laying hens, even though the diet may be well supplied with calcium and phosphorus.

Laying hens fed a vitamin D3-deficient diet exhibit loss of egg production within 2-3 wk, and depending on the degree of deficiency, shell quality deteriorates almost instantaneously. Using a corn-soybean meal diet with no supplemental vitamin D3, shell weight decreases dramatically by about 150 mg/day within 7 days. The less obvious decline in shell quality with suboptimal supplements is more difficult to diagnose than that seen with absolute deficiency, as it is very difficult to assay vitamin D3 in complete feeds.

There is a significant increase in plasma 1,25(OH)2 D3 of birds producing good vs poor eggshells. Feeding purified 1,25(OH)2D3 improves the shell quality of these layers, suggesting a potential inherent problem with metabolism of cholecalciferol.

Retarded growth and severe leg weakness are the first signs noted when chicks are deficient in vitamin D3. Also, beaks and claws become soft and pliable. Chicks may have trouble walking and will take a few steps before squatting on their hocks. They often sway from side to side while resting, suggesting loss of equilibrium. Feathering is usually poor, and an abnormal banding of feathers is seen in colored breeds. With chronic vitamin D3 deficiency, skeletal disorders are noted. The spinal column may bend downward, and the sternum may deviate to one side. These structural changes reduce the size of the thorax with subsequent crowding of the internal organs. A characteristic finding in chicks is a beading of the ribs at the junction of the spinal column along with downward, and posterior bending. Poor calcification can be seen at the epiphysis of the tibia and femur. By dipping the split bone in a silver nitrate solution and allowing it to stand under an incandescent light for a few minutes, the calcified areas are easily distinguished from the areas of uncalcified cartilage.

In the laying hen, signs of gross pathology are usually confined to the bones and parathyroid glands. Bones are soft and easily broken, and the ribs may become beaded. The ribs may also show spontaneous fractures in the sternovertebral region. Histologic examination shows deficiency of calcification in the long bones, with excess of osteoid tissue and parathyroid enlargement.

Adding synthetic 1,25(OH)2D3 to the diet of susceptible chicks does reduce the incidence of this condition. Although the response is not significant and varies, this suggest that some leg abnormalities may be a consequence of inefficient metabolism of cholecalciferol.

Vitamin E Deficiency

The 3 main disorders seen in chicks deficient in vitamin E are encephalomalacia, exudative diathesis, and muscular dystrophy. The occurrence of these conditions depends on various dietary and environmental factors.

Encephalomalacia is seen in commercial flocks if diets are low in vitamin E, an antioxidant is either omitted or not present in sufficient quantities, or the diet contains a reasonably high level of an unstable, unsaturated fat. For exudative diathesis to occur, the diet must be deficient in both vitamin E and selenium. Signs of muscular dystrophy are rare in chicks, as the diet must be deficient in both sulfur amino acids and vitamin E. Because the sulfur amino acids are necessary for growth, a deficiency severe enough to induce muscular dystrophy is unlikely to occur under commercial conditions. Signs of exudative diathesis and muscular dystrophy can be reversed in chicks by supplementing the diet with liberal amounts of vitamin E, assuming the deficiency is not too advanced. Encephalomalacia may or may not respond to vitamin E supplementation, depending on the extent of the damage to the cerebellum.

The classical sign of encephalomalacia is ataxia, which results from hemorrhage and edema within the molecular and granular layers of the cerebellum, with pyknosis and eventual disappearance of the Purkinje cells and separation of the molecular and granular layers of the cerebellar folia. Due to its inherently low level of vitamin E, the cerebellum is particularly susceptible to lipid peroxidation. In prevention of encephalomalacia, vitamin E functions as a biologic antioxidant. The quantitative need for vitamin E for this function depends on the amount of linoleic acid and polyunsaturated fatty acids in the diet. Over prolonged periods, antioxidants will prevent encephalomalacia in chicks when added to diets with very low levels of vitamin E, or in chicks fed vitamin E-depleted purified diets. Chicks hatched from breeders that are given additional dietary vitamin E are also less susceptible to lipid peroxidation in the brain. The fact that antioxidants can help prevent encephalomalacia but fail to prevent exudative diathesis or muscular dystrophy in chicks, strongly suggests that vitamin E is acting as an antioxidant. Exudative diathesis results in a severe edema caused by a marked increase in capillary permeability. Electrophoretic patterns of the blood show a decrease in albumin levels, whereas exudative fluids contained a protein pattern similar to that of normal blood plasma.

