7
Signs of Nutritional Deficiencies in Chickens and Turkeys

Clinical manifestation of nutrient deficiencies often occurs in conjunction with an alteration of normal biological processes that are unique for the nutrient. Some enzymes depend on particular vitamins and minerals for their functioning, and their activity diminishes with an inadequacy. In other instances, a particular physiological response or change in metabolite concentration may occur. This information was primarily obtained from formal experiments in which the inadequacies were definitive. Under field conditions, nutrient inadequacies are usually marginal, occasionally multiple, and often confounded with management problems or disease. To supplement physical observation of these signs, the committee has provided biochemical and physiological measurements for use in diagnosis. Table 7-1 presents a summary of the known biochemical and physiological measurements for diagnosing each nutrient deficiency. Additional information is available in the associated references.

Inadequate dietary vitamins and minerals in the chicken or turkey hen's diet are likely to reduce the egg contents accordingly and have adverse effects on embryonic development. Normal embryonic development proceeds through several events at which death of the embryo is common. The largest number of deaths occur during the transition from anaerobic to aerobic respiration with the establishment of the chorioallantois, which takes place between 3 to 4 days incubation and emergence at 18 to 21 days incubation. The same problems occur with other poultry species, and nutrient inadequacies generally accentuate death rates at these times (Couch and Ferguson, 1972).

Embryos are well developed at the end of incubation, and embryos that die as a result of nutrient deficiencies at this time may exhibit typical physical symptoms. These symptoms are assembled for each nutrient in Table 7-2. The symptoms can be similar for different nutrients, and the extent of the inadequacy may change the nature of the symptoms as well as when death occurs. Deficiency symptoms are expressed to a greater extent in growing birds than in adults. Table 7-3 gives a list of these symptoms by tissue affected, as a diagnostic aid. The table also presents information on these changes such that each can be rationalized in terms of nutrient function. References provided are not complete but are intended to be salient and most recent for cross-indexing purposes. Again, such information is usually the product of formal experimentation and not complicated by practical circumstances.

PROTEIN AND AMINO ACID DEFICIENCIES

Protein is made up of amino acids. The need for the essential amino acids determines the need for protein, and a reduction in dietary protein that results in deficiencies of several essential amino acids creates general symptoms. Productive activities suffer the most. For example, the energy used by growing birds is heavily committed to assembling the contractile elements in muscle cells but not to increasing cell number; thus protein inadequacies readily affect muscle size but not fiber number (Timson et al., 1983). Similarly, the effect of protein inadequacies on protein synthesis in the liver and oviduct is greatest with the laying hen (Muramatsu et al., 1987).

Deficiencies of individual essential amino acids usually have the same effect as when protein is deficient; however, additional symptoms may appear that characterize certain amino acids. Inadequate lysine is known to cause depigmentation of the wing feathers in Bronze turkey poults (Vohra and Kratzer, 1959) and certain colored chicks (Klain et al., 1957). A variety of abnormalities in feather development occur with deficiencies of arginine, valine, leucine, isoleucine, tryptophan, phenylalanine, and tyrosine in growing chicks (Newberne et



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Nutrient Requirements of Poultry: Ninth Revised Edition, 1994 7 Signs of Nutritional Deficiencies in Chickens and Turkeys Clinical manifestation of nutrient deficiencies often occurs in conjunction with an alteration of normal biological processes that are unique for the nutrient. Some enzymes depend on particular vitamins and minerals for their functioning, and their activity diminishes with an inadequacy. In other instances, a particular physiological response or change in metabolite concentration may occur. This information was primarily obtained from formal experiments in which the inadequacies were definitive. Under field conditions, nutrient inadequacies are usually marginal, occasionally multiple, and often confounded with management problems or disease. To supplement physical observation of these signs, the committee has provided biochemical and physiological measurements for use in diagnosis. Table 7-1 presents a summary of the known biochemical and physiological measurements for diagnosing each nutrient deficiency. Additional information is available in the associated references. Inadequate dietary vitamins and minerals in the chicken or turkey hen's diet are likely to reduce the egg contents accordingly and have adverse effects on embryonic development. Normal embryonic development proceeds through several events at which death of the embryo is common. The largest number of deaths occur during the transition from anaerobic to aerobic respiration with the establishment of the chorioallantois, which takes place between 3 to 4 days incubation and emergence at 18 to 21 days incubation. The same problems occur with other poultry species, and nutrient inadequacies generally accentuate death rates at these times (Couch and Ferguson, 1972). Embryos are well developed at the end of incubation, and embryos that die as a result of nutrient deficiencies at this time may exhibit typical physical symptoms. These symptoms are assembled for each nutrient in Table 7-2. The symptoms can be similar for different nutrients, and the extent of the inadequacy may change the nature of the symptoms as well as when death occurs. Deficiency symptoms are expressed to a greater extent in growing birds than in adults. Table 7-3 gives a list of these symptoms by tissue affected, as a diagnostic aid. The table also presents information on these changes such that each can be rationalized in terms of nutrient function. References provided are not complete but are intended to be salient and most recent for cross-indexing purposes. Again, such information is usually the product of formal experimentation and not complicated by practical circumstances. PROTEIN AND AMINO ACID DEFICIENCIES Protein is made up of amino acids. The need for the essential amino acids determines the need for protein, and a reduction in dietary protein that results in deficiencies of several essential amino acids creates general symptoms. Productive activities suffer the most. For example, the energy used by growing birds is heavily committed to assembling the contractile elements in muscle cells but not to increasing cell number; thus protein inadequacies readily affect muscle size but not fiber number (Timson et al., 1983). Similarly, the effect of protein inadequacies on protein synthesis in the liver and oviduct is greatest with the laying hen (Muramatsu et al., 1987). Deficiencies of individual essential amino acids usually have the same effect as when protein is deficient; however, additional symptoms may appear that characterize certain amino acids. Inadequate lysine is known to cause depigmentation of the wing feathers in Bronze turkey poults (Vohra and Kratzer, 1959) and certain colored chicks (Klain et al., 1957). A variety of abnormalities in feather development occur with deficiencies of arginine, valine, leucine, isoleucine, tryptophan, phenylalanine, and tyrosine in growing chicks (Newberne et

