NUTRITIONAL REQUIREMENT OF COMMERCIAL POULTRY

NUTRITIONAL REQUIREMENT OF COMMERCIAL POULTRY

Poultry convert feed into food products quickly, efficiently, and with relatively low environmental impact compared with other livestock. The high rate of productivity of poultry results in relatively high nutrient needs. Poultry require the presence of at least 38 dietary nutrients in appropriate concentrations and balance. The nutrient requirement figures published in Nutrient Requirements of Poultry (National Research Council, 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 requirement for a given nutrient include growth, feed efficiency, egg production, prevention of deficiency symptoms, and quality of poultry product. These requirements assume the nutrients are in a highly bioavailable form, and they do not include a margin of safety. Consequently, adjustments should be made based on bioavailability of nutrients in various feedstuffs. A margin of safety should be added based on the length of time the diet will be stored before feeding, changes in rates of feed intake due to environmental temperature or dietary energy content, genetic strain, husbandry conditions (especially the level of sanitation), and the presence of stressors (such as diseases or mycotoxins).
Water
Water is an essential nutrient. Many factors influence water intake, including environmental temperature, relative humidity, salt and protein levels of the diet, birds’ productivity (rate of growth or egg production), and the individual bird’s ability to resorb water in the kidney. As a result, precise water requirements are highly variable. 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, uncontaminated by high levels of minerals or other potential toxic substances, must be available at all times.
Energy Requirements and Feed Intake
The energy requirements of poultry and the energy content of feedstuffs are expressed in kilocalories (1 kcal equals 4.1868 kilojoules). Two different measures of the bioavailable energy in feedstuffs are in use, metabolizable energy (AMEn) and the true metabolizable energy (TMEn). 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. Calculations of TMEn make an additional correction to account for endogenous losses of energy that are not directly attributable to the feedstuff and are usually a more useful measure. AMEn and TMEn are similar for many ingredients. However, the two values differ substantially for some ingredients such as feather meal, rice, wheat middlings, and corn distiller’s grains with solubles.
Poultry can adjust their feed intake over a considerable range of feed energy levels to meet their daily energy needs. Energy needs and, consequently, feed intake also vary considerably with environmental temperature and amount of physical activity. A bird’s daily need for amino acids, vitamins, and minerals are mostly independent of these factors. The nutrient requirement values in the following tables are based on typical rates of intake of birds in a thermoneutral environment consuming a diet that contains a specific energy content (eg, 3,200 kcal/kg for broilers). If a bird consumes a diet that has a higher energy content, it will decrease its feed intake; consequently, that diet must contain a proportionally higher amount of amino acids, vitamins, and minerals. Thus, nutrient density in the ration should be adjusted to provide appropriate nutrient intake based on requirements and the actual feed intake.
Because of the ability of poultry to adjust their feed intake to accommodate a wide range of diets with differing energy content, the energy values listed in the nutrient requirement tables in this section ( Nutrient Requirements of Growing Pullets a through Linoleic Acid, Mineral, and Vitamin Requirements of Turkeys a) should be regarded as guidelines rather than absolute requirements.
Appropriate body weight and fat deposition are important factors in rearing pullets for maximal egg production. Most strains of White Leghorn chickens have relatively low body weights and do not tend, under normal feeding, to become obese. Feed is normally provided for ad lib intake to this strain of pullets. For brown-egg strains of chickens, some degree of restriction is often practiced (~90% of ad lib feeding) to prevent precocial onset of lay. Broiler strains tend to become obese if fed ab lib; feed restriction is necessary for broiler pullets and broiler breeders. When feed restriction is practiced, the feed levels of amino acids, vitamins, and minerals must be proportionally increased to prevent deficiencies. Most large commercial breeders provide feed restriction and dietary nutrient guidelines specific for their strains.
Amino Acid Requirements
Poultry, like all animals, synthesize proteins that contain 20 L-amino acids. Birds are unable to synthesize 9 of these amino acids because of the lack of specific enzymes: arginine, isoleucine, leucine, lysine, methionine, phenylalanine, threonine, tryptophan, and valine. Histidine, glycine, and proline can be synthesized by birds, but the rate is usually insufficient to meet metabolic needs and a dietary source is required. These 12 amino acids are referred to as the essential amino acids. Tyrosine and cysteine can be synthesized from phenylalanine and methionine, respectively, and are referred to as conditionally essential because they must be in the diet if phenylalanine or methionine levels are inadequate. The diet must also supply sufficient amounts of nitrogen to allow the synthesis of nonessential amino acids. Essential amino acids are often added to the diet in purified form (eg, DL-methionine and L-lysine) to minimize the total protein level as well as the cost of the diet. This has the added advantage of minimizing nitrogen excretion.

Vitamins
Requirements for vitamins A, D, and E are expressed in IU. For chickens, 1 IU of vitamin A activity is equivalent to 0.3 mcg of pure retinol, 0.344 mcg of retinyl acetate, or 0.6 mcg of �-carotene. However, young chicks use �-carotene less efficiently.
One IU of vitamin D is equal to 0.025 mcg of cholecalciferol (vitamin D3). Ergocalciferol (vitamin D2) is used with an efficiency of <10% of vitamin D3 in poultry. One IU of vitamin E is equivalent to 1 mg of synthetic dl-a-tocopherol acetate. Vitamin E requirements vary with type and level of fat in the diet, the levels of selenium and trace minerals, and the presence or absence of other antioxidants. When diets high in long-chain highly polyunsaturated fatty acids are fed, vitamin E levels should be increased considerably. 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 also use betaine as a methylating agent. Betaine is widely distributed in practical feedstuffs and can spare the requirement for choline but cannot completely replace it in the diet. All vitamins are subject to degradation over time, and this process is accelerated by moisture, oxygen, trace minerals, heat, and light. Stabilized vitamin preparations and generous margins of safety are often applied to account for these losses. This is especially true if diets are pelleted, extruded, or stored for long periods Minerals Much of the phosphorus in feedstuffs of plant origin is complexed by phytate and is not absorbed efficiently by poultry. Consequently, it is critical that only the available phosphorus and not the total phosphorus levels be considered. Appropriate calcium nutrition depends on both the level of calcium and its ratio to that of available phosphorus. For growing poultry, this ratio should not deviate substantially from 2:1. The calcium requirement of laying hens is very high and increases with the rate of egg production and age of the hen. Other Nutrients and Additives The chick has requirements for 38 nutrients, together with an adequate level of metabolizable energy and water. Some additional nutrients may be necessary for growth and development under certain conditions. These include vitamin C, pyrroloquinoline quinone, and several heavy metals. Non-nutrient antioxidants, such as ethoxyquin, are usually added to poultry diets to protect vitamins and unsaturated fatty acids from oxidation. Antibiotics at low levels (5�25 mg/kg of feed, depending on the antibiotic) and surfeit copper (150 ppm) are sometimes included to improve growth rate and feed efficiency. Enzymes that increase the bioavailability of dietary phosphorus, energy, and protein are often used in poultry diets when their costs are not prohibitive. In some cases, phytase enzymes are used to decrease the amount of phosphorus in the excreta to meet environmental regulations. 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 strain�s breeder company should be followed with regard to the feeding of extra calcium, grit, or whole grain. Fresh, clean water should always be readily available. Broiler houses generally have specific areas designated for brooding. These areas could be throughout the whole house but with rings of cardboard (often referred to as chick guards) used to keep chicks around a heat source; more commonly, an area of the house is curtained off and preheated before chick placement. Either way, the brooder area floor temperature should be between 85��90�F (29.4��32.2�C). As the birds become older, the brooder temperature is lowered 5�F (2.8�C) each week until it is 70�F (21.1�C). At ~1 wk of age, the chick guards are removed or the curtains are opened, and the chicks have access to the additional space in the house. In particularly large chicken houses, there may be a second area curtained off for several days (up to 10�14 days of age) before the chicks are given access to the complete house. Ample space should be provided for feeders and waterers, which should be well distributed in the house. 