1.  Vitamin deficiencies are most commonly due to inadvertent omission of a vitamin premix from the birds’ diet.  Birds that are fed an adequate diet made up from a good commercial feed are unlikely to suffer from nutritional problems unless there are additional factors involved.

2. On the other hand, village, backyard or scavenging poultry are subject to the availability of food in their normal environment, which may occasionally be seasonally deficient in vitamins, minerals or other important dietary components.

3.  Adequate dietary supply.  Vitamin destruction in feeds is a factor of time, temperature, and humidity.  For most feeds, vitamin efficiency is little affected over 2-mo storage within mixed feed.

4.  Knowledge and experience  Testing of formulas  Quality control.  Improper formulation vitamin and mineral deficiencies lack of protection against disease

5.  Health and proper functioning of the skin and lining of the digestive, reproductive and respiratory tracts, and for normal development of bones.

6.  Poor growth.  Poor feathering.  Nasal and ocular discharge.  Drowsiness.  Pale comb and wattles.  Eyelids stuck shut with thick exudate.

7.  Could be fed a vitamin A-deficient diet for 2- 5 mths.  Birds become emaciated and weak with ruffled feathers.  Egg production, hatchability  Embryonic mortality  Watery discharge from the eyes milky white, cheesy material, making it impossible for the birds to see (xerophthalmia).

8.  Mucous glands of the alimentary tract.  The normal epithelium of the glands is replaced by a stratified squamous, keratinized layer, which blocks the ducts of the mucous glands, resulting in distention and necrosis.  Small, white pustules may be found in the nasal passages, mouth, esophagus, and pharynx, and may extend into the crop. Breakdown of the mucous membrane may allow pathogenic microorganisms to invade these tissues and cause secondary infections.

9.  Reared on a vitamin A-deficient diet may show signs within a week.  Chicks with good reserve: 7 wk.  Gross signs in chicks include: Anorexia, growth retardation, drowsiness, weakness, incoordination, emaciation, and ruffled feathers.

10.  If severe, the chicks may exhibit an ataxia similar to that noted with a vitamin E deficiency.  A cheesy material may be noted in the eyes, but xerophthalmia is seldom.  Chronic vitamin A deficiency may also show pustules in the mucous membrane of the esophagus that can extend down the respiratory tract.

11.  Vitamin A in drinking water.  Prevention Supplementation of diet with vitamin A, antioxidant, good quality raw materials.

12.  Bone formation and the metabolism of calcium and phosphorus.  Increasing the absorption of calcium and phosphorus from the gut.  It also mobilizes stores of calcium and phosphorus from the kidney and bone.  In poultry, the effects of vitamin D deficiency include bones and beak that become soft and rubbery as well as reduced growth and egg production.

13.  Rickets in young growing chickens or in osteoporosis and poor eggshell quality in laying hens, even though the diet may be well supplied with calcium and phosphorus.  Laying hens fed a vitamin D-deficient diet exhibit loss of egg production within 2-3 wk, and depending on the degree of deficiency, shell quality deteriorates almost instantaneously.

14.  Retarded growth and severe leg weakness.  Beaks and claws  Loss of equilibrium.  Poor feathering.  With chronic vitamin D deficiency, marked skeletal disorders are noted. The spinal column may bend downward, and the sternum may deviate to one side.

15.  A characteristic finding in chicks is a beading of the ribs at the junction of the spinal column along with downward, and posterior bending.

18.  Confined to the bones and parathyroid glands. Bones are soft and easily broken, and the ribs may become beaded.  Histologic examination shows deficiency of calcification in the long bones.

21.  Adding synthetic D to the diet of susceptible chicks does reduce the incidence of this condition.  Although the response is not dramatic and is quite variable, results suggest that some leg abnormalities may be a consequence of inefficient metabolism of cholecalciferol.

22.  The 3 main disorders seen in chicks deficient in vitamin E are:  Encephalomalacia  Exudative diathesis  Muscular dystrophy.  The occurrence of these conditions depends on various dietary and environmental factors.

23.  Encephalomalacia in commercial flocks  Diets are low in vitamin E  Antioxidant is either omitted or not present  Diet contains a reasonably high level of an unstable, unsaturated fat.

24.  For exudative diathesis : Diet must be deficient in both vitamin E and selenium.  Signs of muscular dystrophy are rare in chicks, as the diet must be deficient in both sulfur amino acids and vitamin E.

25.  Signs of exudative diathesis and muscular dystrophy can be reversed in chicks by supplementing the diet with liberal amounts of vitamin E, assuming the deficiency is not too advanced.  Encephalomalacia may or may not respond to vitamin E supplementation, depending on the extent of the damage to the cerebellum.

26.  The classical sign of encephalomalacia is ataxia.  Exudative diathesis results in a severe edema caused by a marked increase in capillary permeability.  A vitamin E deficiency accompanied by a sulfur amino acid deficiency results in a severe muscular dystrophy in chicks by ~4 wk of age.

28.  Increase Vit. E and Selenium

29.  Nerve and locomotory function.  Signs  Chicks grow slowly  Emaciation  Sprawl on chest  Wings spread out  Curled toe  Clubbed down

30.  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.

32.  Chicks receiving diets only partially deficient in riboflavin may recover spontaneously, indicating that the requirement rapidly decreases with age.

33.  A 100-µg dose should be sufficient for treatment of riboflavin-deficient chicks, followed by incorporation of an adequate level in the diet.  However, when the curled-toe deformity is longstanding, irreparable damage has occurred in the sciatic nerve, and the administration of riboflavin is no longer curative.

34.  Polyneuritis in birds represents the later stages of a thiamine deficiency.  In the initial stages of deficiency, lethargy and head tremors may be noted.

35.  Neuromuscular problems:  Resulting in impaired digestion  General weakness  Star-gazing

36.  Increase Thiamine

37.  Calcium and Phosphorous: A deficiency of either calcium or phosphorus in the diet of young growing birds results in abnormal bone development even though the diet contains adequate vitamin D. The newly hatched chick requires an immediate supply of dietary calcium.

38.  A deficiency of either calcium or phosphorus results in lack of normal skeletal calcification. Diets must provide adequate quantities of calcium and phosphorus to prevent deficiencies.  In laying hens, the provision of Oyster Shells, other broken or coarse ground shells, and/or Limestone grit provides a good source of calcium.

39.  A deficiency of manganese in the diet of young growing chickens is one of the causes of perosis (bone deformities) and of thin- shelled eggs and poor hatchability.  Commercial poultry feeds should be supplemented with a source of available manganese.

40.  Most green feeds contain adequate amounts of manganese, so scavenging poultry should not suffer from a deficiency. However, problems are likely to be encountered in caged birds if the feed does not contain sufficient available manganese.