Vitamin Deficiencies in Poultry
Vitamin deficiencies are most commonly due to inadvertent omission of a complete vitamin premix from the birds’ diet. Multiple signs are therefore seen, although in general, signs of B vitamin deficiencies appear first. Because there are some stores of fat-soluble vitamins in the body, it often takes longer for these deficiencies to affect the bird, and it may take months for vitamin A deficiency to affect adult birds.
Treatment and prevention rely on an adequate dietary supply, usually microencapsulated in gelatin or starch along with an antioxidant. Vitamin destruction in feeds is a factor of time, temperature, and humidity. For most feeds, efficacy of vitamins is little affected over 2-mo storage within mixed feed.
Depending on liver stores, adult birds could be fed a vitamin A–deficient diet for 2–5 mo before signs of deficiency develop. Eventually, birds become emaciated and weak with ruffled feathers. Egg production drops markedly, hatchability decreases, and embryonic mortality increases. As egg production declines, there will likely be only small 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 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 upper alimentary tract. The normal epithelium is replaced by a stratified squamous, keratinized layer. This blocks the ducts of the mucous glands, resulting in necrotic secretions. Small, white pustules may be found in the nasal passages, mouth, esophagus, and pharynx, and these may extend into the crop. Breakdown of the mucous membrane usually allows 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 within 7 days. However, chicks with a good reserve of maternal vitamin A may not show signs of a deficiency for up to 7 wk. Gross signs in chicks include anorexia, growth retardation, drowsiness, weakness, incoordination, emaciation, and ruffled feathers. If the deficiency is severe, the chicks may become ataxic, which is also seen with vitamin E deficiency (see Vitamin E Deficiency). 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. Secondary infection may play a role in many of the deaths noted with acute vitamin A deficiency.
Young chicks with chronic vitamin A deficiency may also develop pustules in the mucous membrane of the esophagus that usually affect the respiratory tract. Kidneys may be pale and the tubules distended because of uric acid deposits, and in extreme cases, the ureters may be plugged with urates. Blood levels of uric acid can rise from a normal level of ~5 mg to as high as 40 mg/100 mL. 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.
Although vitamin A–deficient chicks can be ataxic, similar to those with 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 (see Vitamin E Deficiency). The livers of ataxic vitamin A–deficient chicks contain little or no vitamin A.
Because stabilized vitamin A supplements are almost universally used in poultry diets, it is unlikely that a deficiency will be encountered. However, if a deficiency does develop because of either inadvertent omission of the vitamin A supplement or inadequate feed preparation, up to 2 times the normally recommended level, should be fed for ~2 wk. Vitamin A can be administered through the drinking water, and such treatment usually results in faster recovery than supplemtation via the feed.
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/or poor eggshell quality in laying hens, even though the diet may be well supplied with calcium and phosphorus. Abnormal skeletal development is discussed under calcium and phosphorus imbalances (see Calcium and Phosphorus Imbalances) and manganese deficiency (see Manganese Deficiency).
Laying hens fed a vitamin D3–deficient diet show loss of egg production within 2–3 wk, and depending on the degree of deficiency, shell quality deteriorates almost instantly. Using a corn-soybean meal diet with no supplemental vitamin D3, shell weight decreases dramatically by ~150 mg/day throughout the first 7 days of deficiency. The less obvious decline in shell quality with suboptimal, rather than deficient, supplements is more difficult to diagnose, especially because it is very difficult to assay vitamin D3 in complete feeds.
There is a significant increase in plasma 1,25(OH)2D3 of birds producing good versus poor eggshells. Feeding purified 1,25(OH)2D3 improves the shell quality of these inferior 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. Beaks and claws become soft and pliable. Chicks may have trouble walking and will take a few steps before squatting on their hocks. While resting, they often sway from side to side, suggesting loss of equilibrium. Feathering is usually poor, and an abnormal banding of feathers may be seen in colored breeds. With chronic vitamin D3 deficiency, marked 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, especially the air sacs. A characteristic finding in chicks is a beading of the ribs at the junction of the spinal column along with a downward and posterior bending. Poor calcification can also be seen at the epiphysis of the tibia and femur. By immersing the split bone in a silver nitrate solution and allowing it to stand under incandescent light for a few minutes, the calcified areas are easily distinguished from the areas of cartilage. Adding synthetic 1,25(OH)2D3 to the diet of susceptible chicks reduces the incidence of this condition. Although response is variable, results suggest that some leg abnormalities may be a consequence of inefficient metabolism of cholecalciferol.
In laying hens, 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 decreased calcification in the long bones, with excess of osteoid tissue and parathyroid enlargement.
