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 Nutrition and Management: Poultry: Vitamin D3 Deficiency). A deficiency of either calcium or phosphorus results in lack of normal skeletal calcification. Rickets is seen mainly in growing birds, while calcium deficiency in laying hens results in reduced shell quality and osteoporosis. This depletion of bone structure causes a disorder that is 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 most commonly occurs 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 poults can exhibit lameness at 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 disorganized cartilage matrix, with an irregular vascular penetration. 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. 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 provide optimal utilization of fat-soluble compounds. Diets must also provide a correct balance of calcium to available phosphorus. For this reason, ingredients that are notoriously variable in their content of these minerals should be used with 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)2 D3, 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.
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 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. Incidence can quickly be altered through genetic selection, suggesting that it is affected by a major sex-linked recessive gene. 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 and 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.
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. 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 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 4.0% Ca) for at least 7 days prior to 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.
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, 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, 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.
A deficiency of manganese in the diet of immature chickens and turkeys is one of the causes of perosis and of thin-shelled eggs and poor hatchability in mature birds (also see Nutrition and Management: Poultry: Calcium and Phosphorus Imbalances). It can also cause chondrodystrophy.
The most dramatic 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 chondyles. Elevated intakes of calcium and/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, 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 usually 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 otoliths of the inner ear are defective or absent.
Deformities cannot be corrected by feeding more manganese. Effects of manganese deficiency on egg production are fully corrected by feeding a diet containing 30–40 mg of Mn/kg, provided the diet does not contain excess calcium and/or 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 the pigmentation process. Ochratoxin at 4–8 μg/g diet also causes an iron deficiency characterized by hypochromic microcytic anemia. Aflatoxin also reduces iron absorption.
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 resemble the changes noted in birds with a vitamin A deficiency. 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 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 Cu in the liver, compared to 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-nitrophenylarsionic 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 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.
Natural feed ingredients are rich in magnesium, thus deficiency is rare and magnesium is rarely added to diets. Newly hatched chicks fed a diet 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 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 classes of chicken seem to be ~500–600 ppm Mg, 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 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.
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 uptake of potassium. As liver glycogen is restored, potassium returns to the liver.
Birds that are fed a diet low in protein and potassium or that are starving grow slowly but do not show a potassium deficiency. Potassium derived from metabolized 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 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 decrease, 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 balance is described by the formula of Na + K – Cl expressed as mEq/kg of diet. An overall dietary balance of 250–300 mEq/kg is generally 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 chlorine 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 3 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 attempts to maintain the 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 change to 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 occur in the body 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.
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%. Therefore, care must be taken to meet the minimum chloride requirements when, for example, NaHCO3 replaces NaCl in a diet.
A deficiency of selenium in growing chickens causes exudative diathesis. 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, 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 may be used in poultry rations and are good sources of selenium. Fish meal and dried brewer's yeast are also rich in selenium.
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 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, 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, 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. 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.
Last full review/revision March 2012 by Alex J. Bermudez, DVM, MS, DACPV; Mahmoud El-Begearmi, PhD; Steven Leeson, PhD; Kirk C. Klasing, BS, MS, PhD