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. When rearing pullets to be used as commercial egg laying or meat type breeding hens, 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 beak trimmed at the hatchery or, in rare cases, within the first 7 days after hatch. In controlled environment housing, day lengths are controlled more precisely; with dim lights, beak trimming 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 geographic area (see Vaccination Programs in Poultry). Many commercial egg laying type 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. 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 1 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 Water Requirements Egg-production birds usually spend their entire lives in cages. Although some broiler breeders are similarly housed, most are reared on litter floors or in pens in which as much as two-thirds of the floor is slatted. For egg-strain pullets 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 nipple- and 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. See table: Minimum Space Requirements for White Leghorn Egg-Strain Birds a and see Table: Space Requirements for Meat-Strain Birds for space requirements for egg-strain and meat-strain birds. Environmental housing and various types of ventilation may alter these specifications. Layers per Cage Within the guidelines indicated in Minimum Space Requirements for White Leghorn Egg-Strain Birds a and Space Requirements for Meat-Strain Birds, most colony cages house 5�10 layers. The ideal flock size depends on several factors, including labor and cost, and is best determined by the individual poultry manager or producer. Organic Poultry According to livestock standards, birds for slaughter designated as organic must be raised under organic management starting no later than the second day of life. Preventive management practices, including the use of vaccines to keep animals healthy, are used; however, antibiotics cannot be used for any reason, and federal regulations prohibit the use of hormones in all poultry. Organic management standards prohibit producers from withholding treatment from a sick or injured animal, but animals treated with a prohibited medication may not be sold as organic. All organically raised animals must have access to the outdoors; they may be temporarily confined only for reasons of health, safety, or to protect soil or water quality. For a product to be labeled with the �USDA organic� seal, it must comply with USDA National Organic Standards. Congress passed the Organic Foods Production Act in 1990, and the USDA established national organic standards in 2002. As of 2011, the organic layer flock in the USA was approximately 6.5 million hens, and the average number of organic broilers processed each week was approximately 0.5 million birds. This represents approximately 2.3% of the layer population and 0.3% of the broiler production. In the years from 2001 to 2011, the organic layer flock has grown 400%, and broilers processed as organic has grown 900%. However, it is important to realize that there are years in the past 10 when both layer and broiler organic numbers have shrunk from one year to the next. Growth of these areas is not a straight and predictable line. The first step toward organic certification for a poultry producer is to select a third-party certifier. The USDA keeps an actively updated list of accredited certification agencies, all of which follow the same USDA National Organic Standards. The producer then submits an application and Organic System Plan (OSP) to the selected certification agency. In livestock production, this plan includes information on the animal source, feeding practices, management practices, health care, recordkeeping, and product labeling. The certifier then reviews the OSP and, if it is deemed adequate, assigns a qualified organic inspector to the livestock facility. The inspector conducts a detailed evaluation of the OSP and the actual farm practices, provides a written exit interview of findings to the producer, and prepares a report to the certifier. If the farm is found to meet all National Organic Program standards, an organic certificate may be issued. The livestock product must be labeled with information identifying both the producer and certifier (�Certified organic by...�). The use of the USDA organic seal on packaging is optional. Organic certification requires annual inspections of the poultry farm. Animal Production Claims and �Natural� Claims The USDA Food Safety and Inspection Service (FSIS) permits the use of animal production claims and the term �natural.� FSIS permits the application of �animal production claims� (ie, truthful statements about the raising of animals from which meat and poultry products are derived) on the labeling of meat and poultry products. For many years, animal production claims have served as an alternative to the use of the term �organic� on the labeling of meat and poultry products in the absence of a uniformly accepted definition. Thus, producers may wish to continue the use of animal production claims (eg, �Raised Without Added Hormones,� �Free Range,� "No Antibiotics Ever," "All Vegetarian Diet") on meat and poultry labeling. The system FSIS has in place to evaluate the necessary supporting documentation to ensure the accuracy of animal production claims, such as producer affidavits of specific raising protocols or independent third-party programs with audits, will continue to be used whenever these types of claims are made. The term �natural� may be used when products contain no artificial ingredients and are no more than minimally processed in accordance with FSIS Policy Memo 055. This term may be used in combination with the claim �certified organic by (a certifying entity)� when these requirements are met. The definition of "naturally raised" is being reviewed by the USDA and may result in changes to these definitions. A nutritional deficiency may be due to a nutrient being omitted from the diet, adverse interaction between nutrients in otherwise apparently well-fortified diets, or the overriding effect of specific antinutrients. The latter two scenarios are difficult to diagnose, because diet analysis suggests a normal level of the nutrient(s) under investigation. Micronutrients such as vitamins and trace minerals are usually added to diets in the form of stand-alone micro premixes, so it is rare to see classic symptoms of deficiency of individual nutrients�rather, the effect seen is more commonly 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, necropsies, and tissue analyses. Unfortunately, tissue, and especially liver and serum analysis, can be misleading, because relative to the time of initial occurrence of any deficiency, the bird often sequesters nutrients in the liver, and so even with deficient diets, liver assays show erroneously high values. This latter effect is most significant for minerals such as copper. A diet that, by analysis, appears to contain just enough of one or more nutrients may actually be deficient to some degree in those nutrients. Stress (bacterial, parasitic, or viral infections; high or low temperatures; etc) may either interfere with absorption of a nutrient or increase the quantity required. Thus, a toxin or microorganism, for example, may destroy or render unavailable to the bird a particular nutrient that is present in the diet at apparently adequate levels according to conventional chemical or physical assay procedures. The optimal level of balanced protein intake for growing chicks is ~18%�23% of the diet; for growing poults and gallinaceous upland game birds, ~26%�30%; and for growing ducklings and goslings, ~20%�22%. 