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Nutrient Requirements of Poultry: Ninth Revised Edition, 1994 TABLE 7-1 Biochemical and Physiological Measurements for Diagnosis of Nutrient Deficiencies in Chickens and Turkeys Nutrients Biochemical and Physiological Measurements References Histidine Reduced breast muscle anserine and carnosine. Robbins et al., 1977; Amend et al., 1979 Lysine Reduced hemoglobin and hematocrit. Braham et al., 1961 Vitamin A Hepatic vitamin A is indicative of a deficiency, but blood level is not. Liver xanthine dehydrogenase and kidney arginase both increase even in the first stages of a deficiency. Reduced glycogen phosphorylase in liver, and red and white muscles. Increased thyroid size and reduced T3 and T4. Rogers, 1969; Nockels and Phillips, 1971; Jensen, 1974; Bruckental and Ascarelli, 1975; Nockels et al., 1984 Vitamin D Calcium-binding protein of intestine; 1,25-(OH)2-D3 versus 24,25-(OH)2-D2 in serum (complicated by dietary calcium and phosphorus); plasma alkaline phosphatase; nonproteolipid phospholipid content of rachitic cartilage. Bar et al., 1972; Ohmdahl and DeLuca, 1973; Morrissey et al., 1977; Boyan and Ritter, 1984; Kaetzel and Soares, 1985 Vitamin E Superoxide dismutase; glutamic-oxaloacetictransaminase; plasma and tissue vitamin E concentration (all measurements affected by selenium as well). Walter and Jensen, 1964; Arnold et al., 1974; Sklan et al., 1981; Sklan and Donoghue, 1982 Vitamin K Prothrombin clotting time of plasma. Griminger et al., 1970 Thiamin Transketolase in erythrocytes and leucocytes; plasma pyruvic acid. Lofland et al., 1963; Anonymous, 1977 Riboflavin Liver xanthine dehydrogenase; erythrocyte glutathione reductase. Chou, 1971; Lee, 1982 Niacin Level and ratio of niacin excretion products N'-methyl-nicotinamide and N'-methyl-2-pyridone-5-carboxyamide (untested for fowl). Darby et al., 1975 Biotin Blood pyruvate carboxylase; ratio of C 16:1 to C 18:0 fatty acids in blood. Edwards, 1974; Whitehead and Bannister, 1980 Pantothenic acid Hepatic coenzyme A. Cupo and Donaldson, 1986 Pyridoxine Serum glutamic oxaloacetic transaminase; plasma glycine-serine ratio aspartic aminotransferase. Daghir and Balloun, 1963; Sifri et al., 1972; Lee et al., 1976 Folacin Dihydrofolic acid reductase in liver; serine hydroxymethyl transferase in liver. Rabbani et al., 1973; Zamierowski and Wagner, 1977 Vitamin B12 B12 in blood; excretion of methylmalonic acid. Cox and White, 1962; Lau et al., 1965 Choline Serum phospholipids. Seifter et al., 1972 Linoleic acid Linoleate, arachidonate, and eicosatrienoate concentrations in liver lipids. Machlin and Gordon, 1960 Calcium Calcium in hen's blood (but not in chick's unless deficiency is severe); intestinal calcium-binding protein (complicated by D3 metabolites and phosphorus); turkey poults differ from chicks. Bar et al., 1972, 1978a,b; Bar and Hurwitz, 1973 Chlorine Hemoconcentration; alkalosis. Leach and Nesheim, 1963; Cohen and Hurwitz, 1974; Hamilton and Thompson, 1980 Copper Plasma ceruloplasmin; lysyl oxidase in aorta, liver, tendon, and bone; erythrocyte superoxide dismutase. Kim and Hill, 1966; Miller and Stake, 1974; Bettger et al., 1979; Opsahl et al., 1982 Iodine Plasma thyroxine and tri-iodothyronine. Singh et al., 1968 Iron Hematocrit; blood hemoglobin concentration; transferrin saturation; anemia with lipemia. Davis et al., 1962; Waddell and Sell, 1964; Planas, 1967 Magnesium Magnesium concentration in blood. Sell et al., 1967; Hajj and Sell, 1969 Manganese Chondroitin sulfate in bone; manganese concentration in bone; superoxide dismutase. Leach, 1968; Reid et al., 1973; DeRosa et al., 1980 Phosphorus Serum inorganic phosphorus; renal calcium-binding protein. Miller and Stake, 1974; Bar et al., 1978a,b Potassium Plasma potassium; metabolic acidosis (complicated by sodium). Burns et al., 1953; Cohen and Hurwitz, 1974 Selenium Plasma glutathionine peroxidase. Noguchi et al., 1973; Dean and Combs, 1981; Cantor et al., 1982 Sodium Metabolic acidosis (complicated by potassium). Nott and Combs, 1969; Cohen and Hurwitz, 1974 Zinc Plasma and bone zinc; thymidine kinase; alkaline phosphatase and collagenase in bone. Miller and Stake, 1974; Oberleas and Prasad, 1974; Starcher et al., 1980; Bettger et al., 1979

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Nutrient Requirements of Poultry: Ninth Revised Edition, 1994 TABLE 7-2 Signs of Deficiency in the Embryo Nutrients Deficiency Signs References Vitamin A Death at about 48 hours of incubation from failure to develop the circulatory system; abnormalities of kidneys, eyes, and skeleton. Asmundson and Kratzer, 1952; Thompson et al., 1965; Heine et al., 1985 Vitamin D Death at about 18 or 19 days of incubation, with malpositions, soft bones, and with a defective upper mandible prominent. Sunde et al., 1978; Narbaitz and Tsang, 1989 Vitamin E Early death at about 84 to 96 hours of incubation, with hemorrhaging and circulatory failure (implicated with selenium). Card et al., 1930; Latshaw and Osman, 1974 Vitamin K No physical deformities from a simple deficiency, nor can they be provoked by antivitamins, but mortality occurs between 18 days and hatching, with variable hemorrhaging. Griminger, 1964; Hauschka and Reid, 1978a Thiamin High embryonic mortality during emergence but no obvious symptoms other than polyneuritis in those that survive. Polin et al., 1962; Charles et al., 1972 Riboflavin Mortality peaks at 60 hours, 14 days, and 20 days of incubation, with peaks prominent early as deficiency becomes severe. Altered limb and mandible development, dwarfism, and clubbing of down are defects expressed by embryo. Romanoff and Bauernfeind, 1942; Landauer, 1967 Niacin Embryo readily synthesizes sufficient niacin from tryptophan. Various bone and beak malformations occur when certain antagonists are administered during incubation. Snell and Quarles, 1941; Landauer, 1956; Caplan, 1972 Biotin High death rate at 19 to 21 days of incubation, and embryos have parrot beak, chondrodystrophy, several skeletal deformities, and webbing between the toes. Cravens et al., 1994; Couch et al., 1947 Pantothenic acid Deaths appear around 14 days of incubation, although marginal levels may delay problems until emergence. Variable subcutaneous hemorrhaging and edema; wirey down in poults. Kratzer et al., 1955; Beer et al., 1963 Pyridoxine Early embryonic mortality based on antivitamin use. Landauer, 1967 Folic acid Mortality at about 20 days of incubation. The dead generally appear normal, but many have bent tibiotarsus, syndactyly, and mandible malformations. In poults, mortality at 26 to 28 days of incubation with abnormalities of extremities and circulatory system. Sunde et al., 1950a; Kratzer et al., 1956a Vitamin B12 Mortality at about 20 days of incubation, with atrophy of legs, edema, hemorrhaging, fatty organs, and head between thighs malposition. Olcese et al., 1950; Ferguson et al., 1955 Manganese Peak deaths prior to emergence. Chondrodystrophy, dwarfism, long bone shortening, head malformations, edema, and abnormal feathering are prominent. Lyons and Insko, 1937 Zinc Deaths prior to emergence, and the appearance of rumplessness, depletion of vertebral column, eyes underdeveloped, and missing limbs. Kienholz et al., 1961; Turk, 1965 Copper Deaths at early blood stage with no malformations. Bird et al., 1963 Iodine Prolongation of hatching time, reduced thyroid size, and incomplete abdominal closure. Rogler et al., 1959a, b Iron Low hematocrit; low blood hemoglobin; poor extra-embryonic circulation in candled eggs. Dewar et al., 1974; Morck and Austic, 1981 Selenium High incidence of dead embryos early in incubation. Latshaw et al., 1977

