POULTRY NUTRITION

Nutritional Requirements: Water Energy, Protein, and Amino Acids Vitamins Minerals Unidentified Nutrients

Poultry continue to rank high in their ability to convert feed into food products. Such high efficiency has increased progressively in recent decades. The nutrient requirement figures published in Nutrient Requirements of Poultry (National Academy of Sciences, 1994) are the most recent available and should be viewed as minimal nutrient needs for poultry. They are derived from experimentally determined levels after an extensive review of the published data. Criteria used to determine the adequacy of a given nutrient include growth, feed efficiency, health, productivity, and quality of poultry product. These requirements do not, however, include a margin of safety. Consequently, under practical conditions in which there may be different strains, energy content of the diets, environmental temperatures, type of floor, availability of nutrients from various feedstuffs, destruction or loss of nutrients in the gut, pro-oxidants, intestinal parasites, mycotoxins, diseases, and many other stresses, nutritionists should make the proper adjustment by adding a margin of safety to the nutrient requirements.
Water:

Many factors influence water intake, including environmental temperature, relative humidity, composition of the diet, birds productivity (rate of growth or egg production), and the individual birds ability to resorb water in the kidney. As a result, precise water requirements cannot be determined. However, water is of vital importance and is considered an essential nutrient. Water deprivation for 12 hr has an adverse effect on growth of young poultry and egg production of layers; water deprivation for 36 hr results in a marked increase in mortality of both young and mature poultry. Cool, clean water must be available at all times.
Energy, Protein, and Amino Acids:

The apparent metabolizable energy (AMEn) and the true metabolizable energy (TMEn) values are used for numerous feedstuffs in poultry rations. AMEn is the gross energy of the feed minus the gross energy of the excreta after a correction for the nitrogen retained in the body. Similarly, TMEn is the gross energy of the feed consumed minus the gross energy of the excreta of food origin after a correction for the nitrogen retained in the body. AMEn and TMEn are similar for many ingredients. However, the 2 values could differ substantially for some ingredients such as feather meal, rice bran, wheat middlings, and corn distillers grains with solubles. AMEn is the energy value used by most poultry nutritionists in feed formulation. Because chickens and other fowl can adjust their feed intake over a considerable range of feed energy levels to meet their daily energy needs, dietary energy levels are used to set the levels of other nutrients, including

protein and amino acids. As a result, the concept of the calorie to protein and amino acids ratio has been used extensively in poultry feed formulation. However, recent research indicated that changes in feed intake of both broilers and layers were not inversely proportional to changes in dietary energy levels. This is particularly true when birds were fed high-energy diets (layers) or moderate- to high-energy diets (broilers). Consequently, the use of these specific ratios must be carefully evaluated. Because factors other than dietary energy could also affect feed intake, including ambient temperature (which can have a considerable impact on feed consumption), nutrient density in the ration should be adjusted to provide appropriate nutrient intake based on requirements and the actual feed intake. Poultry can synthesize glycine but often not in sufficient amounts. Cystine and tyrosine are considered essential even though they can be synthesized from methionine and phenylalanine, respectively. In practical feed formulation, methionine can spare choline as a methyl donor, and tryptophan can be used to synthesize niacin. These relationships are important because the 2 vitamins can be supplied in diets more economically than the 2 amino acids. Body weight and composition are important factors in rearing pullets of any strain for maximum egg production. Most strains of White Leghorn chickens have relatively low body weights and do not tend, under normal feeding, to become obese. Feed should be unrestricted to enable these birds to reach adequate body weights at onset of lay. There may be times when, for various reasons, pullets are to be delayed in coming into production. Under such circumstances, feed restriction is necessary to restrict body weight gain of the pullets. For brown-egg strains of chickens, some degree of restriction is often practiced (~90% of ad lib feeding). Some type of feed restriction program is particularly important for broiler-strain pullets, which tend to become obese if fed ad lib. Feed inake of the broiler breeder is also restricted during the laying period. Pullets now come into production and reach peak production weeks earlier than they did several years ago. This is true both for commercial layers and broiler breeders. Thus, it is of utmost importance that the starting, growing, and developer feeds are fully adequate for development of strong pullets of normal body weight at onset of lay.
Vitamins:

One IU of vitamin A activity is equivalent to 1.3 g of pure retinol (or 0.344 g of retinyl acetate). In chickens, 0.6 g of -carotene is considered equivalent to 1 IU of vitamin A. However, young chicks are not efficient in using -carotene. The vitamin A requirements currently recommended are based on use of stabilized vitamin A preparations and thus are somewhat lower than previously recommended levels. Requirements for vitamin D are expressed in IU. Birds use vitamin D3 from fish oils and irradiated animal sterols quite effectively but cannot use vitamin D2 . Metabolic forms of vitamin D have been isolated and synthesized; these are 25-hydroxy vitamin D3, which is synthesized in the liver, and 1,25-

dihydroxy vitamin D3, which is synthesized in the kidneys. One IU of vitamin D represents the vitamin D activity of 0.025 g of pure vitamin D3 One IU of vitamin E is equivalent to 1 mg of synthetic dl--tocopherol acetate. Vitamin E requirements vary with the type and level of fat in the diet, the levels of selenium and trace minerals, and the presence or absence of other antioxidants. Choline is required as an integral part of the body phospholipid, as a part of acetylcholine, and as a source of methyl groups. Growing chickens can use betaine as a methylating agent, but betaine cannot replace choline in preventing perosis. Betaine is widely distributed in practical feedstuffs and may be important in sparing choline. Adequate dietary vitamin B12 helps pullets develop the ability to biosynthesize choline. The choline requirement values apply to diets containing the specified levels of vitamin B12.
Minerals:

The calcium requirement of laying hens is difficult to define. Too much dietary calcium interferes with the use of several other minerals, as well as fat, and tends to reduce palatability. For laying, the recommended level of 3.6-5.0% is adequate in most cases, depending on strain, level of egg production, body weight, and egg mass. Older hens, and especially those subjected to high environmental temperature, may require levels up to and perhaps >3.75%.
Unidentified Nutrients:

The chick has requirements for 40 nutrients, together with an adequate level of metabolizable energy. Some unidentified growth and hatchability factors may improve performance under certain stress conditions. However, with the identification of vitamins and the significant role of many trace elements, many poultry nutritionists disregard the importance of such factors

Antibiotics:

Antibiotics at low levels (5-25 mg/kg of feed, depending on the antibiotic) are used in poultry feeds to improve growth rate and feed efficiency. However, in some countries, regulations restrict this usage for certain antibiotics.

Feeding and Management Practices:

Success of the feeding program should be measured by how it achieves the breeders goals for proper weight and development specific to each strain. Most diets used in feeding poultry are nutritionally complete diets that are commercially mixed, ie, prepared by feed manufacturing companies, most of which employ trained nutritionists. The formulation and mixing of poultry feeds requires knowledge and experience in purchasing ingredients, experimental testing of formulas, laboratory control of ingredient quality, and computer applications. Improper mixing can result in vitamin and mineral deficiencies, lack of protection against disease, or drug toxicity. The physical form of the feed influences the expected results. Most feeds for starting and growing birds are produced as pellets or crumbles. In the pelleting process, the mash is treated with steam and then passed through a suitably sized die under pressure. The pellets are then cooled quickly and dried by means of a forced air draft. The conditions under which pelleting occurs (eg, use of an expander rather than an extruder, exposure to high

temperature, use of soft pellets) have an important effect on the nutritional quality of the pellets, or of the crumbles that are produced by crushing the pellets.