Dry, stabilized forms of vitamin D3 are recommended to treat deficiencies. In cases of severe mycotoxicosis, a water-miscible form of vitamin D3 is administered in the drinking water to provide the amount normally supplied in the diet. In cases of impaired liver function, metabolites of vitamin D are the usual choice for treatment.
The three main disorders seen in chicks deficient in vitamin E are encephalomalacia, exudative diathesis, and muscular dystrophy. The occurrence of these conditions depends on various other dietary and environmental factors.
Encephalomalacia is seen in commercial flocks if diets are very low in vitamin E, if an antioxidant is either omitted or is not present in sufficient quantities, or if the diet contains a reasonably high level of an unstable and 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, because 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 respond to vitamin E supplementation, depending on the extent of the damage to the cerebellum.
The classic sign of encephalomalacia is ataxia. The results from hemorrhage and edema within the granular layers of the cerebellum, with pyknosis and eventual disappearance of the Purkinje cells and separation of the granular layers of the cerebellar folia. Because of 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 have been shown to 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 seem 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 in this situation. 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.
Vitamin E deficiency accompanied by sulfur amino acid deficiency results in 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, which appear to function in the breakdown and removal of the products of dystrophic degeneration. Initial studies involving the effects of dietary vitamin E on muscular dystrophy show 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 also 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 alone had been shown to have no effect on the disease. Throughout the past few years, the incidence of “muscular dystrophy–type” lesions in the breast muscle of older (>35 day) broilers has increased. Characteristic parallel white striations on the muscle are similar to those seen in chicks with muscular dystrophy, yet on analysis the diet of these birds seems adequate in vitamin E as well as selenium.
Studies with chicks on the interrelationships between antioxidants, linoleic acid, selenium, and sulfur amino acids have shown that selenium and vitamin E play supportive roles in several processes, one of which involves cysteine metabolism and its role in prevention of muscular dystrophy in chickens. Glutathione peroxidase is soluble and located in the aqueous portions of the cell, whereas vitamin E is located mainly in the hydrophobic environments of membranes and in adipose tissue and other 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 prevention of deficiency signs.
Only stabilized fat should be used in feeds. Adequate levels of stabilized vitamin E should be used in conjunction with a commercial antioxidant and at least 0.3 ppm selenium. Signs of exudative diathesis and muscular dystrophy due to vitamin E deficiency can be reversed if treatment is begun early by administering vitamin E through the feed or drinking water. Oral administration of a single dose of vitamin E (300 IU per bird) usually causes remission.
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, and in the young chick, plasma levels are as low as 2% of normal. Because the prothrombin content of newly hatched chicks is only ~40% that of adult birds, young chicks are readily affected by a vitamin K–deficient diet. A carryover of vitamin K from the hen to eggs, and subsequently to 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 prolonged blood clotting 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 development of hypoplastic bone marrow. Although blood-clotting time is a reasonable measure of the degree 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, lack of intestinal synthesis, extent of coprophagy, or the presence of sulfur drugs and other feed additives in the diet. Chicks with coccidiosis can have severe damage to their intestinal wall and can bleed excessively. Antimicrobial agents can suppress intestinal synthesis of vitamin K, rendering the bird completely dependent on the diet for its supply of the vitamin. Synthesis of vitamin K does occur in the bacteria resident in the bird’s digestive tract; however, such vitamin K remains inside the bacterial cell, so the only benefit to the bird arises from the bacterial cell digestion or via coprophagy.
The inclusion of menadione at 1–4 mg/ton of feed is an effective and common practice to prevent vitamin K deficiency. If signs of deficiency are seen, the level should be doubled. A number of stress factors (eg, coccidiosis and other intestinal parasitic diseases) increase the requirements for vitamin K. Dicumarol, sulfaquinoxaline, and warfarin are antimetabolites of vitamin K.
Vitamin B12 is an essential part of several enzyme systems, with most reactions involving the transfer or synthesis of methyl groups. Although 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 vitamin B12 results in reduced weight gain and feed intake, along with poor feathering and nervous disorders. Although deficiency may lead to perosis, this is probably a secondary effect due to a dietary deficiency of methionine or choline as sources of methyl groups. Vitamin B12 may alleviate perosis because of its effect on the synthesis of methyl groups. Other signs reported in poultry are anemia, gizzard erosion, and fatty infiltration of the heart, liver, and kidneys. Laying hens initially appear to be able to maintain body weight and egg production; however, egg size is reduced. In breeders, hatchability can be markedly reduced, although several weeks may be needed for signs of deficiency 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 mid-term embryo deaths.
