Vitamin Deficiencies in Poultry part 2

 (Nicotinic Acid) Deficiency

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.

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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.

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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.

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Pantothenic Acid Deficiency

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.

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 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.

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 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.

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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 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.

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. 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.

Thiamine Deficiency

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.

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