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Nutrient Requirements of Poultry: Ninth Revised Edition, 1994 TABLE 7-3 Nutrients Associated with Various Signs of Deficiency in Growing Birds Deficiency Signs Descriptions Species Associated Nutrients Skin lesions Crusting and scab formation around eyes and beak Chick, poult, Biotin, pantothenic acid   Bottoms of feet rough and calloused with hemorrhagic cracks Chick, poult Biotin, pantothenic acid   Scaliness on feet Chick Zinc, niacin   Lesions around eyes, eyelids stuck together Chick, poult Vitamin A   Mouth, inflammation of oral mucosa (chicken black tongue) Poult, chick Niacin Feather abnormalities Uneven feather growth, abnormally long primary feathers, feathers not lying smoothly Chick, poult Protein, amino acid imbalance   Frizzled and rough Chick, poult Zinc, niacin, pantothenic acid, folic acid, lysine   Black pigmentation in breeds with red and brown feathers Chick Vitamin D   Depigmentation Chick, poult, Copper, iron, folacin Nervous disorders Convulsions with head retraction Chick, pigeon Thiamin   Convulsions with hyperexcitability Chick, poult, duckling Pyridoxine   Hyperirritability Chick, poult, duckling Magnesium, sodium chloride   Characteristic fright reaction with tetanic spasms Chick Chloride   Spastic cervical paralysis, neck extended with birds appearing to look down Poult Folacin   Curled-toe paralysis, gross enlargement of sciatic and brachial nerves with myelin degeneration Chick Riboflavin   Encephalomalacia, tetanic spasms with head retraction, hemorrhagic lesions in cerebellum Chick Vitamin E Blood and vascular system Anemia All poultry     Macrocytic   Vitamin B12   Macrocytic, hyperchromic   Folacin   Microcytic, hypochromic   Iron, copper   Microcytic   Pyridoxine   Hemorrhage, intramuscular, subcutaneous, internal from aortic rupture Chick, poult Vitamin K, copper   Exudative diathesis Chick, poult Selenium, vitamin E   Enlarged heart Chick, poult Copper Muscle Muscular dystrophy, white areas of degeneration in skeletal muscle Chick, duck, poult Vitamin E, selenium   Cardiac myopathy Poult Vitamin E, selenium   Gizzard myopathy Poult Vitamin E, selenium Bone disorders Soft, easily bent bones and beak (rickets) All poultry Vitamin D, calcium or phosphorus deficiency or imbalance   Hock enlargement Poult, chick, gosling, duckling Niacin, zinc   Perosis Chick, poult Biotin, choline, vitamin B12, manganese, zinc, folacin   Bowed legs Duck Niacin   Shortening and thickening of leg bones Chick zinc, manganese   Curled toes Chick Riboflavin Diarrhea   Chick, duck, poult Niacin, riboflavin, biotin NOTE: Slow growth and general lack of vigor are generally associated with malnutrition. The signs listed in this table are more specific indications of deficiencies of particular nutrients.

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Nutrient Requirements of Poultry: Ninth Revised Edition, 1994 al., 1960; Robel, 1977; Penz and Kratzer, 1984). Chavez and Kratzer (1974) observed a foot pad dermatitis in poults when methionine was deficient, but cystine had to be adequate for the dermatitis to occur. Grau (1945) reported a tongue deformity in chicks fed a purified diet deficient in leucine, isoleucine, or phenylalanine, but these observations were not confirmed by Bragg (1953) with practical feedstuffs. VITAMIN DEFICIENCIES Vitamin A Substitution of the body's secretory epithelia by keratinized surfaces is the most important change occurring with a vitamin A deficiency. Corneal, conjunctival, esophageal, and tracheal secretory membranes are all altered in chickens (Aydelotte, 1963). Mucus formation depends on vitamin A (DeLuca et al., 1971). Loss of membrane integrity, in turn, alters water retention (Lopen et al., 1973) and impairs the ability to withstand infection (Singh and Donovan, 1973; Sijtsma et al., 1989). Inadequate vitamin A also reduces the immune system's response to challenge and further contributes to disease susceptibility (Davis and Sell, 1989; Sklan et al., 1989). The appearance of keratinized secretory surfaces is followed by a typical ataxia. Alterations in bone growth create several areas of compression on the central nervous system that cause a loss in mobility (Howell and Thompson, 1967). Inadequate vitamin A also adversely affects the pituitary-gonadal axis to create other symptoms that are not readily obvious (Fletcher, 1971). Nockels et al. (1984) reported that hypothyroidism is an early indication of vitamin A deficiency in chicks. Reductions in testes size, circulating testosterone, and fertility have been reported during vitamin A deficiency in cockerels (Padedes and Garcia, 1959; Hall et al., 1980). Muscles in vitamin-A-deficient birds have a high level of glycogen, which cannot be readily used because phosphorylase activity is inordinately low (Nockels and Phillips, 1971; Sundeen et al., 1980). Alternatively, glucose is provided by extensive gluconeogenesis from protein (Nir and Ascarelli, 1967; Bruckental et al., 1974), and nitrogen end products increase such that deposits of uric acid appear in the kidneys and ureters (Bruckental and Ascarelli, 1975; Chandra et al., 1984). Vitamin A in feedstuffs is labile, and concentrated supplements are normally given to ensure that the requirement is met. Misuse of these concentrates has led to occasional toxicosis problems. Skin lesions at the commissure of the beak, nose, and eyes attributable to mucus membrane hyperplastic activity have been shown to occur in chicks within 72 hours after oral dosing with 60,000 IU (Kriz and Holman, 1969). The appearance of rachitic bones together with a hyperplastic parathyroid results from the antagonism known to exist with vitamin D (Metz et al., 1985; Tang et al., 1985; Veltmann et al., 1987). Excessive vitamin A has also been shown to antagonize vitamin E (Vahl and Van't Klooster, 1987) and increase the likelihood of a deficiency when vitamin E and selenium nutriture is marginal (Combs, 1976). Plant source feedstuffs usually provide carotenoid pigments that may be converted into vitamin A. The most favorable such pigment in this respect is ß-carotene (Flegal et al., 1971), and conversion largely occurs at the intestine during absorption (Sklan, 1983). Because of the susceptibility of vitamin A sources to oxidative losses, synthetic antioxidants often are included in premixes and complete feeds (Grundboeck et al., 1977). Vitamin D Poultry require vitamin D to effectively use calcium. After absorption, the vitamin is hydroxylated at the 25-position in the liver and then transferred to the kidney, where the 1,25-dihydroxy metabolite is formed (Ameenuddin et al., 1985). All of the vitamin metabolites affect calcium utilization in one way or another, but the 1,25-dihydroxy-vitamin D seems to have the greatest impact. Vitamin D metabolites induce the synthesis of calcium-binding proteins in the intestine, kidney, and uterus through the efforts of vitamin D metabolites at both transcriptional and post-transcriptional levels. Calcium-binding proteins enhance calcium absorption from the intestine, recovery from the urine, and shell deposition, respectively (Coty, 1980; Jande et al., 1981; Roth et al., 1981; Clemens et al., 1988). Vitamin D also induces the formation of osteocalcin, a protein in bone (Anonymous, 1981). Osteocalcin is believed to participate in the organic-inorganic matrix. Vitamin D is implicated by converting specific glutamic acid residues in osteocalcin to ?-carboxylglutamic acid metabolites that interact with calcium. Bone alterations associated with osteocalcin appear to be more involved with resorption and turnover when calcium is needed elsewhere in the body than growth. Presumably, vitamin D also provides proliferative signals for undifferentiated cells in the intestine (Cross and Peterlik, 1983) and pancreatic islets (Clark et al., 1987). Vitamin D2 represents the plant source of this vitamin and arises from the ultraviolet irradiation of ergosterol (Kobayashi and Yasumura, 1973), whereas vitamin D3 occurs in animals upon irradiation of 7-dehydro-cholesterol in skin (Beadle, 1977). Vitamin D3 is about 10-fold more effective with chicks than vitamin D2 (Hurwitz et al., 1967). A large part of this difference in

