Mineral Deficiencies

A nutritional deficiency can arise simply due to a nutrient being omitted from the diet, or due to interaction between nutrients or between nutrients and anti-nutritional factors. The latter situations are difficult to diagnose because, on analysis, the diet is found to contain a normal level of the suspect nutrient. Micronutrients are often packaged into premixes, so it is rare to see classic individual deficiency signs—rather the effect is a compilation of many individual metabolic conditions. In many instances, a correct diagnosis can be made only by obtaining complete information about diet and management, clinical signs in the affected living birds, and results of necropsies and tissue analyses.

The composition of individual ingredients in a diet is variable; some nutrients are comparatively unstable, while others are unavailable in their natural form. A diet that, by analysis, appears to contain just enough of one or more nutrients may actually be deficient to some degree. Stress due to bacterial, parasitic, or viral infections; high or low temperatures; low humidity; or drugs may either interfere with absorption of a nutrient or increase the quantity required. Thus, a toxin, microorganism, or other stressor may destroy or render unavailable a particular nutrient that is present in the diet at normally adequate levels.
Only deficiencies occurring in practical diets in the field are discussed below.

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. This condition, rickets, can also be caused by a dietary deficiency of vitamin D3, which is necessary for absorption of calcium. A deficiency of either calcium or phosphorus results in lack of normal skeletal calcification. Rickets is seen mainly in growing birds. Calcium deficiency in adult laying hens usually results in reduced shell quality and osteoporosis. This depletion of bone structure causes a disorder commonly referred to as “cage layer fatigue.” When calcium is mobilized from bone to overcome a dietary deficiency, the cortical bone erodes and is unable to support the weight of the hen.
Rickets most commonly occurs in young meat birds. The primary pathologic change is inadequate bone mineralization. Calcium deficiency at the cellular level is the main problem, which may result from feeding a diet deficient or imbalanced in calcium, phosphorus, or vitamin D3. Young broilers and poults exhibit lameness, usually around 10-14 days of age. Their bones are rubbery, and the rib cage is flattened and beaded at the attachment of the vertebrae. Rachitic birds exhibit a very disorganized cartilage matrix, with an irregular penetration of vascular canals. Rickets is not caused by a failure in the initiation of bone mineralization, but rather by the early maturation of this process. There is often an enlargement of the ends of the long bones, with a widening of the epiphyseal plate. A determination of whether rickets is due to deficiencies of calcium, phosphorus, or vitamin D3, or to an excess of calcium (which induces a phosphorus deficiency) may require analysis of blood phosphorus levels and parathyroid activity.

In most field cases of rickets, a deficiency of vitamin D3 is suspected, due to simple dietary deficiency, inadequate potency of the D3 supplement, or other factors that reduce the absorption of vitamin D3. Rickets can best be prevented by providing adequate levels and potency of vitamin D3 supplements, and by ensuring that the diet is formulated to provide optimal utilization of fat-soluble compounds. Diets must also provide a correct calcium:phosphorus ratio. For this reason, ingredients that are notoriously variable in their content of these minerals should be used with caution.
Tibial Dyschondroplasia (Osteochondrosis):
Tibial dyschondroplasia is identified by an abnormal cartilage mass in the proximal head of the tibio-tarsus. It is seen in all fast-growing meat birds (most  in broiler). Rarely seen in early stage, usually seen at 21-35 days of age. Birds are unwilling  to move, and when forced to walk, do so with a swaying motion or stiff gait. Tibial dyschondroplasia is results of 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 happen. The abnormal cartilage is made of severely degenerated cells, with cytoplasm and nuclei appearing shrunken.

The exact cause of tibial dyschondroplasia is not established, a genetic component is likely in some cases. Dietary electrolyte imbalances, and particularly high levels of chloride, seem to be a major contributor in many field outbreaks. More tibial dyschondroplasia is also seen when the level of dietary calcium is relatively low to that of available phosphorus. Treatment involves dietary adjustment of the calcium:phosphorus ratio, consideration of dietary electrolyte balance, and higher levels or potency of vitamin D3 supplementation. Diet changes don’t result in complete recovery. Tibial dyschondroplasia can be prevented by reducing growth rate by  changing feed programs  which can have economic consequences.
Cage Layer Fatigue:
High-producing laying hens maintained in cages sometimes show paralysis around the time of peak egg production due to a fracture of the vertebrae that subsequently affects the spinal cord. The fracture is caused by an impaired calcium flux related to the high output of calcium in the eggshell. Because medullary bone reserves become depleted, the bird uses cortical bone as a source of calcium for the eggshell. The condition is rarely seen in floor-housed birds, suggesting that lack of activity or exercise is one of reasons. Affected birds are found on their sides in the back of the cage. At the time of initial paralysis, birds appear healthy and have a shelled egg in the oviduct and an active ovary. Death occurs from starvation or dehydration because the birds cannot reach feed or water.

