Vitamins are an essential component of a well-balanced diet and their major function is the metabolism and utilization of nutrients. The recommended dietary inclusion of vitamins is aimed at preventing clinical deficiencies by administration of specific vitamins. Under commercial conditions, dietary nutrients are considered adequate when economic parameters such as growth and reproduction are adequately taken care.
The vitamin deficiency syndrome is a gradual process, and this influences various metabolic and biochemical reactions in vivo. The signs of vitamin deficiency should be referred to as marginal, sub-clinical and clinical. Through research into the biological mechanisms of vitamin action, it has now been established that substantially higher intake of some vitamins may significantly influence the immune process in chickens.
In field conditions, the chicken is exposed to a variety of stress factors which may adversely influence the immune system. For a practical disease control program, proper vaccination procedures and an efficient immune system leading to optimum response are essential. Until recently most of the studies overlooked the potential role of vitamins in optimizing immune response in the chicks, particularly in response to infections from bacteria and viruses.
The conditions under which suboptimal immune response is often observed include infectious bursal disease, malabsorption syndrome, Reovirus infections, Adenovirus infections, Marek's disease, chicken anemia agent, mycotoxins, coccidiosis, stress factors and others. An effective disease prevention program may be provided by proper vaccination and suitable supplementation with a given vitamin to provide optimum immune response.
In commercial poultry, a number of therapeutic substances are being used in combating various pathogens. The ultimate success of therapeutics is based not only on the direct effect on a pathogen, but also efficiency of the immune response. Therefore vitamin supplementation may be used as an adjunct to both therapeutic and prophylactic treatments.
Vitamin A is essential for the integrity of epithelial tissues, which represent a major defense against the entry of pathogens. The effect of vitamin A deficiency on growth and development of chicken is well documented. Recent studies in broiler chickens have shown to have a detrimental effect on lymphoid tissues in vitamin A deficient chickens. Chickens receiving 0.2 ug vitamin A/g in their diet have relatively smaller bursa of Fabricius than the chicks receiving 2.0 ug vitamin A/g. Thymus weight is only decreased with total vitamin A deficiency.
Following primary immunization, the chickens deficient in vitamin A show the lowest antibody titer. The difference in antibody titer is the maximum on 7th day post-immunization. Supplementation of Vitamin A either on the day of vaccination or few days afterwards increased antibody titer. It has been demonstrated that the optimum HI titer against Newcastle disease was obtained when the feed contained 20,000 I.U. Vitamin A per kg of feed.
Biotin is required in several enzymes particularly for trans-amination and decarboxylation of amino acids. It has been demonstrated that double the NRC requirement of biotin is required for optimum antibody production in infected flocks.
Pyridoxine (vit. B-6) is essential for the development and maintenance of lymphoid tissues. Pyridoxine deficient birds exhibit reduced capacity to synthesize DNA and there is therefore an adverse effect on cell multiplication and the immune function. The marginal deficiency of vitamin B-6 (0.95%) results in a significant reduction in antibody levels. However, it has been demonstrated that marginal B-6 deficiency alone does not severely impair immune response during the first four weeks of age.
Under normal conditions, Vitamin C (ascorbic acid) is synthesized in sufficient amounts by all species of poultry. However, under prolonged exposure to stress the ascorbic acid utilization may exceed the ability of chicken and turkeys to synthesize ascorbic acid. It is observed that ascorbic acid supplementation increases that HA level from 4 to 6 days post-vaccination. The mechanism by which ascorbic acid ameliorates steroid mediated immuno-suppression is either by reducing adrenal synthesis of corticoids or by protecting the lymphoid tissues.
Chicks from breeders with higher levels of vitamin E (alpha tocopherol) have significantly higher levels of antibodies. In E.coli infection the effect of vitamin E on humoral immunity and phagocytosis was investigated in broilers. The mortality among the vitamin E supplemented groups was significantly reduced which appeared to be aided by improved phagocytosis. The phagocytosis was three to four times faster in all immunized and vitamin E. The chicken receiving higher vitamin E in the diet showed an increase in the weight of the spleen and liver which corresponded to a directly proportional increase in the HA antibody titers. This increase in volume of lymphatic organs is accompanied by an increased production of antibodies. It was concluded that supplementation with vitamin E at 300 IU/kg in the diet may be a useful adjunct to vaccination procedures, as well as protection against E. coil infections.
The influence of higher doses of vitamin E on immune response against Newcastle disease was measured. It was reported that higher doses of vitamin E (300 IU/kg feed) were effective in improving immune response against both the viral and bacterial infections. The target of vitamin E is T cells and the effect of vitamin E is more pronounced when antigens are administered at higher concentrations. Optimum vitamin E supplement response is during the age when the immune system is developing i.e. between 3-4 weeks. However, there is evidence that immune response may be enhanced with 300 IU vitamin E/kg of feed even after the age of 4 weeks.
Dietary supplementation with vitamin E reduced mortality and increased body weight gains of non-immunized chickens infected with 150,000 oocysts of E. tenella. Vitamin E supplementation enhances immunization of chickens against coccidiosis.