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Nutrient Requirements of Poultry: Ninth Revised Edition, 1994 activity seems to involve metabolite formation in the liver, where enhanced glucuronidation of the 25-hydroxy-vitamin D2 favors biliary excretion (Le Van et al., 1981). Gross symptoms occurring because of a vitamin D deficiency can largely be attributed to a reduction of intestinal binding protein and lack of calcium recovered from feed (McCarthy et al., 1984). During vitamin D deficiency, growing birds develop hypocalcemia, which, in turn, stunts skeletal development through widened cartilage at epiphyses of long bones and weakened shafts (Noff et al., 1982; Long et al., 1984). For some reason, an abnormal blackening of the feathers also occurs with some pigmented chicks (Glazener and Briggs, 1948). Once the skeleton has assumed adult size, a vitaminosis D is obvious only with hens in production. Egg production and egg weight decrease while the eggshell thins as bone reserves are progressively depleted (Vohra et al., 1979). Hens in production cyclically release estrogen from the ovary to maximize 1,25-dihydroxy-vitamin D production concurrent with eggshell formation (Castillo et al., 1979). As a result, levels of calcium-binding protein in the uterus (Navickis et al., 1979) and calcium in the medullary bone (Takahashi et al., 1983) are altered to facilitate eggshell formation. Vitamin D nutriture of the hen also influences its content in egg yolk and the subsequent need for this vitamin by the chick (Bethke et al., 1936; Griminger, 1966; Stevens and Blair, 1985). Vitamin D removed from the yolk is metabolized by the embryo as it is by the adult, and 1,25-dihydroxy-vitamin D is the dominant metabolite (Bishop and Norman, 1975). An additional activity for this metabolite is recovery of calcium from the shell at the chorioalloic membrane to support skeletal mineralization prior to hatching (Narbaitz, 1987). The yolk sac membrane also responds to 1,25-dihydroxy-vitamin D at the same time, and a portion of the calcium from the shell is transferred into the yolk for later use upon hatching (Clark et al., 1989); however, one or more of the other metabolites must also be present if complete embryonic development and emergence from the shell is to occur (Ameenuddin et al., 1982). The very low content of vitamin D in feedstuffs is generally ignored in feed formulation, and the complete requirement is satisfied by using concentrated premixes. Overuse of vitamin D concentrates can lead to a toxicity. High levels of 1,25-dihydroxy-vitamin D occur with a toxicosis, along with hypercalcemia and soft tissue mineralization (Morrissey et al., 1977; Ratkowski et al., 1982). Leg problems may arise with growing birds because of bone calcium loss (Cruickshank and Sim, 1987), but few obvious changes occur with hens other than a general depression in performance (Ameenuddin et al., 1986). Toxic levels of vitamin D may be transferred into the egg to create similar problems for the embryo; however, the hypercalcemia occurs from shell resorption, and bone mineralization is enhanced (Narbaitz and Fragiskos, 1984). Vitamin D in feed may not be totally available to poultry. This vitamin is susceptible to destruction by oxidation and significant losses may occur unless supplemental antioxidants are used (Fritz et al., 1942). Also, mycotoxins in feeds interfere with the utilization of dietary vitamin D (Bird, 1978; Gedek et al., 1978; Kohler et al., 1978). Losses of vitamin D because of oxidation and poor utilization may result in a deficiency of the vitamin even though initial dietary concentrations of vitamin D substantially exceed known requirements. Vitamin E Vitamin E is composed of an array of tocopherols derived from plant sources that act as antioxidants within the animal. Hydrophobic areas of tissues, particularly cell membranes, are the sites of action for vitamin E (Erin et al., 1984), whereas selenium is a cofactor for complementary antioxidant activities in the aqueous portion (Xu and Diplock, 1983). Dietary vitamin E is absorbed from the intestine with fat, and its dissemination follows depletion of lipoprotein contents from circulation (Massey, 1984). In turn, tissue vitamin E content parallels feed vitamin E levels, and tissues receiving the highest proportions are intestine, liver, fat depots, and muscle (Astrup, 1979). The amount of vitamin E needed to avoid a deficiency largely depends on the adequacy of the accompanying selenium and on circumstances presenting oxidative threats to the system. An inadequacy of both vitamin E and selenium leads to exudative diathesis, which is a subdermal accumulation of viscous blue-green-colored exudate from endothelial failures in portions of the vascular system (Scott, 1966a). Myopathies of the gizzard, heart, and, to a lesser extent, the skeletal muscles are also apparent. Skeletal muscles, particularly the breast, become more myopathic when the sulfur amino acids are also deficient. Exudative diathesis can be eliminated and most myopathies can be greatly relieved when selenium alone is increased (Combs and Scott, 1974). Vitamin E deficiency symptoms that do not benefit from increased selenium are encephalomalacia (Hassan et al., 1985) and the susceptibility of red blood cells to hemolysis (Dobinska et al., 1982). Degeneration of the Perkinji layer of cells in the cerebellum results in nervous symptoms typified as sudden prostration with toes and legs outstretched, toes flexed, and head outstretched. High concentrations of dietary PUFA lead to