Feeding Methods:

For newly hatched birds of any species, a complete feed in crumble form is the program of choice, regardless of other considerations. A complete feed program for growing stock, particularly for laying and breeding stock, is also highly recommended. Advantages of the complete feed program over the mash and grain system include the simplicity of feeding, accuracy of medication, improved balance of dietary nutrients, and superior feed conversion efficiency. Regardless of the system of feeding, recommendations of the feed manufacturer or the strains breeder company should be followed with regard to the feeding of extra calcium, grit, or whole grain. Fresh, clean water should be readily available.

Vaccination Programs:
Vaccination Program for Broilers*

Age

Vaccine

Route

Type

1 day

Mareks disease

SC

Turkey herpesvirus and SB1

1 day or 14-21 days 1 day or 14-21 days 14-21 days

*

Newcastle disease Newcastle disease

Coarse spray Water or coarse spray

B1 B1 or LaSota

Infectious bronchitis Infectious bronchitis

Coarse spray Water or coarse spray

Massachusetts Massachusetts

Infectious bursal disease

Water

Intermediate

This is an example of a typical vaccination program. Individual programs are highly variable and reflect local conditions, disease prevalence, severity of challenge, and individual preferences.
Vaccination Program for Broiler Breeders*

Age

Vaccine

Route

Type

1 day 6 -7 days 14-21 days

Mareks disease Tenosynovitis Newcastle/infectious bronchitis

SC SC Water

Turkey herpesvirus Live (Mild) B1/Mass

14-28 days 4 wk

Infectious bursal disease Newcastle/infectious bronchitis

Water Water or coarse spray SC Water or coarse spray

Intermediate B1/Mass

6-8 wk 8-10 wk

Tenosynovitis Infectious bursal disease

Live (Mild) Live

8-10 wk

Newcastle/infectious bronchitis

Water or coarse spray Wing web

B1 or LaSota/Mass

10-12 wk

Encephalomyelitis

Live, chick-embryo origin

10-12 wk 10-12 wk 10-12 wk 10-12 wk 10-12 wk or 12-14 wk

Fowlpox Chicken infectious anemia Laryngotracheitis Tenosynovitis Fowl cholera Fowl cholera Newcastle/infectious bronchitis

Wing web Wing web Intraocular Parenteral Parenteral Wing web Water or aerosol

Modified live Modified live Modified live Inactivated Inactivated Live CU, PM-1, or M9 B1 or LaSota/Mass

14-18 wk or 16-18 wk 16-18 wk 16-18 wk and every 60-90 days or 18 wk

*

Fowl cholera Fowl cholera Infectious bursal disease Tenosynovitis Newcastle/infectious bronchitis Newcastle/infectious bronchitis

Parenteral Wing web Parenteral Parenteral Water or aerosol

Inactivated Live CU, PM-1, or M9 Inactivated Inactivated B1 or LaSota/Mass

Parenteral

Inactivated

This is an example of a vaccination program. Individual programs are highly variable and reflect local conditions, disease prevalence, severity of challenge, and individual preferences. SB-1 or MDV301 may be combined with turkey herpesvirus in some areas. Vaccination for fowlpox and laryngotracheitis depends on local requirements. Other strains of infectious bronchitis (Connecticut, Arkansas 99, Florida 88, etc) are included in some areas.

Vaccination Program for Commercial Layers*

Age

Vaccine

Route

Type

1 day

Mareks disease

SC

Turkey herpesvirus and SB-1

14 -21 days

Newcastle/infectious bronchitis

Water

B1/Mass

14-21 days 5 wk

Infectious bursal disease Newcastle/infectious bronchitis

Water Water or coarse spray Water or coarse spray Wing web

Intermediate B1/Mass

8-10 wk

Newcastle/infectious bronchitis

B1 or LaSota/Mass

10-12 wk

Encephalomyelitis

Live, chick-embryo origin

10-12 wk 10-12 wk 10-14 wk

Fowlpox Laryngotracheitis Mycoplasma gallisepticum

Wing web Intraocular Intraocular or spray Parenteral Water or aerosol

Modified live Modified live Mild live strain

or 18 wk 12-14 wk

M gallisepticum Newcastle/infectious bronchitis

Inactivated B1 or LaSota/Mass

16-18 wk and every 60-90 days or 18 wk

*

Newcastle/infectious bronchitis Newcastle/infectious bronchitis

Water or aerosol

B1 or LaSota/Mass

Parenteral

Inactivated

This is an example of a vaccination program. Individual programs are highly variable and reflect local conditions, disease prevalence, severity of challenge, and individual preferences. The use of M gallisepticum vaccine is regulated or prohibited in some states. SB-1 or MDV301 may be combined with turkey herpesvirus in some areas. Vaccination for infectious bursal disease, laryngotracheitis, and fowlpox depends on local requirements. Other strains of infectious bronchitis (Connecticut, Arkansas 99, Florida 88, etc) are included in some areas. M gallisepticum and Haemophilus gallinarum (coryza) are used only on infected, multiage premises in some areas.

Management of Growing Chickens:

Heated brooders for chicks are surrounded by a chick guard to keep the birds near the heat source. At placement the brooder floor temperature should be between 85-90F (29.4-32.2C). As the birds become older, the brooder

temperature is lowered 5F (2.8C) each week until the temperature is 70F (21.1C). The chick guard is typically removed at 1 wk of age, and the birds then have the run of the whole pen. Ample space should be provided for feeders and waterers, which should be well distributed in the pen. At least 3 in. (7.5 cm) of suitable litter, clean for each brood and spread to an even depth, should be provided at the start. Litter must be free of mold; it should absorb moisture without caking, be nontoxic, and of large enough particle size to discourage consumption. Chicks are started with 24 hr of light for several days; thereafter, light is reduced. Both length of day and intensity of light are important. Lighting programs vary widely, depending on whether housing is windowless or open-sided, and should comply with recommendations of major breeders in similar situations. Feeding systems are often combined with day-length control during rearing to influence the rate at which birds mature. Under certain conditions, pullets may be debeaked at 4-7 days of age. In controlled environment housing, day lengths are controlled more precisely; with dim lights, debeaking may be delayed until later in the growing period. Pullets should be treated for external and internal parasites as required. Vaccination should be used to control problem diseases of the area Many pullets are reared in cages. The cage manufacturer usually supplies specific instructions regarding heating, bird density, and feeding space. Most commercial rations are fortified with sufficient nutrients to meet the requirements of cage-reared birds.

Management of Laying Chickens: Artificial Lights Record Keeping Floor Space, Feeding, and Watering Requirements Layers per Cage
Most laying pullets are housed in cages and should be moved to these facilities at least 1 wk before egg production begins. Breeders moved from a growing house to an adult house should also be given at least 1 wk to adjust to their new environment before the stress of egg production begins. Beaks should be retrimmed as necessary, and cull birds removed at the time of rehousing. Feeders and waterers should be of the proper type, size, and height for the stock and management system. Feeders that are too shallow, too narrow, or lacking a lip or flange on the upper edge may permit excess feed waste. Uneven distribution of waterers or lack of water space results in reduced intake and thus reduced performance.
Artificial Lights:

Day length should be increased gradually as the pullets come into egg production and should reach a 14- to 16-hr light period/day at peak production for both market-egg and hatching-egg layers. An intensity of at least one foot-candle of light (10 lux) at the feed trough should be provided; this is about equal to one 60-watt light bulb to each 100 sq ft (~9 sq m), hanging 7 ft (2.1 m) above the birds. Production may decrease if day length

or light intensity is reduced during the laying period. With cage systems of all types, illumination is more even if smaller wattage bulbs placed closer together are used, rather than large bulbs suspended over the center of each aisle. With tiered cages, the bulbs are suspended 6-7 in. (15-18 cm) above the level of the top cage.