A vitamin E deficiency accompanied by a sulfur amino acid deficiency results in a severe muscular dystrophy in chicks by ~4 wk of age. This condition is characterized by degeneration of the muscle fibers, usually in the breast but sometimes also in the leg muscles. Histologic examination shows Zenker’s degeneration, with perivascular infiltration and marked accumulation of infiltrated eosinophils, lymphocytes, and histocytes. Accumulation of these cells in dystrophic tissue results in an increase in lysosomal enzymes, the function of which appears to be the breakdown and removal of the products of dystrophic degeneration. Initial studies involving the effects of dietary vitamin E on muscular dystrophy showed that the addition of selenium at 1-5 mg/kg diet reduced the incidence of muscular dystrophy in chicks receiving a vitamin E-deficient diet that was low in methionine and cysteine, but did not completely prevent the disease. However, selenium was completely effective in preventing muscular dystrophy in chicks when the diet contained a low level of vitamin E, which by itself had no effect on the disease.

Studies on the interrelationships between antioxidants, linoleic acid, selenium, and sulfur amino acids have brought some order to the previous confusion about the role of vitamin E in chick nutrition. It is now apparent that selenium and vitamin E play supportive roles in several processes, one of which involves cysteine metabolism and its role in the prevention of muscular dystrophy in the chicken. Glutathione peroxidase is soluble and is therefore located in the aqueous portions of the cell, while vitamin E is located mainly in the hydrophobic environments of membranes and in lipid storage cells. The overlapping manner in which vitamin E and selenium function in the cellular antioxidant system suggest that they spare one another in the prevention of deficiency signs.

Vitamin K Deficiency

Impairment of blood coagulation is the major clinical sign of vitamin K deficiency. With a severe deficiency, subcutaneous and internal hemorrhages can prove fatal. Vitamin K deficiency results in a reduction in prothrombin content of the blood; in the young chick, plasma levels are as low as 2% of what is considered normal. Because the prothrombin content of newly hatched chicks is only about 40% that of adult birds, the young chick is readily affected by a vitamin K-deficient diet. A carryover of vitamin K from the dam to eggs, and subsequently hatched chicks, has been demonstrated, so breeder diets should be well fortified. Hemorrhagic syndrome in day-old chicks has been attributed to a deficiency of vitamin K in the diet of the breeder hens. Gross deficiency of vitamin K results in such a prolonged blood clotting time that severely deficient chicks may bleed to death from a slight bruise or other injury. Borderline deficiencies often cause small hemorrhagic blemishes. Hemorrhages may appear on the breast, legs, wings, in the abdominal cavity, and on the surface of the intestine. Chicks are anemic, which may be due in part to loss of blood but also to the development of hypoplastic bone marrow. Although blood-clotting time is a fairly good measure of vitamin K deficiency, a more accurate measure is obtained by determining the prothrombin time. Prothrombin times in severely deficient chicks may be extended from a normal of 17-20 sec to 5-6 min or longer. No major heart lesions are seen in vitamin K-deficient chicks such as those that occur in pigs.

A vitamin K deficiency in poultry may be related to low dietary levels of the vitamin, low levels in the maternal diet, degree of intestinal synthesis, extent of coprophagy, presence of sulfur drugs and other feed additives in the diet, and the presence of disease. Chicks with coccidiosis may have severe damage to their intestinal wall, leading to excessive bleeding in addition to depressed vitamin K absorption. Antimicrobial agents can suppress intestinal synthesis of vitamin K, leaving the bird completely dependent on the diet for its supply of the vitamin.

Vitamin B12 Deficiency

Vitamin B12 is an essential part of several enzyme systems, with most reactions involving the transfer or synthesis of one-carbon units (eg, methyl groups). While the most important function of vitamin B12 is in the metabolism of nucleic acids and proteins, it also functions in carbohydrate and fat metabolism.