Deficiency of vitamin B12 is highly unlikely, especially for birds grown on litter or where animal-based ingredients are used. Treatment involves feeding up to 20 mcg/g feed for 1–2 wk.
In addition to poor growth, the classic 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 ~12–13 mg of choline/g of dried whole egg. A large egg contains ~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 are provided for a prolonged period. Under these conditions, the choline content of eggs is not reduced, suggesting possible intestinal synthesis by the bird.
Diets that contain appreciable quantities of soybean meal, wheat bran, and wheat shorts are unlikely to be deficient in choline. Soybean meal is a good source of choline, and wheat byproducts are good sources of betaine, which can perform the methyl-donor function of choline. Other good sources of choline are distiller’s grains, fishmeal, liver meal, meat meals, distiller’s solubles, and yeast. A number of commercial choline supplements are available, and supplemental choline is routinely used in most poultry feeds.
There is considerable evidence that poultry, and even chick and turkey embryos, can synthesize niacin but at a rate too slow for optimal growth. It has been claimed that a marked deficiency of niacin cannot occur in chickens unless there is a concomitant deficiency of the amino acid tryptophan, which is a niacin precursor.
Niacin deficiency is characterized by severe disorders in the skin and digestive organs. The first signs are usually loss of appetite, retarded growth, general weakness, and diarrhea. Deficiency produces enlargement of the tibiotarsal joint, valgus-varus bowing of the legs, poor feathering, and dermatitis on the head and feet.
Niacin deficiency in chicks can also result in “black tongue.” At ~2 wk of age, the tongue, oral cavity, and esophagus become distinctly inflamed. 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 as seen in manganese and choline deficiency is that with niacin deficiency the Achilles tendon seldom slips from its condyles.
Niacin deficiency in chickens may be prevented by feeding a diet that contains niacin at ≥30 mg/kg; however, many nutritionists recommend 2–2.5 times as much. An allowance of 55–70 mg/kg of feed appears to be satisfactory for ducks, geese, and turkeys. Ample niacin should be provided in poultry diets so as to spare the utilization of tryptophan.
Pantothenic acid is the prosthetic group within coenzyme A, an important coenzyme involved in many reversible acetylation reactions in carbohydrate, fat, and amino acid metabolism. Signs of deficiency therefore 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 before this event. Embryos from hens with pantothenic acid deficiency can have subcutaneous hemorrhages and severe edema, with most mortality showing up during the later part of the incubation period. In chicks, the first signs are reduced growth and feed consumption, poor feathering with feathers becoming ruffled and brittle, and a rapidly developing dermatitis. The corners of the beak and the area below the beak are usually the worst affected regions for dermatitis, but the condition is also noted on the feet. In severe cases, the skin of the feet may cornify, and wart-like lumps occur on the balls of the feet. The foot problem often leads to bacterial infection.
Liver concentration of pantothenic acid is reduced during a deficiency, with the liver becoming atrophied, with a faint dirty yellow color developing. Nerve fibers of the spinal cord may show myelin degeneration. Pantothenic acid–deficient chicks show lymphoid cell necrosis in the bursa of Fabricius and thymus, together with lymphocytic paucity in the spleen. The foot condition in chicks and the poor feathering are difficult to differentiate from signs of a biotin deficiency. In a pantothenic acid deficiency, dermatitis of the feet is usually noted first on the toes; in contrast, a biotin deficiency primarily affects the foot pads and is usually more severe. Ducks do not show the usual signs noted for chickens and turkeys, except for retarded growth, but mortality can be quite high.
Most poultry diets contain supplements of calcium pantothenate. Periodically, growing chickens fed practical diets develop a scaly condition of the skin, the exact cause of which is not known. Treatment with both calcium pantothenate (2 g) and riboflavin (0.5 g) in the drinking water (50 gal [190 L]) for a few days has been successful in some instances. Diets usually contain supplemental pantothenic acid at 12 mg/kg.
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 the diet is inadvertently devoid of the entire spectrum of vitamins, it is signs of riboflavin deficiency that first appear. 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; sciatic nerves usually show the most pronounced effects. Histologic examination of the affected nerves shows degenerative changes in the myelin sheaths that, when severe, pinch the nerve. This produces a permanent stimulus, which causes the curled-toe paralysis.