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, optimal 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. If a diet is deficient in protein or certain amino acids, the bird may initially consume more feed in an attempt to resolve the deficiency. After a few days, this transient increase in feed intake shifts to a situation of reduced feed intake. Consequently, there will be inferior feed efficiency, and the birds are invariably fatter as a consequence of overconsuming energy. All commercial breeds of poultry have an amazing ability to consume energy to requirement regardless of dietary energy concentration, assuming they can physically eat enough feed in extreme situations. A deficiency of energy can therefore occur only if the diet is so low in energy concentration that the bird physically cannot eat a sufficient quantity of feed to normalize energy intake. With a deficiency of energy, the bird will grow slowly or stop ovulating. As sources of energy, protein and amino acids will be deaminated, and any lipids will undergo �-oxidation. The latter condition can lead to ketosis, which more commonly occurs in mammals, yet the classic signs are similar. Calcium and Phosphorus Imbalances 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 (see Vitamin D 3 Deficiency). A deficiency of either calcium or phosphorus results in lack of normal skeletal calcification. Rickets is seen mainly in growing birds, whereas calcium deficiency in laying hens results in reduced shell quality and subsequently 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 occurs most commonly in young meat birds; the main characteristic is inadequate bone mineralization. Calcium deficiency at the cellular level is the main cause, although feeding a diet deficient or imbalanced in calcium, phosphorus, or vitamin D3 can also induce this problem. Young broilers and turkey poults can exhibit lameness at ~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 disorganized cartilage matrix, with an irregular vascular penetration. There is an indication of impaired metabolism of collagen precursors such as hyaluronic acid and desmosine. Rickets is not caused by a failure in the initiation of bone mineralization but rather by impairment of 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 investigation of parathyroid activity. In most field cases of rickets, a deficiency of vitamin D3 is suspected. This can be 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 ensure optimal utilization of all fat-soluble compounds. Young birds have limited ability to digest saturated fats, and these undigested compounds can complex with calcium to form insoluble soaps, leading to an induced deficiency of calcium. Again, this situation cannot be diagnosed through diet assay for calcium but rather through excreta assay of this mineral. Diets must also provide a correct balance of calcium to available phosphorus. For this reason, ingredients notoriously variable in their content of these minerals, such as animal proteins, should be used with extra caution. In recent years, the use of 25(OH)D3 has become very popular as a partial replacement for vitamin D3, with reports of greatly reduced incidence of rickets, especially in poults. This metabolite is similar to that naturally produced in the liver of birds in the first step of conversion of vitamin D3 to 1,25(OH)2D3, the active form of the vitamin. The commercial form of 25(OH)D3 is therefore especially useful if normal liver metabolism is compromised in any way, such as occurs with mycotoxins or other �natural� toxins in the feed that potentially impair liver metabolism. Tibial Dyschondroplasia (Osteochondrosis) Tibial dyschondroplasia is characterized by an abnormal cartilage mass in the proximal head of the tibiotarsus. It has been seen in all fast-growing types of meat birds but is most common in broiler chickens. Regardless of diet or environmental conditions, fast versus slow growth rate seems to at least double the incidence of tibial dyschondroplasia. Signs can occur early but more usually are not initially seen until 14�25 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 the normal process of ossification does not occur. The abnormal cartilage is composed of severely degenerated cells, with cytoplasm and nuclei appearing shrunken. Affected cartilage contains less protein and less DNA. The exact cause of tibial dyschondroplasia is unknown. Incidence can quickly be altered through genetic selection and is likely affected by a major sex-linked recessive gene. Imbalance of dietary electrolyte, and particularly high levels of chloride relative to other dietary cations, 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, or more commonly when diet phosphorus is high relative to calcium. Treatment involves dietary adjustment of the calcium:phosphorus ratio and by achieving a dietary electrolyte balance of ~250 mEq/kg. Dietary changes rarely result in complete recovery. Tibial dyschondroplasia can be prevented by tempering growth rate; however, programs of light or feed restriction must be considered in relation to economic consequences of reduced growth rate. There is evidence that replacement of some of the dietary vitamin D3 with metabolites such as 1,25(OH)D3 improves chondrocyte differentiation and hence limits occurrence of this skeletal disorder. Cage Layer Fatigue High-producing laying hens maintained in cages sometimes show paralysis during and just after the period 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. Layers are capable of early egg production exceeding 95% for at least 6 mo, which places even more pressure on maintenance of adequate calcium flux between the diet, the skeleton, and the oviduct. 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 within the cage is a predisposing or associated 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 simply 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 4% calcium) for at least 7 days before first oviposition. Older caged layers are also susceptible to bone breakage during removal from the cage and transport to processing. It is not known whether cage layer fatigue and bone breakage are related. However, bone strength cannot practically be improved without adverse consequences to other economically important traits such as eggshell quality. Cage layer fatigue is undoubtedly related to high, sustained egg output and associated clutch lengths of 200�230 eggs laid on successive days. Diets must provide adequate quantities of calcium and phosphorus to prevent deficiencies. However, feeding diets that contain >2.5% calcium during the immature growing period (<16 wk) produces a high incidence of nephritis, visceral gout, calcium urate deposits in the ureters, and sometimes high mortality, especially in the presence of infectious bronchitis virus. Eggshell strength and bone strength can both be improved by feeding ~50% of the dietary calcium supplement in the form of coarse limestone, with the remaining half as fine particle limestone. Offering the coarse supplement permits the birds to satisfy their requirements when they need it most, allowing the coarse material to be retained in the gizzard where the calcium can be absorbed continually and especially at night-time when the bird is not feeding. A readily available calcium and/or calcium phosphate supplement is often effective if started very soon after paralysis is first observed. Although these supplements may be advantageous to afflicted layers, they are not ideal for the regular birds in the flock; therefore, decisions regarding treatment are often influenced by the severity of the condition and the proportion of the flock affected. Manganese Deficiency A deficiency of manganese in the diet of immature chickens and turkeys is one of the potential causes of perosis and chondrodystrophy, and also the production of thin-shelled eggs and poor hatchability in mature birds (also see Calcium and Phosphorus Imbalances). The most dramatic classic effect of manganese deficiency syndrome is perosis, 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 tendon from its condyles. Increased intakes of calcium and/or phosphorus will aggravate the condition because of reduced absorption of manganese via the action of 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, thickened legs and shortened wings. Other signs can include 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 occurring just above the atlas joint of the neck and extending posteriorly, and protruding of the abdomen due to unassimilated yolk. Growth is also reduced, and development of down and feathers is retarded. A manganese-deficient chick has a characteristic star-gazing posture, because the physiology of the inner ear becomes defective. Deformities cannot be corrected by feeding more manganese. Effects of manganese deficiency on egg production are fully corrected by feeding a diet that contains at least 30�40 mg of manganese/kg, provided the diet does not contain excess calcium and/or phosphorus. There is an indication of the need for Fe2+ ions as well as manganese to correct the deficiency, although most commercial poultry diets contain a surfeit of iron. 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 and lines of demarcation on the feathers are part of diagnosis. 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 the pigmentation process. Ochratoxin at 4�8 mcg/g diet also causes an iron deficiency characterized by hypochromic microcytic anemia. Aflatoxin also reduces iron absorption. Young chicks become lame within 2�4 wk when fed a copper-deficient diet. Bones are fragile and easily broken, the epiphyseal cartilage becomes thickened, and vascular penetration of the thickened cartilage is markedly reduced. These bone lesions resemble the changes noted in birds with a vitamin A deficiency. Copper is required for cartilage formation, and certain antinutrients such as some grain fumigants have been shown to impact skeletal development, likely via interaction with copper metabolism. Copper-deficient chickens may also display 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 three 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 ions, molybdenum, and also 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 physically complex with copper. 