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and adversely affect commercial parameters. The causative agents include Eimeria spp, Histomonads, several pathogenic and opportunistic bacteria, bacterial toxins, fungi and their toxins as well as several strains of viruses. All the pathogens tend to persist in poultry environments and infections become endemic in commercial flocks. The clinical disease may vary significantly from subacute with minimal clinical symptoms to an acute form with classical symptoms and often with significant mortality. The significant economic effect of gastroenteritis results from poor digestion and absorption of nutrients from the feed as well as rapid passage of nutrients due to excessive intake and excretion of water. The loss of water-soluble nutrients through excessive loss of intestinal water such as water-soluble vitamins is often not fully appreciated in practice. Similarly the intestinal dysfunction significantly influences the bioconversion and transportation of vitamins essential for metabolic functions.
Block to absorption
Vitamins are absorbed intact from the intestinal contents active and passive processes into the mucosal cells lining the intestine. The integrity of mucosal cells is not only essential for the absorption of vitamins but also for the bioconversion or activation for some vitamins prior to being absorbed into the blood circulation. The absorption of fatsoluble vitamins (A, E &D3) in excess of normal physiological and metabolic requirements results in storage in the liver in case vitamin intake or absorption is inadequate. Storage and availability of fat-soluble vitamins in day old chickens depends upon the maternal supply of vitamins into fertile eggs, which are ultimately transferred to the liver prior to hatching.
VITAMIN
on all the major visceral organs that contribute directly or indirectly to the most commonly recognised signs and lesions. The toxins affect all body organs, however the most common signs exhibited under practical conditions are invariably related to the function of those organs. The signs commonly observed in chickens as a result of mycotoxin intake invariably relate to organs such as liver, kidneys, reproductive tract, bursa, skeleton, vascular system and gastrointestinal tract. The adverse effects associated with mycotoxins include lesions of the mucous membranes, dermal and footpad lesions, bursal atrophy, fatty infiltration both of liver and kidneys, bile duct proliferation, etc. The clinically recognised parameters include depressed appetite, lesions in the mouth, gizzard and intestines, thin egg shell, decreased fertility and hatchability, poor feathering, poor growth rate and feed conversion, immunosuppression, bruising, diarrhoea and rickets.
ability and growth up to 14 days (Table 3), whilst Jadev and colleagues (1997) found that in 7-week old chicks, weight gain could be improved from 1315 to 1658 g by B-complex supplementation. The effect of gradual depletion of vitamins has also been demonstrated in controlled studies (Table 4). In adult hens the inadequate supplement or deficiency of vitamins is expected to affect not only gradual decline in egg production, and in breeder flocks adversely affects fertility, hatchability and the liveability of the progeny.
Both the pathological and clinical signs of mycotoxicosis resemble the signs that result from vitamin deficiencies. Vitamin deficiency symptoms are the direct result of incomplete or absence of specific vitamin participation in the biochemical and metabolic pathways necessary to utilise nutrients and maintain tissue integrity. The mechanism of mycotoxin induced tissue and organ damage is the result of complex biochemical processes that may react with other enzymes and cofactors (Table 5). Absorption and bioconversion of vitamins may be adversely affected due to cell membrane damage caused by mycotoxins and their metabolites in organs such as the gastrointestinal tract, liver or the kidneys. These arguments lead to the evaluation of whether mycotoxins induce vitamin deficiency-like signs are due to: 1. Higher requirement of specific vitamins to metabolise toxins 2. Vitamins required to eliminate toxin metabolites from the tissues 3. Vitamins are destroyed by mould growth in the feed ingredients 4. Lower intake of vitamins due to appetite depression and reduced feed intake 5. Nutritional interaction or some unknown factors 6. Tissue regeneration to repair organ damage 7. Protein synthesis such as antibody production as a result of immunosupression.
WORLD POULTRY -Vitamin special 2001
Figure 3. Aflatoxin B1 (1mg/kg) and response to biotin supplementation (200mg/kg) (adapted from Bryden et al., 1979)
plasma; thiamine, pyridoxine, pantothenic acid, choline, folate and niacin decreased by more than 19% in the liver. These results suggest that aflatoxins significantly influence the vitamin status of the chicken and are therefore implicated in inducing vitamin inadequacy in affected flocks.
Supplementation vital
Apart from measuring vitamin status, there have been several studies reporting the response to vitamin supplementation to improve specific economically important parameters, which are measurable in practical terms. The high incidence of thin eggshells and broken eggs can be reduced significantly by supplementation of ascorbic acid in the feed as illustrated in Figures 1 and 2. Similarly, accumulation of lipids in visceral organs may be reduced by adequate supplementation of biotin in the feed (Figure 3). Fat-soluble vitamins normally have reason-
able tissue reserves that can only be maintained with adequate supplementation in the feed to prevent appearances of deficiency signs. Vitamin E is important for its antioxidant functions in the body and maintaining its tissue levels by adequate supplementation would be necessary during mycotoxicosis (Table 7). Vitamin E is very important in maintaining immune function; therefore during mycotoxicosis substantially higher supplementation may be necessary to meet normal physiological requirements. Under practical conditions, supplementation of vitamins is frequently practised to alleviate clinical signs or to improve commercial parameters suggestive of mycotoxicosis in the flock. The application or involvement of vitamins in mycotoxicoses is summarised in Table 8 as a guide for practical considerations. The level and duration of vitamin supplementation varies widely depending upon personal experience in the field and the incidence of mycotoxicosis. For the proper use of vitamins a basic understanding of their function and application is essential to achieve practical results.
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