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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.
Source: This article has previously been published in THE VETERINARY
NEWS & VIEWS [WEEKLY] and on World Veterinary Association
web site (Oct 23, 2003 - 02:43 PM). |