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 subsequent enlargement of the thyroid gland, usually termed goiter. The enlarged gland results from hypertrophy and hyperplasia of the thyroid follicles, which increases the secretory surface of the follicles. Lack of thyroid activity or inhibition of the thyroid by administration of thiouracil or thiourea causes hens to cease laying and become obese. It 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 hen�s 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 can be avoided by supplementing the feed with as little as 0.5 mg of iodine/kg, although a level of 2�3 mg/kg is more commonly provided to sustain good feathering in fast-growing birds. Magnesium Deficiency Natural feed ingredients are rich in magnesium; thus, deficiency is rare and magnesium is never specifically used as a supplement to poultry diets. Newly hatched chicks fed a diet totally devoid of magnesium live only a few days. They grow slowly, are lethargic, and often pant and gasp. When disturbed, they exhibit brief convulsions and become comatose, which is sometimes temporary but 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 laying hens results in a rapid decline in egg production, 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. Magnesium requirements for most classes of chickens seem to be ~500�600 ppm, a level that is usually achieved with contributions by natural feed ingredients. Potassium, Sodium, and Chloride Deficiencies Although requirements for potassium, sodium, and chloride have been clearly defined, it is also important to maintain a balance of these and all other electrolytes in the body. Often termed electrolyte balance or acid-base balance, the effects of deficiency of any one element are often a 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 increased, 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 uptake of potassium. As liver glycogen is restored, potassium returns to the liver. Birds fed a diet low in both protein and potassium or that are starving grow slowly but do not show a potassium deficiency. Potassium derived from catabolized tissue protein replaces that lost in the urine. The ratio of potassium to nitrogen in urine is relatively constant and is the same as that found in muscle. Thus, tissue nitrogen and potassium are released together from the catabolized 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 both decrease, PCV 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, such as GI losses from diarrhea or urinary losses due to renal or adrenal damage. Electrolyte Imbalance Electrolyte balance is commonly described by the simple formula of Na + K � Cl expressed as mEq/kg of diet. An overall dietary balance of 250�300 mEq/kg is generally considered optimal for normal physiologic function. The buffering systems in the body ensure the maintenance of near normal physiologic pH, preventing electrolyte imbalance. The primary role of electrolytes is in maintenance of body water and ionic balance. Thus, requirements for elements such as sodium, potassium, and chloride cannot be considered individually, because it is the overall balance that is important. Electrolyte balance, also referred to as acid-base balance, is affected by three factors: the balance and proportion of these electrolytes in the diet, endogenous acid production, and the rate of renal clearance. In most situations, the body maintains a normal balance between cations and anions in the body such that physiologic pH is maintained. If there is a shift toward acid or base conditions, metabolic processes return the body to a normal pH. Actual electrolyte imbalances are rare, because regulatory mechanisms must sustain optimal cellular pH and osmolarity. Electrolyte balance can therefore more correctly be described as the changes that necessarily occur in the body processes to achieve normal pH. In extreme situations, such modifications in regulatory mechanisms seem to adversely affect other physiologic systems, and they produce or accentuate potentially debilitating conditions. 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 affected 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 seems to occur more frequently when the diet contains an excess of sodium relative to potassium, along with very high chloride levels. The latter situation is most easily remedied by substitution of sodium bicarbonate for sodium chloride in the diet. 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, it is critical to make adjustments to the dietary cations to maintain overall balance. Alternatively, chloride levels can be reduced, although chickens have requirements of ~0.12%�0.15% of the diet, and deficiency signs will develop with dietary levels <0.12%. Sodium content of drinking water can have a meaningful impact on total sodium intake of the bird. When drinking water contains >300 ppm of sodium, it may be necessary to reduce sodium levels in the diet. A recent innovation in poultry nutrition that impacts electrolyte balance is the use of phytase enzyme. This commonly used exogenous enzyme supplement is intended to reduce dependence on supplemental phosphorus, but it has been shown to concomitantly reduce renal excretion of sodium. Diets therefore need less supplemental sodium when they contain phytase enzyme.
Selenium Deficiency
A deficiency of selenium in growing chickens causes exudative diathesis. Early signs of unthriftiness and ruffled feathers usually occur at 3�6 wk of age, depending on the degree of deficiency. 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, and large scabs often form on old bruises. In laying hens, such 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 selenite and, more recently, organic selenium chelates. Feeds grown on high-selenium soils are sometimes necessarily used in poultry rations and are good sources of selenium. Fish meal and dried brewer�s yeast are also rich in available selenium.
Zinc Deficiency
Zinc requirements and signs of deficiency are influenced by dietary ingredients. In semipurified diets, it is difficult to show a response to zinc levels much above 25�30 mg/kg diet, whereas in practical corn-soybean meal diets, requirement values are increased to 60�80 mg/kg. Such variable zinc 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, the need for supplemental zinc is reduced by up to 10 mg/kg diet.
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, loss of appetite, and in severe cases, mortality. Although 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. Zinc-deficient 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 are most commonly due to inadvertent omission of a complete vitamin premix from the birds’ diet. Multiple signs are therefore seen, although in general, signs of B vitamin deficiencies appear first. Because there are some stores of fat-soluble vitamins in the body, it often takes longer for these deficiencies to affect the bird, and it may take months for vitamin A deficiency to affect adult birds.
Treatment and prevention rely on an adequate dietary supply, usually microencapsulated in gelatin or starch along with an antioxidant. Vitamin destruction in feeds is a factor of time, temperature, and humidity. For most feeds, efficacy of vitamins is little affected over 2-mo storage within mixed feed.
Vitamin A Deficiency
Depending on liver stores, adult birds could be fed a vitamin A�deficient diet for 2�5 mo before signs of deficiency develop. Eventually, birds become emaciated and weak with ruffled feathers. Egg production drops markedly, hatchability decreases, and embryonic mortality increases. As egg production declines, there will likely be only small follicles in the ovary, some of which show signs of hemorrhage. A watery discharge from the eyes may also be noted. As the deficiency continues, milky white, cheesy material accumulates in the eyes, making it impossible for birds to see (xerophthalmia). The eye, in many cases, may be destroyed.
The first lesion usually noted in adult birds is in the mucous glands of the upper alimentary tract. The normal epithelium is replaced by a stratified squamous, keratinized layer. This blocks the ducts of the mucous glands, resulting in necrotic secretions. Small, white pustules may be found in the nasal passages, mouth, esophagus, and pharynx, and these may extend into the crop. Breakdown of the mucous membrane usually allows pathogenic microorganisms to invade these tissues and cause secondary infections.
Depending on the quantity of vitamin A passed on from the breeder hen, day-old chicks reared on a vitamin A�deficient diet may show signs within 7 days. However, chicks with a good reserve of maternal vitamin A may not show signs of a deficiency for up to 7 wk. Gross signs in chicks include anorexia, growth retardation, drowsiness, weakness, incoordination, emaciation, and ruffled feathers. If the deficiency is severe, the chicks may become ataxic, which is also seen with vitamin E deficiency (see Vitamin E Deficiency). The yellow pigment in the shanks and beaks is usually lost, and the comb and wattles are pale. A cheesy material may be noted in the eyes, but xerophthalmia is seldom seen because chicks usually die before the eyes become affected. Secondary infection may play a role in many of the deaths noted with acute vitamin A deficiency.