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Nutrient Requirements of Poultry: Ninth Revised Edition, 1994 increased contents in cell membranes and, in turn, the additional susceptibility to oxidative stress may enhance the possibilities of encephalomalacia (Budowski and Crawford, 1986). Other stressors such as ozone in the environment (Bartov et al., 1981) or peroxidized fat (Budowski et al., 1979) or medium-chain fatty acids (Ikumo, 1980) contained in the feed also increase the possibility of a vitamin E deficiency. Adult fowl are less susceptible to a vitamin E deficiency than are actively growing chicks, and the symptoms differ. Males become infertile because sperm become incompetent (Friedrichsen et al., 1980). Reduced egg production and hatchability occur when both vitamin E and selenium are deficient over a prolonged period with hens (Latshaw and Osman, 1974). Although supplemental selenium can completely overcome these problems, chicks from these eggs are particularly susceptible to encephalomalacia (Bartov and Bornstein, 1980) and muscular dystrophy (Ewen and Jenkins, 1967). Adding excessive vitamin E to feed can have adverse effects. Nockels et al. (1976) reported that feeding 8,000 IU/kg reduced body weight gain and gave a waxy appearance to the feathers. Should either vitamin D or vitamin K be marginal when high levels of vitamin E are being fed, then rachitic bones and blood clotting failures, respectively, may occur (March et al., 1973; Murphy et al., 1981; Franchini et al., 1988). However, dietary excesses approximating 100 to 500 IU/kg of feed are advantageous to the oxidative stability of broiler (Lin et al., 1989) and turkey (Sheldon, 1984) meat products. Vitamin K Vitamin K is used as a cofactor to synthesize ?-carboxyglutamic residues from glutamic acid in proteins located in the liver and bone. The liver protein is involved in the synthesis of several blood clotting factors, including prothrombin clotting of blood (Suttie, 1987), and the bone protein, osteocalcin, is implicated in calcification of bone matrix (Hauschka et al., 1989). Although inadequate dietary vitamin K alters bone osteocalcin, symptoms associated with the skeletal system are not as apparent as blood clotting problems (Scott, 1966b; Hauschka and Reid, 1978b). Hemorrhaging may occur subcutaneously, intermuscularly, and internally and may lead to anemia and the appearance of hypoplastic bone marrow. A greatly extended blood clotting time may result in death from exsanguination. Vitamin K adequacy is usually measured in terms of prothrombin clotting time with decalcified plasma (Griminger et al., 1970). Dietary vitamin K may be of three sources. Vitamin K1, or phylloquinone, largely occurs in the leafy parts of plants. Vitamin K2, or menaquinone, is of bacterial origin, particularly those bacterial located in the large intestine. Vitamin K3, or menadione, has been synthesized and does not occur in nature as such. Antivitamin K compounds, whether synthetic (Lowenthal and MacFarlane, 1965) or natural (Griminger, 1987), act as anticoagulants. Menadione generally exhibits the greatest vitamin K activity (Dua and Day, 1966), except when anticoagulants are given and the converse occurs (Griminger, 1965). Dietary anticoagulants lead to vitamin K deficiency symptoms commensurate with the extent of toxicity (Veltmann et al., 1981; Bai and Krishnakumari, 1986). Inadequate vitamin K under practical circumstances is most likely to occur during the starting period, and supplementation of the feed at this time is advantageous (Fritz, 1969). Starting feeds seldom contain forage meals, and a poorly developed intestinal microflora together with the use of antimicrobials further reduces access to the vitamin (Bornstein and Samberg, 1954). Nelson and Norris (1961a) showed that the inclusion of 0.1 percent sulfaquinoxaline increased the chick's need for supplemental vitamin K by fourfold to sevenfold. Adults usually have a well-developed intestinal microflora, and vitamin K inadequacies are unusual. Vitamin K2 is not readily absorbed from the large intestine but it is digested after coprophagy of cecal excreta (Berdanier and Griminger, 1968). The caging of hens minimizes coprophagy, and minimal amounts of vitamin K reach the egg (Cravens et al., 1941). Griminger and Brubacher (1966) observed that dietary vitamin K3 is transferred to the yolk as vitamin K2, but vitamin K1 is best transferred and remains as such. Use of vitamin K by embryos parallels that by adults. A deficiency with the embryo alters bone metabolism, but no physical deformities occur (Hauschka and Reid, 1978a). Adverse effects on blood clotting are not apparent until after hatching, when hemorrhaging and mortality occur should trauma be encountered (Griminger, 1964). Thiamin (Vitamin B1) Thiamin is a cofactor for several enzymes catalyzing decarboxylation- and transketolation-type reactions. Although the activity of all these enzymes is depressed in a thiamin deficiency, the accrual of pyruvic acid from decreased brain pyruvic oxidase seems to manifest the most symptoms (Lofland et al., 1963). Ataxia and awkward backward flexions of the head and neck are typical nervous symptoms (Gries and Scott, 1972b). Deficient birds can rapidly detect and discriminate against feeds that do not provide the vitamin (Hughes and Wood-Gush, 1971) and are high in carbohydrate content (Thornton and Shutze, 1960). Most complete feeds satisfy the thiamin requirement because grains and their by-products usually contain adequate

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Nutrient Requirements of Poultry: Ninth Revised Edition, 1994 amounts. Thiamin is unstable to heat at neutral and alkaline pH (Dwivedi and Arnold, 1973), and pelleting (Guo and Summers, 1969) or extrusion (Beetner et al., 1974) under these circumstances facilitates loss. Amaranth is very low in thiamin, and the level is reduced further if it is heated to destroy growth-inhibiting properties (Laovoravit et al., 1986). Inclusion of certain fish meals having enzymes capable of destroying thiamin may also decrease dietary content (Ishihara et al., 1974; Bryan et al., 1975). Use of medicants acting as a thiamin antagonist can also cause a deficiency (Ott et al., 1965; Shindo et al., 1972). The hen transfers thiamin to the egg in proportion to dietary content (Polin et al., 1963). Although the dietary inadequacies possible under practical terms do not affect breeder flock productivity, high mortality of embryos occurs prior to hatching and chicks that hatch express a polyneuritis (Polin et al., 1962; Charles et al., 1972). Riboflavin (Vitamin B2) Riboflavin acts as a cofactor for many enzymes involved in oxidation-reduction. Erythrocyte glutathione reductase (Lee, 1982) and liver xanthine dehydrogenase (Chou, 1971) are two enzymes in fowl shown to need riboflavin, and their activities reflect dietary adequacy. Prior to the development of concentrated riboflavin sources, milk products were incorporated in feed to avoid deficiencies (Culton and Bird, 1940). Riboflavin deficiencies lead to neurological problems, particularly with the sciatic and brachial nerves, where myelin degeneration, Schwann cell proliferation, and axis cylinder fragmentation have been observed (Phillips and Engel, 1938). Symptoms involving the legs of chickens appear as splay and hock resting postures, and curling of the toes occurs to a lesser extent (Wyatt et al., 1973a; Ruiz and Harms, 1988a). Turkey poults (Ruiz and Harms, 1989a) and pheasants (Scott et al., 1959) exhibit similar symptoms as the chick, whereas ducks (Fritz et al., 1939) and geese (Serafin, 1981) are more likely to have a bowing of the legs in conjunction with perosis. Goff et al. (1953) noted that increased hematocrit, increased mean corpuscular volume, decreased mean hemoglobin concentration, and a marked heterophil leucocytosis appeared in the chick prior to neurological manifestations. Adult cockerels can endure a riboflavin-deficient feed for a prolonged period before neurological and blood problems similar to those of the growing chick appear (Arscott, 1972). Deficiency symptoms can be reversed upon riboflavin administration to adults, but correction with growing birds becomes increasingly difficult as expression progresses. Laying hens transfer riboflavin into the yolk and albumen by hormonally induced binding proteins in the liver and oviduct, respectively (Hamazume et al., 1984). Saturation of these carriers is dependent on dietary riboflavin content (White et al., 1986), and an inadequacy is more likely to adversely affect embryonic development than harm the hen (Tarhay et al., 1975). Severe inadequacies cause death of embryos at 60 hours incubation because of circulatory system failures (Romanoff and Bauernfeind, 1942). Moderate inadequacies result in deaths at 14 days incubation, with the appearance of shortened limbs, malformed mandibles, and clubbing of the down. Marginal deficiencies further delay mortality until pipping, and symptoms are largely dwarfism with clubbed down. Niacin Niacin represents nicotinic acid and nicotinamide, both of which have similar activity in fowl (Ruiz and Harms, 1988b). Many enzymes in glycolysis, lipogenesis, and energy metabolism use niacin as a cofactor. Tryptophan may be converted into niacin; however, the efficiency is poor and not recommended as a substitute for diet supplementation (Ruiz and Harms, 1990). Availability of niacin in grain and grain by-products is generally low (Manoukas et al., 1968; Yen et al., 1977); thus their contribution in determining dietary adequacy is usually ignored. Chicks at hatch have considerable tryptophan contained in the protein of the yolk; thus a niacin deficiency will not readily occur unless the feed is low for both the amino acid and the vitamin (Snell and Quarles, 1941). Briggs et al. (1943) reported that 2 weeks were required to provoke a deficiency with chicks and that an inflammation of the oral cavity and occasional poor feathering, dermatitis, and perosis—a malformation of the bones—were the primary symptoms. Turkey poults (Ruiz and Harms, 1988b), pheasants (Scott et al., 1959), ducks (Heuser and Scott, 1953), and goslings (Serafin, 1981) all expressed perosis as the primary deficiency symptom. Biotin Biotin acts as a cofactor for enzymes performing carboxylations. Acetyl coenzyme A carboxylase, which participates in fatty acid synthesis, and pyruvate carboxylase, which enables gluconeogenesis from intermediates in the Kreb's cycle, are both affected by biotin nutriture (Whitehead and Bannister, 1980; Watkins and Rogel, 1989). Biotin tends to concentrate in liver, kidney, and bone, the primary sites of activity of enzymes requiring this vitamin (Frigg and Torhorst, 1982). Analysis of complete feeds indicates that adequate biotin is