In growing chickens, a deficiency of B12 results in reduced weight gain and feed intake, along with poor feathering and nervous disorders. While deficiency may lead to perosis, this is probably a secondary effect due to a dietary deficiency of methionine, choline, or betaine as sources of methyl groups. Vitamin B12 may alleviate perosis due to its effect on the synthesis of methyl groups. Further clinical signs reported in poultry are anemia, gizzard erosion, and fatty infiltration of heart, liver, and kidneys. Laying hens appear to be able to maintain body weight and egg production in spite of a dietary deficiency of vitamin B12, although egg size may be reduced. Hatchability can be markedly reduced in breeders, but several months may be needed for signs to appear. Changes noted in embryos from B12 -deficient breeders include a general hemorrhagic condition, fatty liver, fewer myelinated fibers in the spinal cord, and high incidence of embryo deaths at 17 days incubation.

Choline Deficiency

In addition to poor growth, the outstanding sign of choline deficiency in chicks and poults is perosis. Perosis is first characterized by pinpoint hemorrhages and a slight puffiness about the hock joint, followed by an apparent flattening of the tibiometatarsal joint caused by a rotation of the metatarsus. The metatarsus continues to twist and may become bent or bowed so that it is out of alignment with the tibia. When this condition exists, the leg cannot adequately support the weight of the bird. The articular cartilage is displaced, and the Achilles tendon slips from its condyles. Perosis is not a specific deficiency sign; it appears with several nutrient deficiencies.

Although choline deficiency readily develops in chicks fed diets low in choline, a deficiency in laying hens is not easily produced. Eggs contain approximately 12-13 mg of choline/g of dried whole egg. A large egg contains about 170 mg of choline, found almost entirely in the phospholipids. Thus, there appears to be a considerable need for choline to produce an egg. In spite of this, producing a marked choline deficiency in laying hens has been difficult even when highly purified diets essentially devoid of choline were provided for a prolonged period of time. The choline content of eggs was not lowered, suggesting synthesis by the bird.

Niacin (Nicotinic Acid) Deficiency

There is good evidence that poultry—even chick and turkey embryos—can synthesize niacin, but at a rate that is too slow for optimal growth. It has been claimed that a marked deficiency of niacin cannot occur in chickens unless there is a deficiency of tryptophan, an amino acid and a niacin precursor.

A niacin deficiency is characterized by severe metabolic disorders in the skin and digestive organs. The first signs are usually loss of appetite, retarded growth, general weakness, and diarrhea. There is conflicting evidence as to whether broilers respond, in terms of growth and feed utilization, to niacin supplementation. However, it has been clearly established that chicks do have a requirement for niacin. Deficiency produces an enlargement of the tibiotarsal joint, bowing of the legs, poor feathering, and dermatitis on the head and feet.

Niacin deficiency in chicks can also result in “black tongue,” in which the tongue, oral cavity, and esophagus become inflamed at ~2 wk of age. In the niacin-deficient hen, weight loss, reduced egg production, and a marked decrease in hatchability can result. Turkeys, ducks, pheasants, and goslings are much more severely affected by niacin deficiency than are chickens. Their apparently higher requirements are likely related to their less efficient conversion of tryptophan to niacin. Ducks and turkeys with a niacin deficiency show a severe bowing of the legs and an enlargement of the hock joint. The main difference between the leg seen in niacin deficiency and perosis seen in manganese and choline deficiency is that with niacin deficiency the Achilles tendon seldom slips from its condyles.

There is good evidence that poultry—even chick and turkey embryos—can synthesize niacin, but at a rate that is too slow for optimal growth. It has been claimed that a marked deficiency of niacin cannot occur in chickens unless there is a deficiency of tryptophan, an amino acid and a niacin precursor.

A niacin deficiency is characterized by severe metabolic disorders in the skin and digestive organs. The first signs are usually loss of appetite, retarded growth, general weakness, and diarrhea. There is conflicting evidence as to whether broilers respond, in terms of growth and feed utilization, to niacin supplementation. However, it has been clearly established that chicks do have a requirement for niacin. Deficiency produces an enlargement of the tibiotarsal joint, bowing of the legs, poor feathering, and dermatitis on the head and feet.