Young chicks with chronic vitamin A deficiency may also develop pustules in the mucous membrane of the esophagus that usually affect the respiratory tract. Kidneys may be pale and the tubules distended because of uric acid deposits, and in extreme cases, the ureters may be plugged with urates. Blood levels of uric acid can rise from a normal level of ~5 mg to as high as 40 mg/100 mL. Vitamin A deficiency does not interfere with uric acid metabolism but does prevent normal excretion of uric acid from the kidney. Histologic findings include atrophy of the cytoplasm and a loss of the cilia in the columnar, ciliated epithelium.
Although vitamin A�deficient chicks can be ataxic, similar to those with vitamin E deficiency, no gross lesions are found in the brain of vitamin A�deficient chicks as compared with degeneration of the Purkinje cells in the cerebellum of vitamin E�deficient chicks (see Vitamin E Deficiency). The livers of ataxic vitamin A�deficient chicks contain little or no vitamin A.
Because stabilized vitamin A supplements are almost universally used in poultry diets, it is unlikely that a deficiency will be encountered. However, if a deficiency does develop because of either inadvertent omission of the vitamin A supplement or inadequate feed preparation, up to 2 times the normally recommended level, should be fed for ~2 wk. Vitamin A can be administered through the drinking water, and such treatment usually results in faster recovery than supplemtation via the feed.
Vitamin D3 Deficiency
Vitamin D3 is required for the normal absorption and metabolism of calcium and phosphorus. A deficiency can result in rickets in young growing chickens or in osteoporosis and/or poor eggshell quality in laying hens, even though the diet may be well supplied with calcium and phosphorus. Abnormal skeletal development is discussed under calcium and phosphorus imbalances (see Calcium and Phosphorus Imbalances) and manganese deficiency (see Manganese Deficiency).
Laying hens fed a vitamin D3�deficient diet show loss of egg production within 2�3 wk, and depending on the degree of deficiency, shell quality deteriorates almost instantly. Using a corn-soybean meal diet with no supplemental vitamin D3, shell weight decreases dramatically by ~150 mg/day throughout the first 7 days of deficiency. The less obvious decline in shell quality with suboptimal, rather than deficient, supplements is more difficult to diagnose, especially because it is very difficult to assay vitamin D3 in complete feeds.
There is a significant increase in plasma 1,25(OH)2D3 of birds producing good versus poor eggshells. Feeding purified 1,25(OH)2D3 improves the shell quality of these inferior layers, suggesting a potential inherent problem with metabolism of cholecalciferol.
Retarded growth and severe leg weakness are the first signs noted when chicks are deficient in vitamin D3. Beaks and claws become soft and pliable. Chicks may have trouble walking and will take a few steps before squatting on their hocks. While resting, they often sway from side to side, suggesting loss of equilibrium. Feathering is usually poor, and an abnormal banding of feathers may be seen in colored breeds. With chronic vitamin D3 deficiency, marked skeletal disorders are noted. The spinal column may bend downward and the sternum may deviate to one side. These structural changes reduce the size of the thorax, with subsequent crowding of the internal organs, especially the air sacs. A characteristic finding in chicks is a beading of the ribs at the junction of the spinal column along with a downward and posterior bending. Poor calcification can also be seen at the epiphysis of the tibia and femur. By immersing the split bone in a silver nitrate solution and allowing it to stand under incandescent light for a few minutes, the calcified areas are easily distinguished from the areas of cartilage. Adding synthetic 1,25(OH)2D3 to the diet of susceptible chicks reduces the incidence of this condition. Although response is variable, results suggest that some leg abnormalities may be a consequence of inefficient metabolism of cholecalciferol.
In laying hens, signs of gross pathology are usually confined to the bones and parathyroid glands. Bones are soft and easily broken, and the ribs may become beaded. The ribs may also show spontaneous fractures in the sternovertebral region. Histologic examination shows decreased calcification in the long bones, with excess of osteoid tissue and parathyroid enlargement.
Dry, stabilized forms of vitamin D3 are recommended to treat deficiencies. In cases of severe mycotoxicosis, a water-miscible form of vitamin D3 is administered in the drinking water to provide the amount normally supplied in the diet. In cases of impaired liver function, metabolites of vitamin D are the usual choice for treatment.
Vitamin E Deficiency
The three main disorders seen in chicks deficient in vitamin E are encephalomalacia, exudative diathesis, and muscular dystrophy. The occurrence of these conditions depends on various other dietary and environmental factors.
Encephalomalacia is seen in commercial flocks if diets are very low in vitamin E, if an antioxidant is either omitted or is not present in sufficient quantities, or if the diet contains a reasonably high level of an unstable and unsaturated fat. For exudative diathesis to occur, the diet must be deficient in both vitamin E and selenium. Signs of muscular dystrophy are rare in chicks, because the diet must be deficient in both sulfur amino acids and vitamin E. Because the sulfur amino acids are necessary for growth, a deficiency severe enough to induce muscular dystrophy is unlikely to occur under commercial conditions. Signs of exudative diathesis and muscular dystrophy can be reversed in chicks by supplementing the diet with liberal amounts of vitamin E, assuming the deficiency is not too advanced. Encephalomalacia may respond to vitamin E supplementation, depending on the extent of the damage to the cerebellum.
The classic sign of encephalomalacia is ataxia. The results from hemorrhage and edema within the granular layers of the cerebellum, with pyknosis and eventual disappearance of the Purkinje cells and separation of the granular layers of the cerebellar folia. Because of its inherently low level of vitamin E, the cerebellum is particularly susceptible to lipid peroxidation. In prevention of encephalomalacia, vitamin E functions as a biologic antioxidant. The quantitative need for vitamin E for this function depends on the amount of linoleic acid and polyunsaturated fatty acids in the diet. Over prolonged periods, antioxidants have been shown to prevent encephalomalacia in chicks when added to diets with very low levels of vitamin E or in chicks fed vitamin E�depleted purified diets. Chicks hatched from breeders that are given additional dietary vitamin E seem less susceptible to lipid peroxidation in the brain. The fact that antioxidants can help prevent encephalomalacia, but fail to prevent exudative diathesis or muscular dystrophy in chicks, strongly suggests that vitamin E is acting as an antioxidant in this situation. Exudative diathesis results in a severe edema caused by a marked increase in capillary permeability. Electrophoretic patterns of the blood show a decrease in albumin levels, whereas exudative fluids contained a protein pattern similar to that of normal blood plasma.
Vitamin E deficiency accompanied by sulfur amino acid deficiency results in severe muscular dystrophy in chicks by ~4 wk of age. This condition is characterized by degeneration of the muscle fibers, usually in the breast but sometimes also in the leg muscles. Histologic examination shows Zenker’s degeneration, with perivascular infiltration and marked accumulation of infiltrated eosinophils, lymphocytes, and histocytes. Accumulation of these cells in dystrophic tissue results in an increase in lysosomal enzymes, which appear to function in the breakdown and removal of the products of dystrophic degeneration. Initial studies involving the effects of dietary vitamin E on muscular dystrophy show that the addition of selenium at 1�5 mg/kg diet reduced the incidence of muscular dystrophy in chicks receiving a vitamin E�deficient diet that was also low in methionine and cysteine, but did not completely prevent the disease. However, selenium was completely effective in preventing muscular dystrophy in chicks when the diet contained a low level of vitamin E, which alone had been shown to have no effect on the disease. Throughout the past few years, the incidence of �muscular dystrophy�type� lesions in the breast muscle of older (>35 day) broilers has increased. Characteristic parallel white striations on the muscle are similar to those seen in chicks with muscular dystrophy, yet on analysis the diet of these birds seems adequate in vitamin E as well as selenium.