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Nutrient Requirements of Poultry: Ninth Revised Edition, 1994 present; however, low availability of biotin from certain grains may result in marginal concentrations in comparison with biotin requirements (Frigg, 1976). Symptoms of a biotin deficiency are skin lesions appearing on the foot pad, shank, and toes, together with eye exfoliation and exudative dermatitis (Marusich et al., 1970). Skin lesions can be related to alterations in the fatty acid composition of associated waxes (Logani et al., 1977). Low dietary fat and the necessity for fatty acid synthesis lead to an abnormal array of fatty acids that predisposes poultry to a fatty liver and kidney syndrome (FLKS) (Whitehead and Randall, 1982). Subjecting these birds to a fast such that gluconeogenesis is accelerated precipitates a high death rate from lack of glucose (Whitehead and Siller, 1983). Tibiotarsal bones are frequently longitudinally distorted. Presumably, reduced biotin prevents ready formation of prostaglandins from essential fatty acids, and bone growth fails to respond to stresses during development (Watkins et al., 1989). Biotin-binding proteins are found in the yolk and albumen of eggs (Bush et al., 1988). The amount of biotin associated with the yolk binding protein changes with biotin content in the feed. Hatchability is affected when the feed is deficient (White et al., 1987). Embryonic mortality because of inadequate biotin occurs largely during the last 3 days of incubation. Dwarfing, chondystrophy, and deformities of the mandibles and skeleton appear at that time (Couch et al., 1947). Chicks hatched from breeder hens given marginal dietary biotin have increased risk of a deficiency (Whitehead et al., 1985). Provoking a deficiency is dependent on many factors, particularly those affecting supplementary biotin synthesis by microbes in the ceca and coprophagy. Caging and use of probiotics and medicants in the feed are influential in this respect (Leeson, 1982). Pantothenic Acid Pantothenic acid serves as a prosthetic group with coenzyme A and thereby is essential in energy metabolism. Inadequate pantothenic acid not only reduces the productive use of available energy (Beagle and Begin, 1976; Cupo and Donaldson, 1986) but also impairs detoxification mechanisms that depend upon acetylation (Kietzmann, 1981). Grains contain low concentrations of pantothenic acid, and complete feeds are usually marginal in satisfying the requirement (Southern and Baker, 1981; Ruiz and Harms, 1989b). Deficiency symptoms are associated with the skin and nervous system of growing chicks (Gries and Scott, 1972b). Skin lesions include crusts and scabs, which first appear at the angles of the eyes and beak. Lesions on the feet are seldom and slight. Biotin deficiency symptoms are similar except lesions on the feet are more severe and appear before those on the head. Although an extensive ataxia also occurs, lesions associated with the nervous system are difficult to detect. Turkey poults present the same symptoms as chicks (Kratzer and Williams, 1948a), but poor feathering is the most prevalent deficiency sign in pheasants and quail (Scott et al., 1964). Adult cockerels receiving inadequate pantothenic acid have reduced semen volume and fertility as well as skin lesions (Goeger and Arscott, 1984). Considerably higher levels of pantothenic acid are needed by chicken and turkey hens to maintain hatchability than for egg production (Kratzer et al., 1955; Balloun and Phillips, 1957a). Embryonic mortality occurs from about 14 days incubation or thereafter, depending on the extent of pantothenic acid inadequacy (Beer et al., 1963). Chicks that hatch are of poor quality and have variable degrees of subcutaneous hemorrhaging and edema (''stunted chick disease"). Pyridoxine (Vitamin B6) Pyridoxine, pyridoxal, and pyridoxamine are the 3 active forms of vitamin B6. Vitamin B6 is a cofactor in decarboxylation and transamination reactions of amino acids. Decarboxylations lead to at least four amines that affect nervous system functioning. Transaminations of certain glycolysis and Kreb's cycle intermediates form most of the nonessential amino acids, whereas the reverse is the basis of gluconeogenesis from protein. Aspartic transaminase in the liver (Lee et al., 1976) and plasma glycine-serine ratio (Sifri et al., 1972) have been employed to evaluate vitamin B6 nutriture. The vitamin B6 content of complete feeds usually satisfies most requirements (Scheiner and DeRitter, 1968). However, the vitamin availability is dependent on the digestibility of each feedstuff (Heard and Annison, 1986). The dietary requirement level may increase as dietary protein increases (Daghir and Shah, 1973), or due to the presence of linatin when linseed meal is used (Kratzer and Williams, 1948b; Klosterman et al., 1967). The inclusion of certain drugs that act as competitive inhibitors may also increase the dietary requirement (Fuller and Dunahoo, 1959). Symptoms exhibited by vitamin-B6-deficient chicks differ with the extent of the inadequacy (Daghir and Balloun, 1963; Gries and Scott, 1972a). A severe deficiency produces an ataxia in combination with nervousness and intermittent episodes of hyperactivity. Prominent pathological findings include hemorrhages at various locations, particularly primary wing feather follicles, and gizzard erosions. Marginal vitamin B6 deficiencies are most likely to be expressed as a perosis because of problems with bone growth. Miller (1963) observed high proportions of pendulous crops with vitamin-B6-deficient chicks.

