PubMed · 4020814
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1985. Mycotoxins.. https://pubmed.ncbi.nlm.nih.gov/4020814/
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The detection and correction of dietary errors plays an important role in avian medicine. Examples of diseases caused in part by a deficiency or abundance of a nutrient include hypovitaminosis A in birds of the parrot (Psittacidae) family, hypocalcemia in the African grey parrot, goitre in budgerigars, and iron storage diseases in the minah and toucan. Hypovitaminosis A can lead to metaplasia of mucous membranes, which in turn can lead to chronic rhinitis and respiratory fungal infections. Vitamin A deficiency is caused by feeding a seed based diet. Seed mixtures are often deficient in calcium, and nutritional secondary hyperparathyroidism can develop if an additional source of calcium, in the form of ground shells, is not provided. Tetanic symptoms as a result of hypocalcemia are only seen in the African grey parrot and the timneh parrot. Over supplementation of vitamin D gives rise to poisoning with polyuria and polydipsia as common initial symptoms. The exact cause of iron storage diseases in toucans and minahs is not known. A diet low in iron and vitamin C is advised as therapy. Goitre can develop in budgerigars as a result of iodine-deficient drinking water and provision of a seed mixture based on millet. An unbalanced or multideficient diet can give rise to reproductive disorders, abnormal feathers, or infections as a result of diminished resistance. It is usually not possible to relate the cause of these diseases in a simple way to the composition of the diet. Obesity, which occurs in the galah, Amazon parrot, and budgerigars, can lead to fatty liver and lipoma. A gradual reduction in weight, by means of calorie restriction, is recommended. Commercially available nutritionally balanced bird food is often effective.
Weaning at the age of 3-4 weeks has great consequences for piglets. The consequences of the change from milk to solid food are discussed with regard to the supply of nutrients, the available enzyme capacity of the digestive tract, and the morphological and functional changes in the gut. A number of preventive measures are discussed, with a distinction being made between general measures, measures related to the composition of the diet, and measures related to specific additives. Future research should clarify the mechanism of action of specific additives and pay more attention to the uptake of nutrients in piglets in the period just after weaning.
The interactions between T. congolense infection and nutritional supplements on onset of puberty and age at first lambing were observed in 24 young Djallonké ewes. As experimental design, a randomised complete block design was used with four treatment combinations, of which two were kept on a restricted diet (L), the remainder on an unrestricted diet (H) and half of each nutritional group being infected with T. congolense (LI and HI), the remainder serving as controls (LC and HC). Infection with T. congolense took place at an average age of 6 months and 15 days. Mortality due to trypanosome infection was zero and clinical symptoms were not obvious. Intensity of parasitaemia and packed cell volume (PCV) drop following trypanosome infection were similar in both infected groups (HI and LI). High dietary supplementation resulted temporarily in a better haematopoietic response following trypanosome infection, measured as a macrocytic anaemia. Dry matter intake (DMI) was significantly depressed in the HI group immediately following infection. Trypanosome infection had a negative effect on live weight gain during the chronic phase, with the difference being most obvious in the HI group (interaction diet x infection; p< or =0.05). Whereas trypanosome infection had no significant effect, high supplementary feeding significantly reduced the age at first cycling. Age at first lambing was similarly reduced by the diet. Trypanosome infection tended (p< or =0.09) to delay age at first lambing with a mean difference of 31.5+/-22.4 days between infected and controls. Interactions between diet and infection for age at first cycling/lambing were not significant, indicating these effects were just additive. Neither birth weights nor growth rates of offspring born to the experimental animals were significantly affected by previous trypanosome infection, nor by the diet of the dam. In contrast, lamb mortality up to 3 months of age was significantly increased by infection of the dam and most losses arose in group LI. In conclusion, the effects of trypanosome infection on puberty and age at first lambing were indirectly mediated through depression of growth rates. Nutritional supplementation enabled a better erythropoietic response to T. congolense infection and better offspring survival rates but resulted in more depressed weight gains. The results however clearly indicated the delaying effect of insufficient feeding on onset of puberty and reproductive performance in young Djallonké sheep.