Studies with chicks on the interrelationships between antioxidants, linoleic acid, selenium, and sulfur amino acids have shown that selenium and vitamin E play supportive roles in several processes, one of which involves cysteine metabolism and its role in prevention of muscular dystrophy in chickens. Glutathione peroxidase is soluble and located in the aqueous portions of the cell, whereas vitamin E is located mainly in the hydrophobic environments of membranes and in adipose tissue and other lipid storage cells. The overlapping manner in which vitamin E and selenium function in the cellular antioxidant system suggest that they spare one another in prevention of deficiency signs.
Only stabilized fat should be used in feeds. Adequate levels of stabilized vitamin E should be used in conjunction with a commercial antioxidant and at least 0.3 ppm selenium. Signs of exudative diathesis and muscular dystrophy due to vitamin E deficiency can be reversed if treatment is begun early by administering vitamin E through the feed or drinking water. Oral administration of a single dose of vitamin E (300 IU per bird) usually causes remission.
Vitamin K Deficiency
Impairment of blood coagulation is the major clinical sign of vitamin K deficiency. With a severe deficiency, subcutaneous and internal hemorrhages can prove fatal. Vitamin K deficiency results in a reduction in prothrombin content of the blood, and in the young chick, plasma levels are as low as 2% of normal. Because the prothrombin content of newly hatched chicks is only ~40% that of adult birds, young chicks are readily affected by a vitamin K�deficient diet. A carryover of vitamin K from the hen to eggs, and subsequently to hatched chicks, has been demonstrated, so breeder diets should be well fortified. Hemorrhagic syndrome in day-old chicks has been attributed to a deficiency of vitamin K in the diet of the breeder hens. Gross deficiency of vitamin K results in such prolonged blood clotting that severely deficient chicks may bleed to death from a slight bruise or other injury. Borderline deficiencies often cause small hemorrhagic blemishes. Hemorrhages may appear on the breast, legs, wings, in the abdominal cavity, and on the surface of the intestine. Chicks are anemic, which may be due in part to loss of blood but also to development of hypoplastic bone marrow. Although blood-clotting time is a reasonable measure of the degree of vitamin K deficiency, a more accurate measure is obtained by determining the prothrombin time. Prothrombin times in severely deficient chicks may be extended from a normal of 17�20 sec to 5�6 min or longer. No major heart lesions are seen in vitamin K�deficient chicks such as those that occur in pigs.
A vitamin K deficiency in poultry may be related to low dietary levels of the vitamin, low levels in the maternal diet, lack of intestinal synthesis, extent of coprophagy, or the presence of sulfur drugs and other feed additives in the diet. Chicks with coccidiosis can have severe damage to their intestinal wall and can bleed excessively. Antimicrobial agents can suppress intestinal synthesis of vitamin K, rendering the bird completely dependent on the diet for its supply of the vitamin. Synthesis of vitamin K does occur in the bacteria resident in the bird’s digestive tract; however, such vitamin K remains inside the bacterial cell, so the only benefit to the bird arises from the bacterial cell digestion or via coprophagy.
The inclusion of menadione at 1�4 mg/ton of feed is an effective and common practice to prevent vitamin K deficiency. If signs of deficiency are seen, the level should be doubled. A number of stress factors (eg, coccidiosis and other intestinal parasitic diseases) increase the requirements for vitamin K. Dicumarol, sulfaquinoxaline, and warfarin are antimetabolites of vitamin K.
Vitamin B12Deficiency
Vitamin B12 is an essential part of several enzyme systems, with most reactions involving the transfer or synthesis of methyl groups. Although the most important function of vitamin B12 is in the metabolism of nucleic acids and proteins, it also functions in carbohydrate and fat metabolism.
In growing chickens, a deficiency of vitamin B12 results in reduced weight gain and feed intake, along with poor feathering and nervous disorders. Although deficiency may lead to perosis, this is probably a secondary effect due to a dietary deficiency of methionine or choline as sources of methyl groups. Vitamin B12 may alleviate perosis because of its effect on the synthesis of methyl groups. Other signs reported in poultry are anemia, gizzard erosion, and fatty infiltration of the heart, liver, and kidneys. Laying hens initially appear to be able to maintain body weight and egg production; however, egg size is reduced. In breeders, hatchability can be markedly reduced, although several weeks may be needed for signs of deficiency to appear. Changes noted in embryos from B12-deficient breeders include a general hemorrhagic condition, fatty liver, fewer myelinated fibers in the spinal cord, and high incidence of mid-term embryo deaths.
Deficiency of vitamin B12 is highly unlikely, especially for birds grown on litter or where animal-based ingredients are used. Treatment involves feeding up to 20 mcg/g feed for 1�2 wk.
Choline Deficiency
In addition to poor growth, the classic sign of choline deficiency in chicks and poults is perosis. Perosis is first characterized by pinpoint hemorrhages and a slight puffiness about the hock joint, followed by an apparent flattening of the tibiometatarsal joint caused by a rotation of the metatarsus. The metatarsus continues to twist and may become bent or bowed so that it is out of alignment with the tibia. When this condition exists, the leg cannot adequately support the weight of the bird. The articular cartilage is displaced, and the Achilles tendon slips from its condyles. Perosis is not a specific deficiency sign; it appears with several nutrient deficiencies.
Although choline deficiency readily develops in chicks fed diets low in choline, a deficiency in laying hens is not easily produced. Eggs contain ~12�13 mg of choline/g of dried whole egg. A large egg contains ~170 mg of choline, found almost entirely in the phospholipids. Thus, there appears to be a considerable need for choline to produce an egg. In spite of this, producing a marked choline deficiency in laying hens has been difficult, even when highly purified diets essentially devoid of choline are provided for a prolonged period. Under these conditions, the choline content of eggs is not reduced, suggesting possible intestinal synthesis by the bird.
Diets that contain appreciable quantities of soybean meal, wheat bran, and wheat shorts are unlikely to be deficient in choline. Soybean meal is a good source of choline, and wheat byproducts are good sources of betaine, which can perform the methyl-donor function of choline. Other good sources of choline are distiller’s grains, fishmeal, liver meal, meat meals, distiller’s solubles, and yeast. A number of commercial choline supplements are available, and supplemental choline is routinely used in most poultry feeds.
Niacin(Nicotinic Acid) Deficiency
There is considerable evidence that poultry, and even chick and turkey embryos, can synthesize niacin but at a rate too slow for optimal growth. It has been claimed that a marked deficiency of niacin cannot occur in chickens unless there is a concomitant deficiency of the amino acid tryptophan, which is a niacin precursor.
