Vitamin Deficiencies in Poultry
Vitamin A Deficiency
Vitamin D 3 Deficiency
Vitamin E Deficiency
Vitamin K Deficiency
Vitamin B 12 Deficiency
Niacin (Nicotinic Acid) Deficiency
This is also a huge issue with water fowl, not just poultry
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
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.
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.