Record Keeping:

Successful intensive poultry keeping requires good records of all flock activities, including hatch date, regular body weights (to ensure that the pullets will have reached optimal body weight when they are brought into egg production), lighting program, house temperatures, disease history, medication and vaccination dates, quantity and type of feed given (important in calculating efficiency of feed utilization), and mortality.
Floor Space, Feeding, and Watering Requirements:

Egg-production birds usually spend their entire lives in cages. While some broiler breeders are similarly housed, most are reared on litter floors or in pens in which up to two-thirds of the floor is slatted. For egg-strain pullets that are reared in cages, there is little chance of altering the feeding and watering space available, but periodic checks are necessary to ensure that feed and water are being continuously supplied. With the success of nippleand cup-waterers and the various types of automatic feeding systems, it becomes more difficult to give specific recommendations for feeding and watering space. Decisions must be made about optimal floor space and feeding and watering requirements based on advice from equipment manufacturers, primary breeders, careful observation, and past experience as to productivity.
Layers per Cage:

Within the guidelines indicated in Table most colony cages house 5-10 layers. The ideal flock size depends on several factors, including labor and cost, and is best determined only by the individual poultry manager or producer
Space Requirements for Meat-strain Birds

Age

Floor Space

Feeder Space*

Cups or Founts* (per 1,000 birds)

From day 1 From wk 1 From wk 8 Mated adults

Heated area 5 sq ft brooder/100 chicks 1 sq ft/bird

10 trays/1,000 (feed little and often) 2 in./bird

20

2 sq ft/bird

4 in./bird

30

All litter: 3 sq ft/bird 1/2 to 2/3 4 in./bird slats: 21/4 sq ft/bird

30 (60 in hot weather)

A nutritional deficiency can arise simply due to a nutrient being omitted from the diet, or due to interaction between nutrients or between nutrients and antinutritional factors. The latter situations are difficult to diagnose because, on analysis, the diet is found to contain a normal level of the suspect nutrient. Micronutrients are often packaged into premixes, so it is rare to see classic individual deficiency signsrather the effect is a compilation of many individual metabolic conditions. In many instances, a correct diagnosis can be made only by obtaining complete information about diet and management, clinical signs in the affected living birds, and results of necropsies and tissue analyses. The composition of individual ingredients in a diet is variable; some nutrients are comparatively unstable, while others are unavailable in their natural form. A diet that, by analysis, appears to contain just enough of one or more nutrients may actually be deficient to some degree. Stress due to bacterial, parasitic, or viral infections; high or low temperatures; low humidity; or drugs may either interfere with absorption of a nutrient or increase the quantity required. Thus, a toxin, microorganism, or other stressor may destroy or render unavailable a particular nutrient that is present in the diet at normally adequate levels.
Only deficiencies occurring in practical diets in the field are discussed below.

Nutritional Deficiencies:

Protein and Amino Acid Deficiencies:

The optimal level of balanced protein intake changes according to age; for growing chicks it is ~18-23% of the diet; for growing poults and gallinaceous upland game birds, ~26-30%; and for growing ducklings and goslings, ~2022%. If the protein and component amino acid content of the diet is below these levels, birds tend to grow more slowly. Even when a diet contains the recommended quantities of protein, satisfactory growth also requires sufficient quantities and proper balance of all the essential amino acids. Few specific signs are associated with a deficiency of the various amino acids, except for a peculiar cup-shaped appearance of the feathers in chickens with arginine deficiency and loss of pigment in some of the wing feathers in bronze turkeys with lysine deficiency. All deficiencies of essential amino acids result in retarded growth or reduced egg size or egg production. Some deficiencies or even imbalances of amino acids may be related to management problems such as hysteria, pickouts and blowouts, and fatty liver syndrome.

Calcium and Phosphorus Imbalances:

Mineral Deficiencies

A deficiency of either calcium or phosphorus in the diet of young growing birds results in abnormal bone development even when the diet contains adequate vitamin D3. This condition, rickets, can also be caused by a dietary deficiency of vitamin D3 ( Vitamin D3 Deficiency), which is necessary for absorption of calcium. A deficiency of either calcium or phosphorus results in

lack of normal skeletal calcification. Rickets is seen mainly in growing birds. Calcium deficiency in adult laying hens usually results in reduced shell quality and osteoporosis. This depletion of bone structure causes a disorder commonly referred to as cage layer fatigue. When calcium is mobilized from bone to overcome a dietary deficiency, the cortical bone erodes and is unable to support the weight of the hen. Rickets: Rickets most commonly occurs in young meat birds. The primary pathologic change is inadequate bone mineralization. Calcium deficiency at the cellular level is the main problem, which may result from feeding a diet deficient or imbalanced in calcium, phosphorus, or vitamin D3. Young broilers and poults exhibit lameness, usually around 10-14 days of age. Their bones are rubbery, and the rib cage is flattened and beaded at the attachment of the vertebrae. Rachitic birds exhibit a very disorganized cartilage matrix, with an irregular penetration of vascular canals. Rickets is not caused by a failure in the initiation of bone mineralization, but rather by the early maturation of this process. There is often an enlargement of the ends of the long bones, with a widening of the epiphyseal plate. A determination of whether rickets is due to deficiencies of calcium, phosphorus, or vitamin D3, or to an excess of calcium (which induces a phosphorus deficiency) may require analysis of blood phosphorus levels and parathyroid activity In most field cases of rickets, a deficiency of vitamin D3 is suspected, due to simple dietary deficiency, inadequate potency of the D3 supplement, or other factors that reduce the absorption of vitamin D3. Rickets can best be prevented by providing adequate levels and potency of vitamin D3 supplements, and by ensuring that the diet is formulated to provide optimal utilization of fat-soluble compounds. Diets must also provide a correct calcium:phosphorus ratio. For this reason, ingredients that are notoriously variable in their content of these minerals should be used with caution. Tibial Dyschondroplasia (Osteochondrosis): Tibial dyschondroplasia is characterized by an abnormal cartilage mass in the proximal head of the tibiotarsus. It is seen in all fast-growing meat birds but is most common in broiler chickens. Signs can occur early, but more usually are seen at 21-35 days of age. Birds are reluctant to move, and when forced to walk, do so with a swaying motion or stiff gait. Tibial dyschondroplasia results from disruption of the normal metaphyseal blood supply in the proximal tibiotarsal growth plate, where the disruption in nutrient supply means that the normal process of ossification does not occur. The abnormal cartilage is composed of severely degenerated cells, with cytoplasm and nuclei appearing shrunken. The exact cause of tibial dyschondroplasia is unknown, although a genetic component is likely in some cases. Dietary electrolyte imbalances, and particularly high levels of chloride, seem to be a major contributor in many field outbreaks. More tibial dyschondroplasia is also seen when the level of dietary calcium is low relative to that of available phosphorus. Treatment involves dietary adjustment of the calcium:phosphorus ratio, consideration of dietary electrolyte balance, and higher levels of (or more potent) vitamin D3 supplementation. Diet changes rarely result in complete recovery. Tibial