Niacin deficiency is characterized by severe disorders in the skin and digestive organs. The first signs are usually loss of appetite, retarded growth, general weakness, and diarrhea. Deficiency produces enlargement of the tibiotarsal joint, valgus-varus bowing of the legs, poor feathering, and dermatitis on the head and feet.
Niacin deficiency in chicks can also result in �black tongue.� At ~2 wk of age, the tongue, oral cavity, and esophagus become distinctly inflamed. In the niacin-deficient hen, weight loss, reduced egg production, and a marked decrease in hatchability can result. Turkeys, ducks, pheasants, and goslings are much more severely affected by niacin deficiency than are chickens. Their apparently higher requirements are likely related to their less efficient conversion of tryptophan to niacin. Ducks and turkeys with a niacin deficiency show a severe bowing of the legs and an enlargement of the hock joint. The main difference between the leg seen in niacin deficiency and perosis as seen in manganese and choline deficiency is that with niacin deficiency the Achilles tendon seldom slips from its condyles.
Niacin deficiency in chickens may be prevented by feeding a diet that contains niacin at =30 mg/kg; however, many nutritionists recommend 2�2.5 times as much. An allowance of 55�70 mg/kg of feed appears to be satisfactory for ducks, geese, and turkeys. Ample niacin should be provided in poultry diets so as to spare the utilization of tryptophan.
Pantothenic Acid Deficiency
Pantothenic acid is the prosthetic group within coenzyme A, an important coenzyme involved in many reversible acetylation reactions in carbohydrate, fat, and amino acid metabolism. Signs of deficiency therefore relate to general avian metabolism.
The major lesions of pantothenic acid deficiency involve the nervous system, the adrenal cortex, and the skin. Deficiency may result in reduced egg production; however, a marked drop in hatchability is usually noted before this event. Embryos from hens with pantothenic acid deficiency can have subcutaneous hemorrhages and severe edema, with most mortality showing up during the later part of the incubation period. In chicks, the first signs are reduced growth and feed consumption, poor feathering with feathers becoming ruffled and brittle, and a rapidly developing dermatitis. The corners of the beak and the area below the beak are usually the worst affected regions for dermatitis, but the condition is also noted on the feet. In severe cases, the skin of the feet may cornify, and wart-like lumps occur on the balls of the feet. The foot problem often leads to bacterial infection.
Liver concentration of pantothenic acid is reduced during a deficiency, with the liver becoming atrophied, with a faint dirty yellow color developing. Nerve fibers of the spinal cord may show myelin degeneration. Pantothenic acid�deficient chicks show lymphoid cell necrosis in the bursa of Fabricius and thymus, together with lymphocytic paucity in the spleen. The foot condition in chicks and the poor feathering are difficult to differentiate from signs of a biotin deficiency. In a pantothenic acid deficiency, dermatitis of the feet is usually noted first on the toes; in contrast, a biotin deficiency primarily affects the foot pads and is usually more severe. Ducks do not show the usual signs noted for chickens and turkeys, except for retarded growth, but mortality can be quite high.
Most poultry diets contain supplements of calcium pantothenate. Periodically, growing chickens fed practical diets develop a scaly condition of the skin, the exact cause of which is not known. Treatment with both calcium pantothenate (2 g) and riboflavin (0.5 g) in the drinking water (50 gal [190 L]) for a few days has been successful in some instances. Diets usually contain supplemental pantothenic acid at 12 mg/kg.
Riboflavin Deficiency
Many tissues may be affected by riboflavin deficiency, although the epithelium and the myelin sheaths of some of the main nerves are major targets. Changes in the sciatic nerves produce �curled-toe� paralysis in growing chickens. Egg production is affected, and riboflavin-deficient eggs do not hatch. When the diet is inadvertently devoid of the entire spectrum of vitamins, it is signs of riboflavin deficiency that first appear. When chicks are fed a diet deficient in riboflavin, their appetite is fairly good but they grow slowly, become weak and emaciated, and develop diarrhea between the first and second weeks. Deficient chicks are reluctant to move unless forced and then frequently walk on their hocks with the aid of their wings. The leg muscles are atrophied and flabby, and the skin is dry and harsh. In advanced stages of deficiency, the chicks lie prostrate with their legs extended, sometimes in opposite directions. The characteristic sign of riboflavin deficiency is a marked enlargement of the sciatic and brachial nerve sheaths; sciatic nerves usually show the most pronounced effects. Histologic examination of the affected nerves shows degenerative changes in the myelin sheaths that, when severe, pinch the nerve. This produces a permanent stimulus, which causes the curled-toe paralysis.
Signs of riboflavin deficiency in hens are decreased egg production, increased embryonic mortality, and an increase in size and fat content of the liver. Hatchability declines within 2 wk when hens are fed a riboflavin-deficient diet but returns to near normal when riboflavin is restored. Affected embryos are dwarfed and show characteristically defective �clubbed� down. The nervous system of these embryos shows degenerative changes much like those described in riboflavin-deficient chicks. Clubbed down is periodically seen in cases of poor hatchability, when the �reject� chicks or dead embryos show this condition, even though the breeder diet is apparently adequate in riboflavin. Anecdotal evidence suggests greater occurrence of this clubbed-down condition in farms that select �floor-eggs� for incubation.
Signs of riboflavin deficiency first appear at 10 days of incubation, when embryos become hypoglycemic and accumulate intermediates of fatty acid oxidation. Although flavin-dependent enzymes are depressed with riboflavin deficiency, the main effect seems to be impaired fatty acid oxidation, which is a critical function in the developing embryo. An autosomal recessive trait blocks the formation of the riboflavin-binding protein needed for transport of riboflavin to the egg. Although the adults appear normal, their eggs fail to hatch regardless of dietary riboflavin content. As eggs become deficient in riboflavin, the egg albumen loses its characteristic yellow color. In fact, albumen color score has been used to assess riboflavin status of birds.
Chicks receiving diets only partially deficient in riboflavin may recover spontaneously, indicating that the requirement rapidly decreases with age. A 100-mcg dose should be sufficient for treatment of riboflavin-deficient chicks, followed by incorporation of an adequate level in the diet. However, when the curled-toe deformity is longstanding, irreparable damage occurs in the sciatic nerve, and the administration of riboflavin is no longer curative.
Most diets contain up to 10 mg of riboflavin/kg. Treatment can be given as two sequential daily 100-mcg doses for chicks or poults, followed by an adequate amount of riboflavin in feed.
Folic Acid (Folacin) Deficiency
A folacin deficiency results in a macrocytic (megaloblastic) anemia and leukopenia. Tissues with a rapid turnover, such as epithelial linings, GI tract, epidermis, and bone marrow, as well as cell growth and tissue regeneration, are principally affected.
Poultry seem more susceptible to folacin deficiency than other farm animals. Deficiency results in poor feathering, slow growth, an anemic appearance, and sometimes perosis. As anemia develops, the comb becomes a waxy-white color, and pale mucous membranes in the mouth are noted. Increased erythrocyte phosphoribosylpyrophosphate concentration can be used as a diagnostic tool in folacin-deficient chicks. There may also be damage to liver parenchyma and depleted glycogen reserves. Although turkey poults show some of the same signs as chickens, mortality is usually higher and the birds develop a spastic type of cervical paralysis that results in the neck becoming stiff and extended.