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Nutrient Requirements of Poultry: Ninth Revised Edition, 1994 Blood alterations are also typical of a vitamin B6 inadequacy. An extreme deficiency leads to a microcytic, polychromatic hypochromic anemia in conjunction with atrophy of the spleen, thymus, and bursa of Fabricius (Asmar et al., 1968). Marginal deficiencies provoke a microcytic, normochromic polycythemia (Blalock and Thaxton, 1984), and deficient chicks show a decreased immunoglobulin M and immunoglobulin G response to antibody challenge (Blalock et al., 1984). Although specific symptoms of vitamin B6 deficiency are not obvious in adult chickens, deficient hens lose body weight and exhibit reduced egg production (Attar et al., 1967). Deficient hens also have relatively low serum glutamic-oxaloacetic acid transaminase activities and high serum nonprotein nitrogen levels (Attar et al., 1967). The vitamin B6 content of eggs reflects that in the feed, and the level necessary to maintain egg production is one-half of that required for hatchability (Fuller et al., 1961). Characteristics of vitamin-B6-deficient embryos have not been reported, but antivitamins injected into eggs cause early deaths (Landauer, 1967). Folic acid Folacin represents folic acid (pteroyl-?-monoglutamic acid) and the array of extended glutamic acid conjugates. Enzymes engaged in one-carbon metabolism use folic acid as a cofactor in methyl and methylene group synthesis. Dietary folacin is absorbed and converted to the reduced form (5-methyl-tetrahydrofolic acid) by the intestine and is distributed throughout the body. Although most complete feeds provide sufficient folic acid from their natural ingredients, marginal inadequacies are possible (Cropper and Scott, 1967). The requirement decreases with age because diminished growth rate reduces the need for deoxyribonucleic acid synthesis (Naber et al., 1957; Balek and Morse, 1976). Accentuated formation of uric acid with excessive dietary protein increases the folic acid requirement (Creek and Vasaitis, 1963), as does inadequate choline (Young et al., 1955) and serine (Rabbani et al., 1973). Use of medicants that antagonize folic acid formation by cecal microflora and management that prevents coprophagy also increases the dietary requirement (Stokstad and Jukes, 1987). The most obvious symptom of inadequate folic acid is perosis with the chick (Daniel et al., 1946) and cervical paralysis with turkey poults (Miller and Balloun, 1967). Macrocytic anemia, abnormal nuclear bodies in erythrocytes, and numerous mitoses and hypersegmented granulocytes occur with marginal deficiencies when no physical symptoms are manifested (Maxwell et al., 1988). Inadequate folic acid with the hen impairs the oviduct's response to estrogen and ability to form albumen (Anderson and Jackson, 1975; Burns and Jackson, 1979). More folic acid is needed to sustain hatchability than egg production; thus the embryo will suffer before the hen (Sunde et al., 1950a). High embryonic mortality occurs around 20 days of incubation, and the dead from severely depleted hens exhibit a marked bending of the tibiotarsus, and, to a lesser extent, syndactyly and deformed mandibles. Chicks that successfully emerge are stunted and have feathers that are poorly developed and abnormally pigmented (Lillie et al., 1950). Vitamin B12 (Cobalamin) Vitamin B12 is a cofactor for enzymes transferring one-carbon units and catalyzing rearrangements in the carbon skeleton of several metabolic intermediates. In fowl, vitamin-B12-mediated one-carbon transfers involve methionine, serine, choline, and thymidine (Gillis and Norris, 1949; Henderson and Henderson, 1966; Langer and Kratzer, 1967), whereas the interconversion of methylmalonyl coenzyme A to succinyl coenzyme A is one of the rearrangement reactions requiring vitamin B12 (Ward et al., 1988). The spleen, bone marrow, liver, kidney, and skin have high concentrations of vitamin B12 (Monroe et al., 1952). Although plant feedstuffs are devoid of vitamin B12, its availability from animal products and cecal microflora after coprophagy makes deficiencies unlikely (Milligan et al., 1952). Deficiencies in chicks have been created by greatly increasing dietary protein content such that carbon rearrangement enzyme activities are accentuated (Rys and Koreleski, 1974; Patel and McGinnis, 1980; Ward et al., 1985). Poor feathering and mortality are the most obvious symptoms of a vitamin B12 deficiency, and gizzard erosions may also appear (Mushett and Ott, 1949; Milligan et al., 1952). Yacowitz et al. (1952) fed a high-protein all-vegetable diet devoid of vitamin B12 to hens in cages and reported a reduction in hatchability. Olcese et al. (1950) observed that most embryonic mortality due to vitamin B12 deficiency in hens occurs at about 17 days of incubation, with atrophy of the leg musculature and hemorrhaging common. Ferguson et al. (1955) further observed fatty organs, dwarfing, and edema. Choline Choline may be synthesized in fowl; however, the extent is limited, and supplementation is necessary when demand exceeds biosynthesis capacity. Choline serves a diversity of needs, particularly as a component of phospholipids for the formation of membranes and lipoproteins. Choline also acts as a methyl donor, and its use in this respect becomes important when de novo synthesis of one-carbon units cannot meet demand.