dyschondroplasia can be prevented by reducing growth rate; however, programs of feed restriction must be considered in relation to economic consequences. Cage Layer Fatigue: High-producing laying hens maintained in cages sometimes show paralysis around the time of peak egg production due to a fracture of the vertebrae that subsequently affects the spinal cord. The fracture is caused by an impaired calcium flux related to the high output of calcium in the eggshell. Because medullary bone reserves become depleted, the bird uses cortical bone as a source of calcium for the eggshell. The condition is rarely seen in floor-housed birds, suggesting that reduced activity or exercise is a predisposing factor. Affected birds are invariably found on their sides in the back of the cage. At the time of initial paralysis, birds appear healthy and often have a shelled egg in the oviduct and an active ovary. Death occurs from starvation or dehydration because the birds cannot reach feed or water. Affected birds will recover if moved to the floor. A high incidence of cage layer fatigue can be prevented by ensuring the normal weight-for-age of pullets at sexual maturity and by giving pullets a high-calcium diet (minimum 3.5% calcium) for at least 14 days prior to first oviposition. Diets must provide adequate quantities of calcium and phosphorus to prevent deficiencies. However, feeding diets that contain >2.5% calcium during the growing period produces a high incidence of nephrosis, visceral gout, calcium urate deposits in the ureters, and sometimes high mortality. Feeding high levels of calcium to pullets 2 wk before the onset of egg production is not harmful and may improve productivity. Eggshell strength can be improved by feeding ~50% of the dietary calcium supplement in the form of oyster-shell flakes or coarse limestone, with the remaining half as ground limestone. Oyster shell or any other form of calcium supplement should never be added without an equivalent reduction in the amount of limestone; feeding too much calcium reduces feed consumption and egg production. Offering the coarse supplement permits the birds to satisfy their requirements when they need it most, or allows the coarse material to be retained in the gizzard where the calcium can be absorbed continuously. A readily assimilable calcium and/or calcium phosphate supplement is effective if started very soon after paralysis due to calcium deficiency develops.

Manganese Deficiency:
A deficiency of manganese in the diet of young growing chickens is one of the causes of perosis and of thin-shelled eggs and poor hatchability (see also CALCIUM AND PHOSPHORUS IMBALANCES, Calcium and Phosphorus Imbalances, and VITAMIN D DEFICIENCY, Vitamin D3 Deficiency). It may also cause chondrodystrophy. Perosis, which occurs in young chicks, is characterized by enlargement and malformation of the tibiometatarsal joint, twisting and bending of the distal end of the tibia and the proximal end of the tarsometatarsus, thickening and shortening of the leg bones, and slippage of the gastrocnemius or Achilles tendon from its condyles. Higher intakes of calcium or phosphorus will aggravate the condition due to reduced absorption of magnesium by

precipitated calcium phosphate in the intestinal tract. In laying hens, reduced egg production, markedly reduced hatchability, and eggshell thinning are often noted. A manganese-deficient breeder diet can result in chondrodystrophy in chick embryos. This condition is characterized by shortened and thickened legs, shortened wings, a parrot beak brought about by a disproportionate shortening of the lower mandible, globular contour of the head due to anterior bulging of the skull, edema usually occurring just above the atlas joint of the neck and extending posteriorly, protruding abdomen (apparently due to a relatively large amount of unassimilated yolk), and retarded growth of down and feathers. In the young chick, nervous signs may also be noted, which are characterized by a star-gazing posture similar to that observed in cases of thiamine deficiency. This posture is a result of defective or absent otoliths in the inner ear. Prevention of perosis requires a diet adequate in all necessary nutrients, especially manganese, choline, niacin, biotin, and folic acid. Deformities cannot be corrected by feeding more manganese. Effects of manganese deficiency on egg production are fully corrected by a diet that contains manganese at 30-40 mg/kg, provided that the diet does not contain excess calcium and phosphorus. Calcium intake may be excessive if calcium supplements are provided free-choice. When meat meal is used as the principal source of protein, the feed may contain excess phosphorus.

Iron and Copper Deficiencies:

Deficiencies of both iron and copper can lead to anemia. Iron deficiency causes a severe anemia with a reduction in PCV. In color-feathered strains, there is also loss of pigmentation in the feathers. The birds requirements for RBC synthesis take precedence over metabolism of feather pigments, although if a fortified diet is introduced, all subsequent feather growth is normal. Iron may be needed not only for the red feather pigments, which are known to contain iron, but also to function in an enzyme system involved in feather pigmentation. Ochratoxin at 4-8 g/g diet also causes an iron deficiency characterized by hypochromic microcytic anemia. Aflatoxin also reduces iron absorption. High levels of iron salts can lead to formation of insoluble phosphates in the digesta, with reduced phosphorus absorption and subsequent incidence of rickets. Insoluble iron phosphates produce a colloidal suspension that may also adsorb vitamins and other trace minerals. Such problems will not occur unless supplements exceed normal levels by at least 10-fold. Young chicks become lame in 2-4 wk when fed a copper-deficient diet. Bones are fragile and easily broken, epiphyseal cartilage becomes thickened, and vascular penetration of the thickened cartilage is markedly reduced. These bone lesions in chickens are quite different from those seen in other farm animals and resemble the bone changes noted in birds with vitamin A deficiency. Copper-deficient chickens also show ataxia and spastic paralysis. Copper deficiency in birds, and especially in turkeys, can lead to rupture of the aorta. The biochemical lesion in the copper-deficient aorta is likely related to failure to synthesize desmosine, the cross-link precursor of elastin. The lysine content of copper-deficient elastin is 3 times that seen in control

birds, suggesting failure to incorporate lysine into the desmosine molecule. In field cases of naturally occurring aortic rupture, many birds have <10 ppm copper in the liver, compared with 15-30 ppm normally seen in birds of comparable age. High levels of sulfate, molybdenum, and ascorbic acid can reduce liver copper levels. A high incidence of aortic rupture has been seen in turkeys fed 4-nitrophenylarsonic acid. The problem can be resolved by feeding higher levels of copper, suggesting that products such as 4-nitro may complex with copper. Most practical diets for poultry contain adequate iron and copper. Nevertheless, feed manufacturers often add small amounts as an insurance measure.

Iodine Deficiency:

Iodine deficiency results in a decreased output of thyroxine from the thyroid gland, which in turn stimulates the anterior pituitary to produce and release increased amounts of thyroid stimulating hormone (TSH). This increased production of TSH results in stimulation, with subsequent enlargement of the thyroid gland, termed a goiter. This enlarged gland is an attempt by the thyroid to increase the secretory surface of the thyroid follicles by hypertrophy and hyperplasia of these follicles. Lack of thyroid activity or inhibition of the thyroid by administration of thiouracil or thiourea causes hens to cease laying and become obese, and also results in the growth of abnormally long, lacy feathers. Administration of thyroxine or iodinated casein reverses the effects on egg production, with eggshell quality returning to normal. The iodine content of an egg is markedly influenced by the hens intake of iodine. Eggs from a breeder fed an iodine-deficient diet will exhibit reduced hatchability and delayed yolk sac absorption. Rapeseed meal and, to a lesser extent, canola meal contain goitrogens that cause thyroid enlargement in young birds. Iodine deficiency in poultry is easily prevented by supplementing the feed with as little as 0.35 mg of iodine/kg.

Magnesium Deficiency:

Natural feed ingredients are rich in magnesium, thus deficiency is rare. Magnesium is rarely added to diets in the mineral premix. Newly hatched chicks fed a diet devoid of magnesium live only a few days. They grow slowly when fed diets low in magnesium, are lethargic, and often pant and gasp. When disturbed, they exhibit brief convulsions and go into a comatose state, which is sometimes temporary but more often fatal. Mortality is quite high on diets only marginally deficient in magnesium, even though growth of survivors may approach that of control birds. A magnesium deficiency in the diet of laying hens results in a rapid decline in egg production, blood hypomagnesemia, and a marked withdrawal of magnesium from bones. Egg size, shell weight, and the magnesium content of yolk and shell are decreased. Increasing the dietary calcium of laying hens accentuates these effects. Magnesium seems to play a central role in eggshell formation, although it is not clear whether there is a structural need or whether magnesium simply gets deposited as a cofactor along with calcium.

Requirements for most breeds of chicken appear to be ~500-600 ppm magnesium, a level that is usually achieved with contributions by natural feed ingredients.

