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.

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Vitamin A Deficiency

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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.

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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 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/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.

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.

Vitamin E Deficiency

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.

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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, 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 Deficiency

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.

Choline Deficiency

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.

By Steven Leeso

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