Affected birds will recover if moved to the floor. A high incidence of cage layer fatigue can be prevented by ensuring the normal weight-for-age of pullets at sexual maturity and by giving pullets a high-calcium diet (minimum 3.5% calcium) for at least 14 days before first egg.

Diets must have adequate 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. It is useful to feed high levels of calcium to pullets 2 wk before the onset of egg production to improve productivity.

Eggshell strength can be improved by feeding ~50% of the dietary calcium supplement in the form of oyster-shell flakes or coarse limestone, with the remaining half as ground limestone. Oyster shell or any other form of calcium supplement should never be added without an equivalent reduction in the amount of limestone; feeding too much calcium reduces feed consumption and egg production. Offering the coarse supplement permits the birds to satisfy their requirements when they need it most, or allows the coarse material to be retained in the gizzard where the calcium can be absorbed continuously. A readily assimilable calcium and/or calcium phosphate supplement is effective if started immediately after first case of paralysis noticed.

Manganese Deficiency

A deficiency of manganese in the diet of young growing chickens is one of the causes of perosis and of thin-shelled eggs and poor hatchability  and vitamin d deficiency. It may also cause chondrodystrophy.

Perosis, which occurs in young chicks, identified by enlargement and malformation of the tibiometatarsal joint, twisting and bending of the distal end of the tibia and the proximal end of the tarsometatarsus, thickening and shortening of the leg bones, and slippage of the gastrocnemius or Achilles tendon from its condyles. Higher intakes of calcium or phosphorus will aggravate the condition by reducing absorption of magnesium due to precipitated calcium phosphate in the intestinal tract. In laying hens, reduced egg production,  reduced hatchability, and eggshell thinning is noticed.

A manganese-deficient breeder diet can result in chondrodystrophy in chick embryos. This condition is characterized by shortened and thickened legs, shortened wings, a “parrot beak” caused by a disproportionate shortening of the lower mandible, globular contour of the head caused by bulging of the anterior skull, edema usually occurring just above the atlas joint of the neck and extending to posterior, protruding abdomen (apparently due to a larger amount of unassimilated yolk), and retarded growth of down and feathers. In the young chick, nervous signs(“star-gazing” posture) may also be noted, which are similar to thiamine deficiency. This posture is a result of defective or absent otoliths in the inner ear.

Prevention of perosis requires a diet adequate in all necessary nutrients, especially manganese, choline, niacin, biotin, and folic acid. Deformities cannot be corrected by feeding more manganese. Effects of manganese deficiency on egg production are fully corrected by a diet that contains manganese at 30-40 mg/kg, keeping calcium and phosphorus at required level. If meat meal is used as  major source of protein, phosphorus level may exceed.

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, but also to function in an enzyme system involved in feather pigmentation. Ochratoxin at 4-8 µg/g diet also causes an iron deficiency characterized by hypochromic microcytic anemia. Aflatoxin also reduces iron absorption. High levels of iron salts can lead to formation of insoluble phosphates in the digesta, with reduced phosphorus absorption and subsequent incidence of rickets. Insoluble iron phosphates produce a colloidal suspension that may also adsorb vitamins and other trace minerals. Such problems will not occur unless supplements exceed normal levels by at least 10-fold.

Young chicks become lame in 2-4 wk when fed a copper-deficient diet. Bones are fragile and easily broken, epiphyseal cartilage becomes thickened, and vascular penetration of the thickened cartilage is markedly reduced. These bone lesions in chickens are quite different from those seen in other farm animals and resemble the bone changes noted in birds with vitamin A deficiency. Copper-deficient chickens also show ataxia and spastic paralysis.