Niacin deficiency in chicks can also result in “black tongue,” in which the tongue, oral cavity, and esophagus become inflamed at ~2 wk of age. In the niacin-deficient hen, weight loss, reduced egg production, and a marked decrease in hatchability can result. Turkeys, ducks, pheasants, and goslings are much more severely affected by niacin deficiency than are chickens. Their apparently higher requirements are likely related to their less efficient conversion of tryptophan to niacin. Ducks and turkeys with a niacin deficiency show a severe bowing of the legs and an enlargement of the hock joint. The main difference between the leg seen in niacin deficiency and perosis seen in manganese and choline deficiency is that with niacin deficiency the Achilles tendon seldom slips from its condyles.

Pantothenic Acid Deficiency

Pantothenic acid is the prosthetic group of coenzyme A, an important coenzyme involved in many reversible acetylation reactions in carbohydrate, fat, and amino acid metabolism. Signs of deficiency relate to general avian metabolism.

The major lesions of pantothenic acid deficiency involve the nervous system, the adrenal cortex, and the skin. Deficiency may result in reduced egg production; however, a marked drop in hatchability is usually noted prior to this event. Embryos from hens with pantothenic acid deficiency may have subcutaneous hemorrhages and severe edema, with mortality showing up during the later part of incubation period. In chicks, the first signs are reduced growth and feed consumption; poor feather growth, with feathers becoming ruffled and brittle; and a rapidly developing dermatitis. Corners of the beak and the area below the beak are usually the worst affected, this condition is also noted on the feet. In severe cases, the skin of the feet may cornify, and wart-like lumps may be seen on the balls of the feet, foot problem can lead to bacterial infection.

Liver concentration of pantothenic acid is reduced during a deficiency, with the liver becoming atrophied,faint to dirty yellow colored . Nerve fibers of the spinal cord may show myelin degeneration. Panthothenic acid-deficient chicks show lymphoid cell necrosis in the bursa of fabricius and thymus, together with lymphocytic scarcity in the spleen. The foot condition in chicks and the poor feathering are quite similar to the signs of a biotin deficiency. Except in a pantothenic acid deficiency, dermatitis of the feet is usually noted first on the toes; in contrast, in a biotin deficiency dermatitis primarily affects the footpads and is usually more severe than that in a pantothenic acid deficiency.

Riboflavin Deficiency

Many tissues may be affected by riboflavin deficiency, although the epithelium and the myelin sheaths of some of the main nerves are major targets. Changes in the sciatic nerves produce “curled-toe” paralysis in growing chickens. Egg production is affected, and riboflavin-deficient eggs do not hatch. When chicks are fed a diet deficient in riboflavin, their appetite is fairly good but they grow slowly, become weak and emaciated, and develop diarrhea between the first and second weeks. Deficient chicks are reluctant to move unless forced and then frequently walk on their hocks with the aid of their wings. The leg muscles are atrophied and flabby, and the skin is dry and harsh. In advanced stages of deficiency, the chicks lie prostrate with their legs extended, sometimes in opposite directions. The characteristic sign of riboflavin deficiency is a marked enlargement of the sciatic and brachial nerve sheaths, with sciatic nerves usually showing the most pronounced effects. Histologic examination of the affected nerves shows degenerative changes in the myelin sheaths that, when severe, pinch the nerve, producing a permanent stimulus that results in curled-toe paralysis.

Signs of riboflavin deficiency in the hen are decreased egg production, increased embryonic mortality, and an increase in size and fat content of the liver. Hatchability decreases within 2 wk when hens are fed a riboflavin-deficient diet but returns to near normal when riboflavin is restored. Embryos from the eggs of hens receiving riboflavin-deficient diets are dwarfed and show characteristically defective down (“clubbed” down). The nervous system of these embryos shows degenerative changes much like those described in riboflavin-deficient chicks.