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Nutrient Requirements of Poultry: Ninth Revised Edition, 1994 Need for supplemental choline is the greatest with the starting bird because all facets of use are likely to be maximal (Seifter et al., 1972; Pesti et al., 1980). As growth diminishes, the necessity for choline supplementation disappears (Molitoris and Baker, 1976). Perosis is the primary symptom of a choline deficiency in chicks (Fritz et al., 1967) and turkey poults (Evans et al., 1943), whereas Bobwhite quail develop enlarged hocks and bowed legs (Serafin, 1974). Estrogenic hormones greatly accentuate the choline need for phospholipid synthesis in the hen's liver to support yolk formation (Vigo and Vance, 1981). Supplemental choline may relieve the hepatic accumulation of fat and improve egg yolk formation (Schexnailder and Griffith, 1973; Tsigabe et al., 1988). Minimal dietary choline does not affect hatchability with either chickens (Gish et al., 1949) or turkeys (Ferguson et al., 1975), but Japanese quail and their developing embryos readily express general signs of deficiency (Latshaw and Jensen, 1971, 1972). MINERAL DEFICIENCIES Calcium and Phosphorus Bone formation is highly dependent on the dietary concentrations of calcium and phosphorus as well as on adequate intake of vitamin D3 (Hart et al., 1922; Dunn, 1924; McGowan and Emslie, 1934). Deficiency of any one of these nutrients will result in rickets. Poor growth may also be a sign of calcium or phosphorus deficiency. Dietary excesses of either calcium or phosphorus should be avoided because such excesses can hinder the intestinal absorption of other mineral elements (Gutowska and Parkhurst, 1942; Schaible and Bandemer, 1942; Migicovsky and Emslie, 1947). The phosphorus that comes from plant products (that is, phytin) should not be depended on to fulfill the phosphorus requirement for two reasons: it is not readily available in its natural form to the bird, and it may bind calcium, zinc, iron, and manganese so as to render them unavailable (Nelson and Walker, 1964; Kratzer and Vohra, 1986). Pullets at the beginning of the laying period undergo considerable metabolic stress associated with adjustment to the need to supply approximately 2.4 g of calcium daily to the oviduct for shell formation (Mueller et al., 1964; Hurwitz and Bar, 1971; Scott et al., 1971). Some birds mobilize large amounts of calcium from their skeleton during this period, and the bones may become so demineralized that the birds are unable to stand and appear paralyzed. The sternum and rib bones are frequently deformed, and all bones are easily broken. Dietary management to prevent this condition (generally termed "cage-layer fatigue" but more precisely described as osteoporosis) has not been devised (Roland et al., 1968). Magnesium When fed a diet very deficient in magnesium, chicks grow slowly for about 1 week and then stop growing and become lethargic. Chicks fed diets marginal in magnesium may grow quite well but exhibit reduced levels of plasma magnesium and symptoms of neuromuscular hyperirritability when disturbed (Almquist, 1942; Bird, 1949). Chicks show a brief convulsion and then enter a comatose state from which they usually recover, but sometimes death occurs. A magnesium deficiency in laying hens results in a rapid decline in blood magnesium level, withdrawal of magnesium from bone, decline in egg production, and, eventually, a comatose state and death (Cox and Sell, 1967). Magnesium content and hatchability of eggs also are reduced when hens are fed magnesium-deficient diets (Sell et al., 1967; Hajj and Sell, 1969). Increasing either the calcium or the phosphorus content of the diet accentuates magnesium deficiency (Nugara and Edwards, 1963). Normally, adequate magnesium is present in the natural ingredients of practical diets to meet the requirements of poultry. Manganese Manganese deficiency in chicks and poults results in perosis or slipped tendon (Wilgus et al., 1937; Ringrose et al., 1939). Deficiencies of other nutrients, such as choline and biotin, may also be involved in inducing perosis (Jukes, 1940; Jukes and Bird, 1942). The usual signs of perosis are swelling and flattening of the hock joint, with subsequent slipping of the Achilles tendon from its condyles. The tibia and the tarsometatarsus may exhibit bending near the hock joint and lateral rotation. One or both legs may be affected. A shortening and thickening of the long bones of the wings and legs are also observed. The disorder, insofar as manganese is concerned, is aggravated by excess dietary calcium and phosphorus (Schaible and Bandemer, 1942). In laying and breeding birds, manganese deficiency results in lowered egg production, reduced eggshell strength, poor hatchability, and reduced fertility. Manganese-deficient embryos exhibit shortening of the long bones, parrot beak, and wiry down (Lyons and Insko, 1937; Caskey et al., 1939). Potassium, Sodium, and Chlorine A deficiency of potassium results in high mortality and retarded growth of chicks and causes reduced egg

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Nutrient Requirements of Poultry: Ninth Revised Edition, 1994 production and eggshell thickness in laying hens (Ben-Dor, 1941; Gillis, 1948; Leach, 1974). It is not usually necessary to add potassium to practical feed formulations, since such formulas generally contain about 0.7 to 1.0 percent potassium. A deficiency of sodium in chicken diets results in poor growth, increased adrenal weight, and decreased egg production (Burns et al., 1952, 1953; Nott and Combs, 1969). Frequently, sodium supplementation is minimized to reduce the moisture level in the excreta. Signs of chlorine deficiency in chicks include poor growth, mortality, hemoconcentration, and reduced blood chlorine level (Leach and Nesheim, 1963). Chlorine-deficient chicks show a nervous condition resembling tetany and fall forward with legs extended backward when stimulated by a sharp noise. Iodine Iodine is necessary for the synthesis of thyroid hormones. Iodine deficiency results in goiter, which is the enlargement of the thyroid glands (Wilgus et al., 1953; Rogler et al., 1959a). The glands may increase to many times their usual size. If the deficiency is not too severe, the increased efficiency of the enlarged gland in "trapping" iodine from the bloodstream may compensate for the low dietary concentration. When this is the case, the production of thyroid hormones is normal, although the thyroid glands are enlarged. Inadequate production of thyroid hormones results in poor growth, egg production, and egg size. Iodine deficiency in breeders results in low iodine content of the egg and, consequently, decreased hatchability and thyroid enlargement in the embryos. Copper Copper deficiency in poultry causes an anemia in which the red blood cells are small and low in hemoglobin (Elvehjem and Hart, 1929). Bone deformities can occur (O'Dell et al., 1961). Pigmentation of feathers in New Hampshire and Rhode Island Red chickens is reduced (Hill and Matrone, 1961). Copper is required for the activity of the enzyme needed for the cross-linking of lysine in the protein elastin (O'Dell et al., 1961; Starcher et al., 1964). Dissecting aneurism of the aorta occurs in birds deficient in copper because of the defect in elastin formation. Copper deficiency also results in marked cardiac hypertrophy (Carlton and Henderson, 1963). Iron Iron deficiency in chickens and turkeys causes an anemia in which the red blood cells are reduced in size and low in hemoglobin (Elvehjem and Hart, 1929). In red-feathered chickens, pigmentation does not occur when the diet is deficient in iron (Hill and Matrone, 1961; Davis et al., 1962). Selenium Selenium is closely associated with vitamin E and other antioxidants in practical feed formulation. The principal sign of deficiency in chicks is exudative diathesis (Creech et al., 1957; Patterson et al., 1957; Nesheim and Scott, 1958). A requirement for selenium supplementation, even in the presence of vitamin E, is demonstrated by the poor growth, muscular dystrophy, and mortality of chicks fed purified diets or diets based on grains produced on low-selenium soils (Nesheim and Scott, 1958). Selenium is required for prevention of myopathies of the gizzard and heart in turkeys (Walter and Jensen, 1963; Scott et al., 1967). Pancreatic fibrosis, with resultant reductions in the pancreatic output of lipase, trypsinogen, and chymotrypsinogen, has also been associated with selenium deficiency (Thompson and Scott, 1970; Gries and Scott, 1972c). Selenium is a structural component of glutathione peroxidase, an enzyme needed to quench peroxides generated during metabolism (Rotruck et al., 1973). There is wide variability in the amount and availability of selenium in the soils of different geographic areas (Scott and Thompson, 1971; Scott, 1973). Consequently, cereals and plant-derived feedstuffs are variable sources of selenium. Grains from some areas contain sufficient selenium to render them toxic to chicks. The effects of toxic levels of selenium are listed in Table 8-1. The amount of supplementary selenium permissible in diets is regulated in the United States and Canada. Zinc Zinc has many biochemical functions. Deficiency causes retarded growth and frayed feathers (O'Dell et al., 1958; Sullivan, 1961). The extent of fraying varies from almost no feathers on the wings and tail to only slight defects in the development of some of the barbules and barbicels. The long bones of the legs and wings are shorter and thicker than normal (Kratzer et al., 1958; Morrison and Sarett, 1958; O'Dell et al., 1958). The hock joint may be enlarged. Layer and breeder diets deficient in zinc reduce egg production and hatchability (Kienholz et al., 1961).