Deficiencies of vitamins may occur following inappropriate formulation, the use of impotent commercial preparations or destruction of nutrients in feed by oxidation. The significant deficiencies encountered in commercial poultry production include;

• Avitaminosis A
  Chicks will show poor growth and feathering and in advanced cases, ataxia (inability to stand) and xerophthalmia ("dry eye") and chronic purulent conjunctivitis (accumulation of grey caseous material beneath the eyelids).

  Laying hens subjected to avitaminosis A will show a deterioration in internal egg quality and a high prevalence of blood spots. Fertility and hatchability of breeders will be adversely affected. Since vitamin A is concerned with the integrity of respiratory and gastrointestinal mucosa, flocks subjected to avitaminosis A will show a high prevalence of E. coli and other bacterial infections and will be more severely affected by endoparasites.

  Diagnosis of avitaminosis A can be confirmed by microscopic examination of the trachea and oral mucosa. The characteristic change comprises squamous metaplasia, in which normal columnar epithelial cells regress to multiple layers of flattened cells. Both immature and adult flocks will show kidney degeneration and the accumulation of urate in the ureters. In advanced cases urate deposit on the viscera (visceral gout) is observed at postmortem examination.

• Vitamin D3 (Cholecalciferol) Deficiency
  A deficiency in vitamin D3 will lead to rickets in immature flocks. Affected birds aged 4 to 7 weeks show a disinclination to walk. On examination, swelling of the joints is noted together with depressed growth rate and poor feathering. On post-mortem examination decreased skeletal density is evident, costochondral (rib to spine) junctions are enlarged and the end plates of the long bones are irregular due to defective mineral deposition required for osteogenesis (bone formation). Vitamin D3 deficiency results in gross enlargement of the parathyroid glands.

  Rickets can be confirmed by histological examination of the proximal end plate of the tibia.

  In mature laying and breeding stock, a deficiency of vitamin D3 results in osteomalacia characterized by decreased skeletal density. Affected flocks show a gradual decrease in egg production and a marked deterioration in shell quality. Ascending mortality is associated with paresis and paralysis in caged hens which are unable to stand to feed and drink.

• Vitamin E Deficiency
  Vitamin E is required in complex biochemical functions. Three specific deficiency conditions occur in young chickens.

  Encephalomalacia occurs in chicks fed diets in which vitamin E has been destroyed by oxidative rancidity. The presence of free radicals will result in destruction of vitamin E both in the feed and in vivo.

  Transudative diathesis occurs in chicks fed diets deficient in vitamin E or containing free radicals. Transudative diathesis results from degeneration of the endothelium (lining of the blood vessels) resulting in leakage of plasma into surrounding tissues. Transudative diathesis can be partly reversed by supplementation of diets with adequate quantities of selenium. (0.1 to 0.3 ppm)

  Muscular Dystrophy occurs in the skeletal muscles, the ventriculus (gizzard) and myocardium (heart muscle). The effect of avitaminosis E is exacerbated by concurrent deficiency in sulphur-containing amino acids and selenium.

  Encephalomalacia is the most commonly encountered condition associated with avitaminosis E in tropical countries. Onset is at approximately 10 - 20 days of age and may result in the death of up to 10% of the flock. Infected birds demonstrate ataxia, incoordination, and terminal recumbency with cycling motions of the legs. The characteristic lesion comprises punctate hemorrhages within the cerebellum and occasionally the cerebrum. Malacia (softening) of the brain is evident. The condition can be confirmed by histological examination of brain tissue from affected birds.

  The differential diagnosis of ataxia includes avitaminosis A, avian encephalomyelitis (epidemic tremor), thiamine and pyridoxine deficiencies. Recently, arenavirus infection has emerged which leads to hypoglycemia shown as recumbency and tremors. Organophosphate toxicity which causes incoordination and death preceded by convulsions is usually rapid in onset and involves the entire flock.

  Flocks showing nutritional encephalomalacia will respond to administration of water dispersable vitamin E and stabilization of diets with antioxidants and supplementary vitamin E. Affected birds do not recover.

• Vitamin K Deficiency
  This condition occurs in caged flocks fed rations deficient in vitamin K. Subcutaneous hemorrhages are noted on the head and beneath the wings of affected birds. On post-mortem examination sub-serosal hemorrhage is evident. The condition can be diagnosed by determining the prothrombin time which is delayed from a normal 20 - 30 seconds to values exceeding 5 minutes. Differential diagnoses for vitamin K deficiency include hemorrhagic syndrome, mycotoxicosis, and anticoagulant rodenticide toxicity.

• Vitamin B1 (Thiamine) Deficiency
  This condition occurs as a result of failure to add thiamine to vitamin premixes or occasionally as a result of excessive addition of the anticoccidial, amprolium, to diets. The principal sign of thiamine deficiency in 10 to 20 day old chicks comprises incoordination and an abnormal retraction of the head ("star gazing"). There are no macroscopic lesions associated with thiamine deficiency.

• Vitamin B2 (Riboflavin) Deficiency
  This condition is characterized by rotation of the legs in chicks aged 10 - 30 days, and is referred to as "club foot" or "curled toe paralysis". Affected flocks will demonstrate low growth rate and poor feathering. Breeding flocks fed diets deficient in riboflavin show low egg production and hatchability. Histological examination of the major peripheral nerve tracts will show myelin degeneration.

• Biotin Deficiency
  Affected flocks demonstrate poor growth and feathering and elevated mortality. The principal sign comprises dermatitis of the feet and of the skin adjacent to the angle of the beak. These changes also occur with pantothenic acid deficiency. In breeding flocks, hatchability is lowered and embryonic malformations of the feet are noted.

• Other Vitamin Deficiencies
  Deficiencies of pantothenic acid, niacin, pyridoxine and folic acid can be reproduced under experimental conditions. These avitaminoses are seldom diagnosed as single entities in commercial poultry in tropical countries but contribute to a general pattern of poor growth and depressed reproductive efficiency.

• Calcium and Phosphorus Deficiency
  In immature flocks a deficiency of either calcium or available phosphorus or an imbalance in these nutrients will result in rickets. In laying hens and breeders, osteomalacia may occur. Calcium and phosphate deficiencies may be diagnosed by histological examination of bones and the parathyroid gland, bone ash determinations, and analyses of representative feed samples.

• Manganese Deficiency
  Manganese deficiency leads to chondrodystrophy which results in deformation of the distal tibiotarsus and proximal tarsometatarsus. In extreme cases displacement of the gastrocnemius tendon occurs (perosis or "slipped tendon").

• Sodium and or Chloride Deficiency
  Failure to add supplementary salt to poultry diets comprising maize and soybean meal will result in depressed growth rate and decreased egg production. Young chicks will show tail picking and cannibalism.

• Zinc Deficiency
  Deletion of zinc from the mineral premix will result in decreased growth rate and chondrodystrophy.

It is necessary to implement a comprehensive quality control program to monitor the nutritional value and composition of ingredients and to ensure thorough mixing and correct identification of diets. Standard operating procedures consistent with industry practice should be developed and a quality control program implemented based on laboratory analysis and a review of production records. A commitment to the principle of total quality management generates the following benefits:

• enhanced performance of flocks by obviating toxicity and deficiency in diets.
  
• improving client and in-company acceptance of feeds.
  
• improved market share and profitability.