Signs of riboflavin deficiency first appear at 10 days of incubation, when embryos become hypoglycemic and accumulate intermediates of fatty acid oxidation. Although flavin-dependent enzymes are depressed with riboflavin deficiency, the main effect seems to be impaired fatty acid oxidation, which is a critical function in the developing embryo. An autosomal recessive trait blocks the formation of riboflavin-binding protein, which is needed for transport of riboflavin to the egg. While the adults appear normal, their eggs fail to hatch regardless of dietary riboflavin content. As eggs become deficient in riboflavin, the egg albumen loses its characteristic yellow tinge. In fact, albumen color score has been used to assess riboflavin status of birds.

Chicks receiving diets only partially deficient in riboflavin may recover spontaneously, indicating that the requirement rapidly decreases with age. A 100-µg dose should be sufficient for treatment of riboflavin-deficient chicks, followed by incorporation of an adequate level in the diet. However, when the curled-toe deformity is longstanding, irreparable damage has occurred in the sciatic nerve, and the administration of riboflavin is no longer curative.

Folic Acid (Folacin) Deficiency

A folacin deficiency results in a macrocytic (megaloblastic) anemia and leukopenia. Tissues with a rapid turnover, such as epithelial linings, GI tract, epidermis, and bone marrow, as well as cell growth and tissue regeneration, are principally affected. Poultry seem more susceptible than other farm animals to a folacin deficiency.

Deficiency results in poor feathering, slow growth, an anemic appearance, and perosis. As anemia develops, the comb becomes waxy white, and pale mucous membranes in the mouth are noted. Elevated erythrocyte phosphoribosylpyrophosphate concentration can be used as a diagnostic tool in folate-deficient chicks. There may also be damage to liver parenchyma and depleted glycogen reserves. While turkey poults show some of the same signs as chickens, mortality is usually higher and the birds develop a spastic type of cervical paralysis that results in the neck becoming stiff and extended.

The abnormal feather condition in chickens leads to weak and brittle shafts. Depigmentation develops in colored feathers due to a deficiency of the vitamin. While a folacin deficiency can result in reduced egg production, the main sign noted with breeders is a marked decrease in hatchability associated with an increase in embryonic mortality, usually during the last few days of incubation. Embryos have deformed beaks and often a bending of the tibiotarsus. While birds may exhibit perosis, the lesions seen differ histologically from those seen as a consequence of choline or manganese deficiency. Abnormal structure of the hyaline cartilage and retardation of ossification are noted with folacin deficiency. Increasing protein content of the diet increases the severity of perosis in chicks receiving diets low in folic acid, as there is an increased folacin demand for uric acid synthesis.

Biotin Deficiency

Biotin deficiency results in dermatitis of the feet and the skin around the beak and eyes similar to that described for pantothenic acid (see above). Perosis and footpad dermatitis are also characteristic signs. While signs of classical biotin deficiency are rare, occurrence of fatty liver and kidney syndrome (FLKS) is important to commercial poultry producers. FLKS was first described in Denmark in 1958, but was not a major concern until the late 1960s, especially in Europe and Australia. Chicks ~3 wk of age become lethargic and unable to stand, then die within hours. Mortality is usually quite low at 1-2% but can reach 20-30%. Postmortem examination reveals pale liver and kidney with accumulation of fat.

The condition was usually confined to wheat-fed birds and was most problematic in low-fat, high-energy diets. High vitamin supplementation in general corrected the problem, and biotin was isolated as the causative agent. It is now known that biotin in wheat has exceptionally low availability. The trigger of high-energy diets led to investigation of biotin in carbohydrate metabolism. Chicks suffering from FLKS are invariably hypoglycemic, highlighting the importance of biotin in 2 key enzymes: pyruvate carboxylase and acetyl Co-A carboxylase. Acetyl Co-A carboxylase appears to preferentially sequester biotin, such that with low biotin availability and need for high de novo fat synthesis (high energy, low-fat diet), pyruvate carboxylase activity is severely compromised. Even with this imbalance, birds are able to grow. However, with a concurrent deprivation in feed intake or increased demand for glucose, hypoglycemia develops, leading to adipose catabolism and the characteristic accumulation of fat in both liver and kidney. Birds with FLKS rarely show signs of classic biotin deficiency.