Signs of riboflavin deficiency in hens are decreased egg production, increased embryonic mortality, and an increase in size and fat content of the liver. Hatchability declines within 2 wk when hens are fed a riboflavin-deficient diet but returns to near normal when riboflavin is restored. Affected embryos are dwarfed and show characteristically defective “clubbed” down. The nervous system of these embryos shows degenerative changes much like those described in riboflavin-deficient chicks. Clubbed down is periodically seen in cases of poor hatchability, when the “reject” chicks or dead embryos show this condition, even though the breeder diet is apparently adequate in riboflavin. Anecdotal evidence suggests greater occurrence of this clubbed-down condition in farms that select “floor-eggs” for incubation.
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 the riboflavin-binding protein needed for transport of riboflavin to the egg. Although 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 color. 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-mcg 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 occurs in the sciatic nerve, and the administration of riboflavin is no longer curative.
Most diets contain up to 10 mg of riboflavin/kg. Treatment can be given as two sequential daily 100-mcg doses for chicks or poults, followed by an adequate amount of riboflavin in feed.
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 to folacin deficiency than other farm animals. Deficiency results in poor feathering, slow growth, an anemic appearance, and sometimes perosis. As anemia develops, the comb becomes a waxy-white color, and pale mucous membranes in the mouth are noted. Increased erythrocyte phosphoribosylpyrophosphate concentration can be used as a diagnostic tool in folacin-deficient chicks. There may also be damage to liver parenchyma and depleted glycogen reserves. Although 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, and depigmentation develops in colored feathers. Although 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 bending of the tibiotarsus. Birds may exhibit perosis, but the lesions seen differ histologically from those that develop due to choline or manganese deficiency. Abnormal structure of the hyaline cartilage and retardation of ossification are noted with folacin deficiency. Increasing the protein content of the diet has been shown to increase the severity of perosis in chicks receiving diets low in folic acid, because there is an increased folacin demand for uric acid synthesis.
Signs of folic acid deficiency in poultry can be prevented by ensuring diets contain supplements of up to 1 mg/kg.
Biotin deficiency results in dermatitis of the feet and the skin around the beak and eyes similar to that described for pantothenic acid deficiency (see Pantothenic Acid Deficiency). Perosis and footpad dermatitis are also characteristic signs. Although signs of classic 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, when the condition became more prevalent and especially so in Europe and Australia. Chicks ~3 wk old 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 as described in the 1960s 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 with FLKS are invariably hypoglycemic, emphasizing the importance of biotin in two key enzymes, namely 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 kidneys. Birds with FLKS rarely show signs of classic biotin deficiency.
Plasma biotin levels <100 ng/100 mL have been reported as a sign of 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 kidneys 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 supplemental 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 hens are fed a deficient 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, which is an extensive webbing between the third and fourth toes, is seen in biotin-deficient embryos. Such embryos are chondrodystrophic and characterized by reduced size, parrot beak, crooked tibia, and shortened or twisted tarsometatarsus.
A number of factors increase biotin requirements, including oxidative rancidity of any feed fat, competition by intestinal microorganisms, and lack of carryover into the newly hatched chick or poult. It is good practice to add 150 mg biotin/tonne of feed, especially when significant amounts of wheat or wheat byproducts are used in the diet.
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. Dietary protein is not well utilized, and thus nitrogen excretion increases. Increased iron levels and decreased copper levels are noted in the serum, and iron utilization appears to be markedly decreased. The resulting anemia is likely due to a disturbance in the synthesis of protoporphyrins. Anemia is often noted in ducks but is 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, the chicks may run about aimlessly, flapping their wings and falling with jerking motions. The greater intensity of activity, resulting from vitamin B6 deficiency, distinguishes these signs from those of encephalomalacia. 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 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 rapid involution of the ovary, oviduct, comb, and wattles, and of the testis in cockerels. Feed consumption in vitamin B6–deficient hens and cockerels declines sharply. Although a partial molt is seen in some hens, normal egg production returns within 2 wk after provision of a normal dietary level of pyridoxine.
Deficiency can be prevented by adding pyridoxine at 3–4 mg/kg feed.
Polyneuritis in birds represents the later stages of a thiamine deficiency, probably caused by buildup of the intermediates of carbohydrate metabolism. Because the brain’s immediate source of energy results from the degradation of glucose, it depends on biochemical reactions involving thiamine. In the initial stages of deficiency, lethargy and head tremors may be noted. A marked decrease in appetite is 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, 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 the chickens to resume eating.
Thiamine deficiency is most common when poorly processed fish meals are used, because they contain thiaminase enzyme. In such situations, adding extra thiamine may be ineffective. There is no good evidence suggesting that, unlike in some mammalian species, certain Fusarium mycotoxins can increase the need for supplemental thiamine. In otherwise adequate diets, deficiency is prevented by supplements of thiamine up to 4 mg/kg.