Copper deficiency in birds, and especially in turkeys, can lead to rupture of the aorta. The biochemical lesion in the copper-deficient aorta is likely related to failure to synthesize desmosine, the cross-link precursor of elastin. The lysine content of copper-deficient elastin is 3 times that seen in control birds, suggesting failure to incorporate lysine into the desmosine molecule. In field cases of naturally occurring aortic rupture, many birds have <10 ppm copper in the liver, compared with 15-30 ppm normally seen in birds of comparable age. High levels of sulfate, molybdenum, and ascorbic acid can reduce liver copper levels. A high incidence of aortic rupture has been seen in turkeys fed 4-nitrophenylarsonic acid. The problem can be resolved by feeding higher levels of copper, suggesting that products such as 4-nitro may complex with copper.

Most practical diets for poultry contain adequate iron and copper. Nevertheless, feed manufacturers often add small amounts as an insurance measure.

Iodine Deficiency

Iodine deficiency results in a decreased output of thyroxine from the thyroid gland, which in turn stimulates the anterior pituitary to produce and release increased amounts of thyroid stimulating hormone (TSH). This increased production of TSH results in stimulation, with subsequent enlargement of the thyroid gland, termed a goiter. This enlarged gland is an attempt by the thyroid to increase the secretory surface of the thyroid follicles by hypertrophy and hyperplasia of these follicles.

Lack of thyroid activity or inhibition of the thyroid by administration of thiouracil or thiourea causes hens to cease laying and become obese, and also results in the growth of abnormally long, lacy feathers. Administration of thyroxine or iodinated casein reverses the effects on egg production, with eggshell quality returning to normal. The iodine content of an egg is markedly influenced by the 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 is easily prevented by supplementing the feed with as little as 0.35 mg of iodine/kg.

Magnesium Deficiency

Natural feed ingredients are rich in magnesium, thus deficiency is rare. Magnesium is rarely added to diets in the mineral premix. Newly hatched chicks fed a diet devoid of magnesium live only a few days. They grow slowly when fed diets low in magnesium, are lethargic, and often pant and gasp. When disturbed, they exhibit brief convulsions and go into a comatose state, which is often fatal. Mortality is quite high on diets,even  in marginally deficient in magnesium, though growth of survivors may mach 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 noticable 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 adds to the condition. Magnesium seems to play a central role in eggshell formation, although it is not clear where it is exactly reuired.

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

Potassium, Sodium, and Chloride Deficiency

While requirements for potassium, sodium, and chloride have been clearly defined, it is also important to maintain a balance of electrolytes in the body. Often termed dietary electrolyte balance or acid-base balance, the effects of deficiency of any one element are often the consequence of alteration to this important balance as it affects osmoregulation.
Simple Deficiency:
A deficiency of chloride causes ataxia with classic signs of nervousness, often induced by sudden noise or fright. The main sign of hypokalemia is an overall muscle weakness characterized by weak extremities, poor intestinal tone with intestinal distention, cardiac weakness, and weakness and ultimately failure of the respiratory muscles. Hypokalemia is common to occur during severe stress. Plasma protein is elevated, causing the kidney, under the influence of adreno-cortical hormone, to discharge potassium into the urine. During adaptation to the stress, blood flow to the muscle gradually improves, and the muscle begins to retrieve lost potassium. As liver glycogen is restored, potassium returns to the liver. This may result in temporary prolongation of the hypokalemia. Effects of administering potassium salts to chickens during and following severe stress periods have not been adequately investigated.

When fed a diet low in protein and potassium or when starving, animals grow slowly but do not show a potassium deficiency. Potassium derived from metabolized tissue protein replaces that lost in the urine and lacking in the diet. Under such conditions, less potassium is needed. The ratio of potassium to nitrogen in urine is relatively constant and is the same as that found in fresh muscle. Thus, tissue nitrogen and potassium are released together from metabolized tissue.