Potassium, Sodium, and Chloride Deficiency:

While requirements for potassium, sodium, and chloride have been clearly defined, it is also important to maintain a balance of electrolytes in the body. Often termed dietary electrolyte balance or acid-base balance, the effects of deficiency of any one element are often the consequence of alteration to this important balance as it affects osmoregulation.
Simple Deficiency:

A deficiency of chloride causes ataxia with classic signs of nervousness, often induced by sudden noise or fright. The main sign of hypokalemia is an overall muscle weakness characterized by weak extremities, poor intestinal tone with intestinal distention, cardiac weakness, and weakness and ultimately failure of the respiratory muscles. Hypokalemia is apt to occur during severe stress. Plasma protein is elevated, causing the kidney, under the influence of adrenocortical hormone, to discharge potassium into the urine. During adaptation to the stress, blood flow to the muscle gradually improves, and the muscle begins to retrieve lost potassium. As liver glycogen is restored, potassium returns to the liver. This may result in temporary prolongation of the hypokalemia. Effects of administering potassium salts to chickens during and following severe stress periods have not been adequately investigated. When fed a diet low in protein and potassium or when starving, animals grow slowly but do not show a potassium deficiency. Potassium derived from metabolized tissue protein replaces that lost in the urine and lacking in the diet. Under such conditions, less potassium is needed. The ratio of potassium to nitrogen in urine is relatively constant and is the same as that found in fresh muscle. Thus, tissue nitrogen and potassium are released together from metabolized tissue. A deficiency of sodium leads to a lowering of osmotic pressure and a change in acid-base balance in the body. Cardiac output and blood pressure fall, hematocrit increases, elasticity of subcutaneous tissues decreases, and adrenal function is impaired. This leads to an increase in blood uric acid levels, which can result in shock and death. A less severe sodium deficiency in chicks can result in retarded growth, soft bones, corneal keratinization, impaired food utilization, and a decrease in plasma volume. In layers, reduced egg production, poor growth, and cannibalism may be noted. A number of diseases can result in sodium depletion from the body (eg, GI losses from diarrhea or urinary losses from renal or adrenal damage).
Electrolyte Imbalance:

Most commonly, electrolyte balance is described by the simple formula of Na+ + K+ - Cl- expressed as mEq/kg (or mEq/g) of diet. Generally, an overall diet balance of 250 mEq/kg is optimal for normal physiologic function. The primary role of electrolytes is to maintain body water and ionic balance. Thus, requirements for elements such as sodium, potassium, and chlorine cannot be considered individually, as it is the overall balance that is important. Electrolyte balance is affected by 3 factors, namely the balance

and proportion of these electrolytes in the diet, endogenous acid production, and the rate of renal clearance. In most situations, the body attempts to maintain the balance between cations and anions in the body such that physiologic pH is maintained. If conditions in the body result in a shift toward acid or base conditions, physiologic defense mechanisms alter metabolism to maintain normal pH. Actual electrolyte imbalances rarely occur because these regulatory mechanisms must ensure optimal cellular pH and osmolarity. Electrolyte balance can therefore more correctly be described as the mechanisms that must occur in the body to achieve normal physiologic pH. Electrolyte imbalance causes a number of metabolic disorders in birds, most notably tibial dyschondroplasia and respiratory alkalosis in layers. Tibial dyschondroplasia in young broiler chickens can be effected by the electrolyte balance of the diet. The unusual development of the cartilage plug at the growth plate of the tibia can be induced by a number of factors, although its incidence can be greatly increased by metabolic acidosis induced by feeding products such as NH4Cl. Tibial dyschondroplasia occurs more frequently when the diet contains an excess of sodium relative to potassium and a very high level of chloride. Overall electrolyte balance is always important, but is most critical when chloride or sulfur levels are high. With low dietary chloride levels, there is often little response to the manipulation of electrolyte balance; however, when dietary chloride levels are high, making adjustments to the dietary cations is critical to maintain overall balance. Alternatively, chloride levels can be reduced, although chickens have requirements ~0.12-0.15% of the diet, and deficiency signs will develop with dietary levels <0.12%. Therefore, care must be taken to meet the minimum chloride requirements when, for example, NaHCO3 replaces NaCl in a diet.

Selenium Deficiency:
A deficiency of selenium in growing chickens causes exudative diathesis. The early signs (unthriftiness, ruffled feathers) usually occur at 5-11 wk of age. The edema results in weeping of the skin, which is often seen on the inner surface of the thighs and wings. The birds bruise easily; large scabs often form on old bruises. In laying hens, the tissue damage is unusual, but egg production, hatchability, and feed conversion are adversely affected. The metabolism of selenium is closely linked to that of vitamin E, and signs of deficiency can sometimes be treated with either the mineral or the vitamin. Vitamin E can spare selenium in its role as an antioxidant, and so some selenium-responsive conditions can also be treated by supplemental vitamin E. In most countries, there are limits to the quantity of selenium that can be added to a diet; the upper limit is usually 0.3 ppm. The commonly used forms are sodium selenate and sodium selenite and, more recently, organic selenium chelates. Feeds grown on high-selenium soils may be used in poultry rations and are good sources of selenium. Fish meal and dried brewers yeast are also good sources.

Zinc Deficiency:
Zinc requirements and signs of deficiency are influenced by dietary ingredients. In semipurified diets, it is difficult to show a response to levels much above 25-30 mg/kg diet, whereas in practical corn-soy diets, requirement values are increased to 60-80 mg/kg. Such variable needs likely relate to phytic acid content of the diet, because this ligand is a potent zinc chelator. If phytase enzyme is used in diets, presumably the need for supplemental zinc will be reduced. In young chicks, signs of zinc deficiency include retarded growth, shortening and thickening of leg bones and enlargement of the hock joint, scaling of the skin (especially on the feet), very poor feathering, reduced feed utilization, loss of appetite, and in severe cases, mortality. While zinc deficiency can reduce egg production in aging hens, the most striking effects are seen in developing embryos. Chicks hatched from zinc-deficient hens are weak and cannot stand, eat, or drink. They have accelerated respiratory rates and labored breathing. If the chicks are disturbed, the signs are aggravated and the chicks often die. Retarded feathering and frizzled feathers are also found. However, the major defect is grossly impaired skeletal development. Zincdeficient embryos show micromelia, curvature of the spine, and shortened, fused thoracic and lumbar vertebrae. Toes often are missing and, in extreme cases, the embryos have no lower skeleton or limbs. Some embryos are rumpless, and occasionally the eyes are absent or not developed.

Vitamin deficiencies
Vitamin deficiencies are most commonly due to inadvertent omission of a vitamin premix from the birds diet. Multiple signs are therefore seen, although in general, problems with deficiencies of the B vitamins appear first. Because there are some stores of the fat-soluble vitamins in the body, it often takes longer for these deficiencies to affect the bird. Treatment and prevention rely on an adequate dietary supply, usually protected by gelatin microencapsulation, that also contains an antioxidant. Vitamin destruction in feeds is a factor of time, temperature, and humidity. For most feeds, vitamin efficiency is little affected over 2-mo storage within mixed feed.