Plasma biotin levels <100 ng/100 mL may indicate a deficiency. However, recent evidence suggests that plasma biotin levels are quite insensitive to the birds’ biotin status, and that biotin levels in the liver or kidney are more useful indicators. Plasma pyruvic carboxylase is positively correlated with dietary biotin concentration, and levels plateau much later than does the growth response to biotin.

Embryos are also sensitive to biotin status. Congenital perosis, ataxia, and characteristic skeletal deformities may be seen in embryos and newly hatched chicks when the dams are fed a low-biotin diet. Deformities can be prevented by adding biotin to the diet. Embryonic deformities include a shortened tibiotarsus that is bent posteriorly, a much shortened tarsometatarsus, shortening of the bones of the wing and skull, and shortening and bending of the anterior end of the scapula. Syndactyly—an extensive webbing between the third and fourth toes—in biotin-deficient embryos has been noted. Such embryos are chondrodystrophic and characterized by reduced size, parrot beak, crooked tibia, and shortened or twisted tarsometatarsus

Pyridoxine (Vitamin B6) Deficiency

A vitamin B6 deficiency causes retarded growth, dermatitis, and anemia. Because a major role of the vitamin is in protein metabolism, deficiency can result in reduced nitrogen retention. A deficiency can result in a marked increase in iron and a decrease in copper levels of the serum; iron utilization appears to be markedly decreased. The resulting anemia is believed to be the result of a disturbance in the synthesis of the protoporphyrins. Anemia is often noted in ducks, but seldom seen in chickens and turkeys. Young chicks may show nervous movements of the legs when walking and often undergo spasmodic convulsions, leading to death. During convulsions, chicks may run about aimlessly, flapping their wings and falling with jerking motions. The greater intensity of activity, resulting from pyridine deficiency, distinguishes these signs from those of encephalomalacia. A marked gizzard erosion has been noted in vitamin B6-deficient chicks. It can be prevented by inclusion of 1% taurocholic acid in the diet, leading to the speculation that pyridoxine is involved in taurine synthesis and is important for gizzard integrity. In pyridoxine deficiency, collagen maturation is incomplete, suggesting that this vitamin is essential for integrity of the connective tissue matrix. A chronic or borderline deficiency can result in perosis, with one leg usually being crippled and one or both middle toes bent inward at the first joint.

In adult birds, pyridoxine deficiency results in reduced appetite, leading to reduced egg production and a decline in hatchability. Severe deficiency can cause a rapid involution of the ovary, oviduct, comb, and wattles, and of the testis in cockerels. Feed consumption in B6-deficient hens and cockerels declines sharply, but inanition is not responsible for the marked effects of vitamin B6 deficiency on sexual development. Although a partial molt is observed in some hens, the molt is not serious, and hens return to normal egg production within 2 wk following provision of a normal dietary level of pyridoxine.

Thiamine Deficiency

Polyneuritis in birds represents the later stages of a thiamine deficiency, probably caused by buildup of the intermediates of carbohydrate metabolism. In the initial stages of deficiency, lethargy and head tremors may be noted. A marked decrease in appetite is also seen in birds fed a thiamine-deficient diet. Poultry are also susceptible to neuromuscular problems, resulting in impaired digestion, general weakness, star-gazing, and frequent convulsions.

Polyneuritis may be seen in mature birds ~3 wk after they are fed a thiamine-deficient diet. As the deficiency progresses to the legs, wings, and neck, birds may sit on flexed legs and draw back their heads in a star-gazing position. Retraction of the head is due to paralysis of the anterior neck muscles. Soon after this stage, chickens lose the ability to stand or sit upright and topple to the floor, where they may lie with heads still retracted. Thiamine deficiency may also lead to a decrease in body temperature and respiratory rate. Testicular degeneration may be noted, and the heart may show slight atrophy. Birds consuming a thiamine-deficient diet soon show severe anorexia. They lose all interest in feed and will not resume eating unless given thiamine. If a severe deficiency has developed, thiamine must be force-fed or injected to induce eating.
 
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