A deficiency of sodium leads to a lowering of osmotic pressure and a change in acid-base balance in the body. Cardiac output and blood pressure fall, hematocrit increases, elasticity of subcutaneous tissues decreases, and adrenal function is impaired. This leads to an increase in blood uric acid levels, which can result in shock and death. A less severe sodium deficiency in chicks can result in retarded growth, soft bones, corneal keratinization, impaired food utilization, and a decrease in plasma volume. In layers, reduced egg production, poor growth, and cannibalism may be noted. A number of diseases can result in sodium depletion from the body (eg, diarrhea or  renal or adrenal damage).
Electrolyte Imbalance:
Most commonly, electrolyte balance is described by the simple formula of Na++ K+ - Cl- expressed as mEq/kg (or mEq/g) of diet. Generally, an overall diet balance of 250 mEq/kg is optimal for normal physiologic function. The primary role of electrolytes is to maintain body water and ionic balance. Thus, requirements for elements such as sodium, potassium, and chlorine cannot be considered individually, as it is the overall balance that is important. Electrolyte balance is affected by 3 factors, namely the balance and proportion of these electrolytes in the diet, endogenous acid production, and the rate of renal clearance.

In most situations, the body attempts to maintain the balance between cations and anions in the body so that physiologic pH is maintained. If conditions in the body result in a shift toward acid or base conditions, physiologic defense mechanisms alter metabolism to maintain normal pH. Actual electrolyte imbalances rarely occur because these regulatory mechanisms  ensure optimal cellular pH and osmolarity. Electrolyte balance can therefore more correctly be described as the mechanisms that must occur in the body to achieve normal physiologic pH.

Electrolyte imbalance causes a number of metabolic disorders in birds, most notably tibial dyschondroplasia and respiratory alkalosis in layers. Tibial dyschondroplasia in young broiler chickens can be effected by the electrolyte balance of the diet. The unusual development of the cartilage plug at the growth plate of the tibia can be induced by a number of factors, although its incidence can be greatly increased by metabolic acidosis induced by feeding products such as NH4Cl. Tibial dyschondroplasia occurs more frequently when the diet contains an excess of sodium relative to potassium and a very high level of chloride.

Overall electrolyte balance is always important, but is most critical when chloride or sulfur levels are high. With low dietary chloride levels, there is often little response to the manipulation of electrolyte balance; however, when dietary chloride levels are high, making adjustments to the dietary cations is critical to maintain overall balance. Alternatively, chloride levels can be reduced, although chickens have requirements ~0.12-0.15% of the diet, and deficiency signs will develop with dietary levels <0.12%. Therefore, care must be taken to meet the minimum chloride requirements when, for example, NaHCO3 replaces NaCl in a diet.

Selenium Deficiency

A deficiency of selenium in growing chickens causes exudative diathesis. The early signs (unthriftiness, ruffled feathers) usually occur at 5-11 wk of age. The edema results in weeping of the skin, which is often seen on the inner surface of the thighs and wings. The birds bruise easily; large scabs often form on old bruises. In laying hens, the tissue damage is rare, but egg production, hatchability, and feed conversion are affected.

The metabolism of selenium is closely linked to that of vitamin E, and signs of deficiency can sometimes be treated with either the mineral or the vitamin. Vitamin E can spare selenium in its role as an antioxidant, and so some selenium-responsive conditions can also be treated by supplemental vitamin E. In most countries, there are limits to the quantity of selenium that can be added to a diet; the upper limit is usually 0.3 ppm.

The commonly used forms are sodium selenate and sodium selenite and, more recently, organic selenium chelates. Feeds grown on high-selenium soils, fish meal and dried brewer’s yeast are good sources.

Zinc Deficiency

Zinc requirements and signs of deficiency are influenced by dietary ingredients. In semi-purified diets, it is difficult to show a response to levels much above 25-30 mg/kg diet, whereas in practical corn-soy diets, requirement values are increased to 60-80 mg/kg. Such variable needs likely relate to phytic acid content of the diet, because this ligand is a potent zinc chelator. If phytase enzyme is used in diets, presumably the need for supplemental zinc will be reduced.

In young chicks, signs of zinc deficiency include retarded growth, shortening and thickening of leg bones and enlargement of the hock joint, scaling of the skin (especially on the feet), very poor feathering, reduced feed utilization, loss of appetite, and in severe cases, mortality. While zinc deficiency can reduce egg production in aging hens, the most striking effects are seen in developing embryos. Chicks hatched from zinc-deficient hens are weak and cannot stand, eat, or drink. They have accelerated respiratory rates and labored breathing. If the chicks are disturbed, the signs are aggravated and the chicks often die. Retarded feathering and frizzled feathers are also found. However, the major defect is grossly impaired skeletal development. 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.
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