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

stratified squamous, keratinized layer, which blocks the ducts of the mucous glands, resulting in distention and necrosis. Small, white pustules may be found in the nasal passages, mouth, esophagus, and pharynx, and may extend into the crop. Breakdown of the mucous membrane may allow pathogenic microorganisms to invade these tissues and cause secondary infections. Depending on the quantity of vitamin A passed on from the breeder hen, day-old chicks reared on a vitamin A-deficient diet may show signs within a week. However, chicks with a good reserve of vitamin A may not exhibit signs of 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 exhibit an ataxia similar to that noted with a vitamin E deficiency (see below). The yellow pigment in the shanks and beaks is usually lost, and the comb and wattles are pale. A cheesy material may be noted in the eyes, but xerophthalmia is seldom seen because chicks usually die before the eyes become affected. Infection may play a role in many of the deaths noted with acute vitamin A deficiency. Young chicks with a chronic vitamin A deficiency may also show pustules in the mucous membrane of the esophagus that can extend down the respiratory tract. Kidneys may be pale and the tubules distended due to the uric acid deposits. In extreme cases, the ureters may be filled with urates. Blood levels of uric acid can rise from a normal of ~5 mg to as high as 40 mg/100 mL of blood. Vitamin A deficiency does not interfere with uric acid metabolism but does prevent normal excretion of uric acid from the kidney. Histologic findings include atrophy of the cytoplasm and a loss of the cilia in the columnar, ciliated epithelium. While vitamin A-deficient chicks can show ataxia, similar to that noted with vitamin E deficiency, no gross lesions are found in the brain of vitamin Adeficient chicks as compared with degeneration of the Purkinje cells in the cerebellum of vitamin E-deficient chicks (see below). Also, the livers of ataxic vitamin A-deficient chicks contain little or no vitamin A.

Vitamin D3 Deficiency:
Abnormal development of the bones is discussed under calcium and phosphorus deficiencies ( Calcium and Phosphorus Imbalances) and manganese deficiency ( Manganese Deficiency). Vitamin D3 is required for the normal absorption and metabolism of calcium and phosphorus. A deficiency can result in rickets in young growing chickens or in osteoporosis and poor eggshell quality in laying hens, even though the diet may be well supplied with calcium and phosphorus. Laying hens fed a vitamin D3-deficient diet exhibit loss of egg production within 2-3 wk, and depending on the degree of deficiency, shell quality deteriorates almost instantaneously. Using a corn-soybean meal diet with no supplemental vitamin D3, shell weight decreases dramatically by about 150 mg/day within 7 days. The less obvious decline in shell quality with suboptimal supplements is more difficult to diagnose than that seen with absolute deficiency, as it is very difficult to assay vitamin D3 in complete feeds.

There is a significant increase in plasma 1,25(OH)2 D3 of birds producing good vs poor eggshells. Feeding purified 1,25(OH)2D3 improves the shell quality of these 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. Also, beaks and claws become soft and pliable. Chicks may have trouble walking and will take a few steps before squatting on their hocks. They often sway from side to side while resting, suggesting loss of equilibrium. Feathering is usually poor, and an abnormal banding of feathers is seen in colored breeds. With chronic vitamin D3 deficiency, 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. A characteristic finding in chicks is a beading of the ribs at the junction of the spinal column along with downward, and posterior bending. Poor calcification can be seen at the epiphysis of the tibia and femur. By dipping the split bone in a silver nitrate solution and allowing it to stand under an incandescent light for a few minutes, the calcified areas are easily distinguished from the areas of uncalcified cartilage. In the laying hen, signs of gross pathology are usually confined to the bones and parathyroid glands. Bones are soft and easily broken, and the ribs may become beaded. The ribs may also show spontaneous fractures in the sternovertebral region. Histologic examination shows deficiency of calcification in the long bones, with excess of osteoid tissue and parathyroid enlargement. Adding synthetic 1,25(OH)2D3 to the diet of susceptible chicks does reduce the incidence of this condition. Although the response is not dramatic and is quite variable, results suggest that some leg abnormalities may be a consequence of inefficient metabolism of cholecalciferol.

Vitamin E Deficiency:
The 3 main disorders seen in chicks deficient in vitamin E are encephalomalacia, exudative diathesis(characterised by oxidation of various tissues), and muscular dystrophy. The occurrence of these conditions depends on various dietary and environmental factors. Encephalomalacia is seen in commercial flocks if diets are low in vitamin E, an antioxidant is either omitted or not present in sufficient quantities, or the diet contains a reasonably high level of an unstable, unsaturated fat. For exudative diathesis to occur, the diet must be deficient in both vitamin E and selenium. Signs of muscular dystrophy are rare in chicks, as the diet must be deficient in both sulfur amino acids and vitamin E. Because the sulfur amino acids are necessary for growth, a deficiency severe enough to induce muscular dystrophy is unlikely to occur under commercial conditions. Signs of exudative diathesis and muscular dystrophy can be reversed in chicks by supplementing the diet with liberal amounts of vitamin E, assuming the deficiency is not too advanced. Encephalomalacia may or may not respond to vitamin E supplementation, depending on the extent of the damage to the cerebellum.

The classical sign of encephalomalacia is ataxia, which results from hemorrhage and edema within the molecular and granular layers of the cerebellum, with pyknosis and eventual disappearance of the Purkinje cells and separation of the molecular and granular layers of the cerebellar folia. Due to its inherently low level of vitamin E, the cerebellum is particularly susceptible to lipid peroxidation. In prevention of encephalomalacia, vitamin E functions as a biologic antioxidant. The quantitative need for vitamin E for this function depends on the amount of linoleic acid and polyunsaturated fatty acids in the diet. Over prolonged periods, antioxidants will prevent encephalomalacia in chicks when added to diets with very low levels of vitamin E, or in chicks fed vitamin E-depleted purified diets. Chicks hatched from breeders that are given additional dietary vitamin E are also less susceptible to lipid peroxidation in the brain. The fact that antioxidants can help prevent encephalomalacia but fail to prevent exudative diathesis or muscular dystrophy in chicks, strongly suggests that vitamin E is acting as an antioxidant. Exudative diathesis results in a severe edema caused by a marked increase in capillary permeability. Electrophoretic patterns of the blood show a decrease in albumin levels, whereas exudative fluids contained a protein pattern similar to that of normal blood plasma. A vitamin E deficiency accompanied by a sulfur amino acid deficiency results in a severe muscular dystrophy in chicks by ~4 wk of age. This condition is characterized by degeneration of the muscle fibers, usually in the breast but sometimes also in the leg muscles. Histologic examination shows Zenkers degeneration, with perivascular infiltration and marked accumulation of infiltrated eosinophils, lymphocytes, and histocytes. Accumulation of these cells in dystrophic tissue results in an increase in lysosomal enzymes, the function of which appears to be the breakdown and removal of the products of dystrophic degeneration. Initial studies involving the effects of dietary vitamin E on muscular dystrophy showed that the addition of selenium at 1-5 mg/kg diet reduced the incidence of muscular dystrophy in chicks receiving a vitamin E-deficient diet that was low in methionine and cysteine, but did not completely prevent the disease. However, selenium was completely effective in preventing muscular dystrophy in chicks when the diet contained a low level of vitamin E, which by itself had no effect on the disease. Studies on the interrelationships between antioxidants, linoleic acid, selenium, and sulfur amino acids have brought some order to the previous confusion about the role of vitamin E in chick nutrition. It is now apparent that selenium and vitamin E play supportive roles in several processes, one of which involves cysteine metabolism and its role in the prevention of muscular dystrophy in the chicken. Glutathione peroxidase is soluble and is therefore located in the aqueous portions of the cell, while vitamin E is located mainly in the hydrophobic environments of membranes and in lipid storage cells. The overlapping manner in which vitamin E and selenium function in the cellular antioxidant system suggest that they spare one another in the prevention of deficiency signs.