The abnormal feather condition in chickens leads to weak and brittle shafts, and depigmentation develops in colored feathers. Although a folacin deficiency can result in reduced egg production, the main sign noted with breeders is a marked decrease in hatchability associated with an increase in embryonic mortality, usually during the last few days of incubation. Embryos have deformed beaks and bending of the tibiotarsus. Birds may exhibit perosis, but the lesions seen differ histologically from those that develop due to choline or manganese deficiency. Abnormal structure of the hyaline cartilage and retardation of ossification are noted with folacin deficiency. Increasing the protein content of the diet has been shown to increase the severity of perosis in chicks receiving diets low in folic acid, because there is an increased folacin demand for uric acid synthesis.
Signs of folic acid deficiency in poultry can be prevented by ensuring diets contain supplements of up to 1 mg/kg.
Biotin Deficiency
Biotin deficiency results in dermatitis of the feet and the skin around the beak and eyes similar to that described for pantothenic acid deficiency (see Pantothenic Acid Deficiency). Perosis and footpad dermatitis are also characteristic signs. Although signs of classic biotin deficiency are rare, occurrence of fatty liver and kidney syndrome (FLKS) is important to commercial poultry producers. FLKS was first described in Denmark in 1958 but was not a major concern until the late 1960s, when the condition became more prevalent and especially so in Europe and Australia. Chicks ~3 wk old become lethargic and unable to stand, then die within hours. Mortality is usually quite low at 1%�2% but can reach 20%�30%. Postmortem examination reveals pale liver and kidney with accumulation of fat.
The condition as described in the 1960s was usually confined to wheat-fed birds and was most problematic in low-fat, high-energy diets. High vitamin supplementation in general corrected the problem, and biotin was isolated as the causative agent. It is now known that biotin in wheat has exceptionally low availability. The trigger of high-energy diets led to investigation of biotin in carbohydrate metabolism. Chicks with FLKS are invariably hypoglycemic, emphasizing the importance of biotin in two key enzymes, namely pyruvate carboxylase and acetyl Co-A carboxylase. Acetyl Co-A carboxylase appears to preferentially sequester biotin, such that with low biotin availability and need for high de novo fat synthesis (high-energy, low-fat diet), pyruvate carboxylase activity is severely compromised. Even with this imbalance, birds are able to grow. However, with a concurrent deprivation in feed intake or increased demand for glucose, hypoglycemia develops, leading to adipose catabolism and the characteristic accumulation of fat in both liver and kidneys. Birds with FLKS rarely show signs of classic biotin deficiency.
Plasma biotin levels <100 ng/100 mL have been reported as a sign of deficiency. However, recent evidence suggests that plasma biotin levels are quite insensitive to the birds' biotin status, and that biotin levels in the liver or kidneys are more useful indicators. Plasma pyruvic carboxylase is positively correlated with dietary biotin concentration, and levels plateau much later than does the growth response to supplemental biotin. Embryos are also sensitive to biotin status. Congenital perosis, ataxia, and characteristic skeletal deformities may be seen in embryos and newly hatched chicks when hens are fed a deficient diet. Embryonic deformities include a shortened tibiotarsus that is bent posteriorly, a much shortened tarsometatarsus, shortening of the bones of the wing and skull, and shortening and bending of the anterior end of the scapula. Syndactyly, which is an extensive webbing between the third and fourth toes, is seen in biotin-deficient embryos. Such embryos are chondrodystrophic and characterized by reduced size, parrot beak, crooked tibia, and shortened or twisted tarsometatarsus. A number of factors increase biotin requirements, including oxidative rancidity of any feed fat, competition by intestinal microorganisms, and lack of carryover into the newly hatched chick or poult. It is good practice to add 150 mg biotin/tonne of feed, especially when significant amounts of wheat or wheat byproducts are used in the diet. Pyridoxine (Vitamin B6) Deficiency A vitamin B6 deficiency causes retarded growth, dermatitis, and anemia. Because a major role of the vitamin is in protein metabolism, deficiency can result in reduced nitrogen retention. Dietary protein is not well utilized, and thus nitrogen excretion increases. Increased iron levels and decreased copper levels are noted in the serum, and iron utilization appears to be markedly decreased. The resulting anemia is likely due to a disturbance in the synthesis of protoporphyrins. Anemia is often noted in ducks but is seldom seen in chickens and turkeys. Young chicks may show nervous movements of the legs when walking and often undergo spasmodic convulsions, leading to death. During convulsions, the chicks may run about aimlessly, flapping their wings and falling with jerking motions. The greater intensity of activity, resulting from vitamin B6 deficiency, distinguishes these signs from those of encephalomalacia. Gizzard erosion has been noted in vitamin B6�deficient chicks. It can be prevented by inclusion of 1% taurocholic acid in the diet, leading to the speculation that pyridoxine is involved in taurine synthesis and is important for gizzard integrity. In pyridoxine deficiency, collagen maturation is incomplete, suggesting that this vitamin is essential for integrity of the connective tissue matrix. A chronic deficiency can result in perosis, with one leg usually being crippled and one or both middle toes bent inward at the first joint. In adult birds, pyridoxine deficiency results in reduced appetite, leading to reduced egg production and a decline in hatchability. Severe deficiency can cause rapid involution of the ovary, oviduct, comb, and wattles, and of the testis in cockerels. Feed consumption in vitamin B6�deficient hens and cockerels declines sharply. Although a partial molt is seen in some hens, normal egg production returns within 2 wk after provision of a normal dietary level of pyridoxine. Deficiency can be prevented by adding pyridoxine at 3-4 mg/kg feed. Thiamine Deficiency Polyneuritis in birds represents the later stages of a thiamine deficiency, probably caused by buildup of the intermediates of carbohydrate metabolism. Because the brain's immediate source of energy results from the degradation of glucose, it depends on biochemical reactions involving thiamine. In the initial stages of deficiency, lethargy and head tremors may be noted. A marked decrease in appetite is seen in birds fed a thiamine-deficient diet. Poultry are also susceptible to neuromuscular problems, resulting in impaired digestion, general weakness, star-gazing, and frequent convulsions. Polyneuritis may be seen in mature birds ~3 wk after they are fed a thiamine-deficient diet. As the deficiency progresses, birds may sit on flexed legs and draw back their heads in a star-gazing position. Retraction of the head is due to paralysis of the anterior neck muscles. Soon after this stage, chickens lose the ability to stand or sit upright and topple to the floor, where they may lie with heads still retracted. Thiamine deficiency may also lead to a decrease in body temperature and respiratory rate. Testicular degeneration may be noted, and the heart may show slight atrophy. Birds consuming a thiamine-deficient diet soon show severe anorexia. They lose all interest in feed and will not resume eating unless given thiamine. If a severe deficiency has developed, thiamine must be force-fed or injected to induce the chickens to resume eating. Thiamine deficiency is most common when poorly processed fish meals are used, because they contain thiaminase enzyme. In such situations, adding extra thiamine may be ineffective. There is no good evidence suggesting that, unlike in some mammalian species, certain Fusarium mycotoxins can increase the need for supplemental thiamine. In otherwise adequate diets, deficiency is prevented by supplements of thiamine up to 4 mg/kg.

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