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| NUTRITIONAL DISEASES | ||||||||||||||||||||||||||||
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Vitamin Deficiencies
Mineral Deficiencies 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. 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. Manganese Deficiency A deficiency of manganese in the diet of immature chickens is one of the potential causes of perosis and chondrodystrophy, and also the production of thin-shelled eggs and poor hatchability in mature birds. 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. 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. 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. 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. 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. 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. 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. 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. Zinc Deficiency 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. 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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| Division of Veterinary and Animal Husbandry Extension Education Faculty of Veterinary Sciences and Animal Husbandry, R.S. Pura, SKUAST Jammu | ||||||||||||||||||||||||||||