Vitamin K Deficiency:
Impairment of blood coagulation is the major clinical sign of vitamin K deficiency. With a severe deficiency, subcutaneous and internal hemorrhages can prove fatal. Vitamin K deficiency results in a reduction in prothrombin content of the blood; in the young chick, plasma levels are as low as 2% of what is considered normal. Because the prothrombin content of newly hatched chicks is only about 40% that of adult birds, the young chick is readily affected by a vitamin K-deficient diet. A carryover of vitamin K from the dam to eggs, and subsequently hatched chicks, has been demonstrated, so breeder diets should be well fortified. Hemorrhagic syndrome in day-old chicks has been attributed to a deficiency of vitamin K in the diet of the breeder hens. Gross deficiency of vitamin K results in such a prolonged blood clotting time that severely deficient chicks may bleed to death from a slight bruise or other injury. Borderline deficiencies often cause small hemorrhagic blemishes. Hemorrhages may appear on the breast, legs, wings, in the abdominal cavity, and on the surface of the intestine. Chicks are anemic, which may be due in part to loss of blood but also to the development of hypoplastic bone marrow. Although blood-clotting time is a fairly good measure of vitamin K deficiency, a more accurate measure is obtained by determining the prothrombin time. Prothrombin times in severely deficient chicks may be extended from a normal of 17-20 sec to 5-6 min or longer. No major heart lesions are seen in vitamin K-deficient chicks such as those that occur in pigs. A vitamin K deficiency in poultry may be related to low dietary levels of the vitamin, low levels in the maternal diet, degree of intestinal synthesis, extent of coprophagy, presence of sulfur drugs and other feed additives in the diet, and the presence of disease. Chicks with coccidiosis may have severe damage to their intestinal wall, leading to excessive bleeding in addition to depressed vitamin K absorption. Antimicrobial agents can suppress intestinal synthesis of vitamin K, leaving the bird completely dependent on the diet for its supply of the vitamin.

Vitamin B12 Deficiency:

Vitamin B12 is an essential part of several enzyme systems, with most reactions involving the transfer or synthesis of one-carbon units (eg, methyl groups). While the most important function of vitamin B12 is in the metabolism of nucleic acids and proteins, it also functions in carbohydrate and fat metabolism. In growing chickens, a deficiency of B12 results in reduced weight gain and feed intake, along with poor feathering and nervous disorders. While deficiency may lead to perosis, this is probably a secondary effect due to a dietary deficiency of methionine, choline, or betaine as sources of methyl groups. Vitamin B12 may alleviate perosis due to its effect on the synthesis of methyl groups. Further clinical signs reported in poultry are anemia, gizzard erosion, and fatty infiltration of heart, liver, and kidneys. Laying hens appear to be able to maintain body weight and egg production in spite of a dietary deficiency of vitamin B12, although egg size may be reduced. Hatchability can be markedly reduced in breeders, but several months may be needed for

signs to appear. Changes noted in embryos from B12 -deficient breeders include a general hemorrhagic condition, fatty liver, fewer myelinated fibers in the spinal cord, and high incidence of embryo deaths at 17 days incubation.

Choline Deficiency:
In addition to poor growth, the outstanding sign of choline deficiency in chicks and poults is perosis. Perosis is first characterized by pinpoint hemorrhages and a slight puffiness about the hock joint, followed by an apparent flattening of the tibiometatarsal joint caused by a rotation of the metatarsus. The metatarsus continues to twist and may become bent or bowed so that it is out of alignment with the tibia. When this condition exists, the leg cannot adequately support the weight of the bird. The articular cartilage is displaced, and the Achilles tendon slips from its condyles. Perosis is not a specific deficiency sign; it appears with several nutrient deficiencies. Although choline deficiency readily develops in chicks fed diets low in choline, a deficiency in laying hens is not easily produced. Eggs contain approximately 12-13 mg of choline/g of dried whole egg. A large egg contains about 170 mg of choline, found almost entirely in the phospholipids. Thus, there appears to be a considerable need for choline to produce an egg. In spite of this, producing a marked choline deficiency in laying hens has been difficult even when highly purified diets essentially devoid of choline were provided for a prolonged period of time. The choline content of eggs was not lowered, suggesting synthesis by the bird.

Niacin (Nicotinic Acid) Deficiency:

There is good evidence that poultryeven chick and turkey embryoscan synthesize niacin, but at a rate that is too slow for optimal growth. It has been claimed that a marked deficiency of niacin cannot occur in chickens unless there is a deficiency of tryptophan, an amino acid and a niacin precursor. A niacin deficiency is characterized by severe metabolic disorders in the skin and digestive organs. The first signs are usually loss of appetite, retarded growth, general weakness, and diarrhea. There is conflicting evidence as to whether broilers respond, in terms of growth and feed utilization, to niacin supplementation. However, it has been clearly established that chicks do have a requirement for niacin. Deficiency produces an enlargement of the tibiotarsal joint, bowing of the legs, poor feathering, and dermatitis on the head and feet. Niacin deficiency in chicks can also result in black tongue, in which the tongue, oral cavity, and esophagus become inflamed at ~2 wk of age. In the niacin-deficient hen, weight loss, reduced egg production, and a marked decrease in hatchability can result. Turkeys, ducks, pheasants, and goslings are much more severely affected by niacin deficiency than are chickens. Their apparently higher requirements are likely related to their less efficient conversion of tryptophan to niacin. Ducks and turkeys with a niacin deficiency show a severe bowing of the legs and an enlargement of the hock joint. The main difference between the leg seen in niacin deficiency and perosis seen in manganese and choline deficiency is that with niacin deficiency the Achilles tendon seldom slips from its condyles.

Pantothenic Acid Deficiency:

Pantothenic acid is the prosthetic group of coenzyme A, an important coenzyme involved in many reversible acetylation reactions in carbohydrate, fat, and amino acid metabolism. Signs of deficiency relate to general avian metabolism. The major lesions of pantothenic acid deficiency involve the nervous system, the adrenal cortex, and the skin. Deficiency may result in reduced egg production; however, a marked drop in hatchability is usually noted prior to this event. Embryos from hens with pantothenic acid deficiency may have subcutaneous hemorrhages and severe edema, with most other mortality showing up during the later part of the incubation period. In chicks, the first signs are reduced growth and feed consumption; poor feather growth, with feathers becoming ruffled and brittle; and a rapidly developing dermatitis. Corners of the beak and the area below the beak are usually the worst affected, but the condition is also noted on the feet. In severe cases, the skin of the feet may cornify, and wart-like lumps may be seen on the balls of the feet. The foot problem often leads to bacterial infection. Liver concentration of pantothenic acid is reduced during a deficiency, with the liver becoming atrophied. A faint to dirty yellow color may be noted. Nerve fibers of the spinal cord may show myelin degeneration. Panthothenic acid-deficient chicks show lymphoid cell necrosis in the bursa of Fabricius and thymus, together with lymphocytic 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, in a biotin deficiency dermatitis primarily affects the footpads and is usually more severe than that in a pantothenic acid deficiency. Ducks do not show the usual signs noted for chickens and turkeys, except for in retarded growth, but mortality can be quite high.

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

liver. Hatchability decreases within 2 wk when hens are fed a riboflavindeficient diet but returns to near normal when riboflavin is restored. Embryos from the eggs of hens receiving riboflavin-deficient diets are dwarfed and show characteristically defective down (clubbed down). The nervous system of these embryos shows degenerative changes much like those described in riboflavin-deficient chicks. Signs of riboflavin deficiency first appear at 10 days of incubation, when embryos become hypoglycemic and accumulate intermediates of fatty acid oxidation. Although flavin-dependent enzymes are depressed with riboflavin deficiency, the main effect seems to be impaired fatty acid oxidation, which is a critical function in the developing embryo. An autosomal recessive trait blocks the formation of riboflavin-binding protein, which is needed for transport of riboflavin to the egg. While the adults appear normal, their eggs fail to hatch regardless of dietary riboflavin content. As eggs become deficient in riboflavin, the egg albumen loses its characteristic yellow tinge. In fact, albumen color score has been used to assess riboflavin status of birds. Chicks receiving diets only partially deficient in riboflavin may recover spontaneously, indicating that the requirement rapidly decreases with age. A 100-g dose should be sufficient for treatment of riboflavin-deficient chicks, followed by incorporation of an adequate level in the diet. However, when the curled-toe deformity is longstanding, irreparable damage has occurred in the sciatic nerve, and the administration of riboflavin is no longer curative.

Folic Acid (Folacin) Deficiency:

A folacin deficiency results in a macrocytic (megaloblastic) anemia and leukopenia. Tissues with a rapid turnover, such as epithelial linings, GI tract, epidermis, and bone marrow, as well as cell growth and tissue regeneration, are principally affected. Poultry seem more susceptible than other farm animals to a folacin deficiency. Deficiency results in poor feathering, slow growth, an anemic appearance, and perosis. As anemia develops, the comb becomes waxy white, and pale mucous membranes in the mouth are noted. Elevated erythrocyte phosphoribosylpyrophosphate concentration can be used as a diagnostic tool in folate-deficient chicks. There may also be damage to liver parenchyma and depleted glycogen reserves. While turkey poults show some of the same signs as chickens, mortality is usually higher and the birds develop a spastic type of cervical paralysis that results in the neck becoming stiff and extended. The abnormal feather condition in chickens leads to weak and brittle shafts. Depigmentation develops in colored feathers due to a deficiency of the vitamin. While a folacin deficiency can result in reduced egg production, the main sign noted with breeders is a marked decrease in hatchability associated with an increase in embryonic mortality, usually during the last few days of incubation. Embryos have deformed beaks and often a bending of the tibiotarsus. While birds may exhibit perosis, the lesions seen differ histologically from those seen as a consequence of choline or manganese deficiency. Abnormal structure of the hyaline cartilage and retardation of ossification are noted with folacin deficiency. Increasing protein content of

the diet increases the severity of perosis in chicks receiving diets low in folic acid, as there is an increased folacin demand for uric acid synthesis.

Biotin Deficiency:
Biotin deficiency results in dermatitis of the feet and the skin around the beak and eyes similar to that described for pantothenic acid (see above). Perosis and footpad dermatitis are also characteristic signs. While signs of classical biotin deficiency are rare, occurrence of fatty liver and kidney syndrome (FLKS) is important to commercial poultry producers. FLKS was first described in Denmark in 1958, but was not a major concern until the late 1960s, especially in Europe and Australia. Chicks ~3 wk of age become lethargic and unable to stand, then die within hours. Mortality is usually quite low at 1-2% but can reach 20-30%. Postmortem examination reveals pale liver and kidney with accumulation of fat. The condition was usually confined to wheat-fed birds and was most problematic in low-fat, high-energy diets. High vitamin supplementation in general corrected the problem, and biotin was isolated as the causative agent. It is now known that biotin in wheat has exceptionally low availability. The trigger of high-energy diets led to investigation of biotin in carbohydrate metabolism. Chicks suffering from FLKS are invariably hypoglycemic, highlighting the importance of biotin in 2 key enzymes: pyruvate carboxylase and acetyl Co-A carboxylase. Acetyl Co-A carboxylase appears to preferentially sequester biotin, such that with low biotin availability and need for high de novo fat synthesis (high energy, low-fat diet), pyruvate carboxylase activity is severely compromised. Even with this imbalance, birds are able to grow. However, with a concurrent deprivation in feed intake or increased demand for glucose, hypoglycemia develops, leading to adipose catabolism and the characteristic accumulation of fat in both liver and kidney. Birds with FLKS rarely show signs of classic biotin deficiency. Plasma biotin levels <100 ng/100 mL may indicate a deficiency. However, recent evidence suggests that plasma biotin levels are quite insensitive to the birds biotin status, and that biotin levels in the liver or kidney are more useful indicators. Plasma pyruvic carboxylase is positively correlated with dietary biotin concentration, and levels plateau much later than does the growth response to biotin. Embryos are also sensitive to biotin status. Congenital perosis, ataxia, and characteristic skeletal deformities may be seen in embryos and newly hatched chicks when the dams are fed a low-biotin diet. Deformities can be prevented by adding biotin to the diet. Embryonic deformities include a shortened tibiotarsus that is bent posteriorly, a much shortened tarsometatarsus, shortening of the bones of the wing and skull, and shortening and bending of the anterior end of the scapula. Syndactylyan extensive webbing between the third and fourth toesin biotin-deficient embryos has been noted. Such embryos are chondrodystrophic and characterized by reduced size, parrot beak, crooked tibia, and shortened or twisted tarsometatarsus.

Pyridoxine (Vitamin B6) Deficiency:

A vitamin B6 deficiency causes retarded growth, dermatitis, and anemia. Because a major role of the vitamin is in protein metabolism, deficiency can result in reduced nitrogen retention. A deficiency can result in a marked increase in iron and a decrease in copper levels of the serum; iron utilization appears to be markedly decreased. The resulting anemia is believed to be the result of a disturbance in the synthesis of the protoporphyrins. Anemia is often noted in ducks, but seldom seen in chickens and turkeys. Young chicks may show nervous movements of the legs when walking and often undergo spasmodic convulsions, leading to death. During convulsions, chicks may run about aimlessly, flapping their wings and falling with jerking motions. The greater intensity of activity, resulting from pyridine deficiency, distinguishes these signs from those of encephalomalacia. A marked gizzard erosion has been noted in vitamin B6-deficient chicks. It can be prevented by inclusion of 1% taurocholic acid in the diet, leading to the speculation that pyridoxine is involved in taurine synthesis and is important for gizzard integrity. In pyridoxine deficiency, collagen maturation is incomplete, suggesting that this vitamin is essential for integrity of the connective tissue matrix. A chronic or borderline deficiency can result in perosis, with one leg usually being crippled and one or both middle toes bent inward at the first joint. In adult birds, pyridoxine deficiency results in reduced appetite, leading to reduced egg production and a decline in hatchability. Severe deficiency can cause a rapid involution of the ovary, oviduct, comb, and wattles, and of the testis in cockerels. Feed consumption in B6-deficient hens and cockerels declines sharply, but inanition is not responsible for the marked effects of vitamin B6 deficiency on sexual development. Although a partial molt is observed in some hens, the molt is not serious, and hens return to normal egg production within 2 wk following provision of a normal dietary level of pyridoxine.

Thiamine Deficiency:
Polyneuritis in birds represents the later stages of a thiamine deficiency, probably caused by buildup of the intermediates of carbohydrate metabolism. In the initial stages of deficiency, lethargy and head tremors may be noted. A marked decrease in appetite is also seen in birds fed a thiamine-deficient diet. Poultry are also susceptible to neuromuscular problems, resulting in impaired digestion, general weakness, star-gazing, and frequent convulsions. Polyneuritis may be seen in mature birds ~3 wk after they are fed a thiamine-deficient diet. As the deficiency progresses to the legs, wings, and neck, birds may sit on flexed legs and draw back their heads in a star-gazing position. Retraction of the head is due to paralysis of the anterior neck muscles. Soon after this stage, chickens lose the ability to stand or sit upright and topple to the floor, where they may lie with heads still retracted. Thiamine deficiency may also lead to a decrease in body temperature and respiratory rate. Testicular degeneration may be noted, and the heart may show slight atrophy. Birds consuming a thiamine-deficient diet soon show severe anorexia. They lose all interest in feed and will not resume eating unless given thiamine. If a severe deficiency has developed, thiamine must be force-fed or injected to induce eating.