Pathology of vitamin D deficiency in growing turkeys

Turkey poults were fed a vitamin D-deficient diet and examined for clinical signs and structural changes of bone and parathyroid glands. Vitamin D-deficient poults developed ricketic changes during days 10 to 14. Control poults (deficient diet plus vitamin D) did not develop rickets. In deficient poults, lengths of proliferating-prehypertrophied zones of growth plates increased significantly in the proximal tibiotarsus but were only slightly elongated in the distal tibiotarsus. Unmineralized hypertrophic chondrocyte zones increased in length rapidly in conjunction with a decrease in the length of mineralized hypertrophic degenerative zones; this occurred more rapidly in proximal than in distal tibiotarsus. Other ricketic changes included decreases in bone ash, total femoral bone ash (calcium, phosphorus, magnesium), bone length, and body weight. Plasma alkaline phosphatase was increased, calcium was normal, and phosphorus was normal or elevated. Parathyroids were hyperplastic and had foci of degeneration. Vitamin D3 metabolites 25OHD3, 1,25(OH)2D3, and 24,25(OH)2D3 were rapidly depleted. Increase in bone ash Ca/P ratios in deficient poults suggests that phosphorus may be selectively released from ricketic bone. Low 25OHD3 and 1,25(OH)2D3 of control poults early in the experiment suggests that 1,400 IU of vitamin D3/kg of feed may not be an adequate level of vitamin D3 for growing turkey poults.     

Pathology of experimental vitamin D deficiency in chickens and effects of treatment with vitamin D metabolites

Structural changes in bone, parathyroid, and ultimobranchial body were examined in three groups of chicks fed a vitamin D-deficient diet; one group was treated with vitamin D3 and another with 1,25(OH)2D3. Diets were fed from day of hatching until 5 weeks old, when deficient chicks were near death due to hypocalcemic tetany, loss of fat and muscle, and marked bone deformities. In deficient chicks, parathyroid mass increased linearly to 7.5 times normal at 5 weeks. Parathyroid cells were irregular and vacuolated, with few granules. 1,25(OH)2D3 had normal parathyroids until the fifth week, when parathyroid mass increased greatly. There were few differences in length of growth cartilage, but marked changes in length of metaphyses. Deficient chicks had metaphyses nearly five times longer than vitamin D3-treated chicks. Metaphyses in chicks given 1,25(OH)2D3 were twice as long as those of vitamin D-treated chicks at 5 weeks. Both osteoblasts and osteoclasts were more numerous in deficient chicks. These studies suggest that vitamin D3 is more effective than 1,25(OH)2D3 in preventing parathyroid and bone lesions of vitamin D deficiency.     

An osteodystrophy apparently caused by vitamin D deficiency in growing pigs

An osteodystrophy with features of both rickets and fibrous osteodystrophy was diagnosed in growing pigs housed indoors and fed on a diet deficient in vitamin D. Affected pigs were severely lame and preferred to remain recumbent. At necropsy, the long bones had reduced breaking strength and in one tive-month- old pig the articular surfaces of both proximal humeri were indented due to collapse of subchondral bone.

Microscopic changes in the bones included prominent osteoclastic activity in the proximal metaphyses, variable myelofibrosis, trabecular microfractures, and focal thickening of the hypertrophic zone in some growth plates.

Treatment consisted of an injection of Vitamin D₃, addition of dicalcium phosphate to the diet for 18 days and long-term supplementation of the diet with fat-soluble vitamins. This is the first report of an osteodystrophic disease in pigs in New Zealand.     

An osteodystrophy apparently caused by vitamin D deficiency in growing pigs

An osteodystrophy with features of both rickets and fibrous osteodystrophy was diagnosed in growing pigs housed indoors and fed on a diet deficient in vitamin D. Affected pigs were severely lame and preferred to remain recumbent. At necropsy, the long bones had reduced breaking strength and in one five-month-old pig the articular surfaces of both proximal humeri were indented due to collapse of subchondral bone. Microscopic changes in the bones included prominent osteoclastic activity in the proximal metaphyses, variable myelofibrosis, trabecular microfractures, and focal thickening of the hypertrophic zone in some growth plates. Treatment consisted of an injection of Vitamin D3, addition of dicalcium phosphate to the diet for 18 days and long-term supplementation of the diet with fat-soluble vitamins. This is the first report of an osteodystrophic disease in pigs in New Zealand.     

Management and prevention of vitamin D deficiency rickets in captive-born juvenile chimpanzees (Pan troglodytes).

Vitamin D deficiency rickets was diagnosed in three juvenile chimpanzees (Pan troglodytes) raised indoors under skylights and consuming only breast milk. Two cases detected early had mild but characteristic radiographic changes. More advanced disease presented with florid x-ray features of rickets and pathologic fractures, as well as hypocalcemia, hypophosphatemia, and low serum 25-hydroxyvitamin D levels. Treatment by a single injection of vitamin D2 in sesame oil (slow release) followed by daily oral supplementation with vitamin D2 corrected the condition. On the basis of experience with these cases and comparison with rickets in humans, a prevention protocol for mother-reared, inside-housed, chimpanzee juveniles was developed. Injection with slow release vitamin D2 (5,000 IU i.m. once) at 4 mo of age, followed by oral supplementation of 400 IU vitamin D2 daily until weaning, prevents rickets in juvenile chimpanzees raised indoors.     

Rickets associated with vitamin D deficiency in young sheep

An outbreak of rickets in sheep under a year old (hoggs) appeared clinically as stiffness and rotation of the carpal joints. Histological studies confirmed the diagnosis and biochemical analyses of blood demonstrated a primary vitamin D deficiency.     

Ultrastructure of thyroid C cells in sheep treated with vitamin D3.

Ultrastructural observation was performed in C cells of sheep injected intramuscularly with a dose of 2 million IU of vitamin D3 daily for 10 days, 20 days and 30 days, respectively. After treatment with vitamin D3, hyperplasia and hypertrophy of C cells were noticed mainly at the periphery of the thyroid follicles. Most of hypertrophied C cells degranulated conspicuously and contained many prosecretory granules near the well developed Golgi apparatus which were in the actively secreting and packaging phase of their secretory cycle. The other C cells had prominent lamellar arrays of rough-endoplasmic reticulum and aggregations of free ribosomes in the cytoplasm which were interpreted to be in the actively synthesizing phase of their secretory cycle. Atrophic C cells which contained degenerative organelles in the cytoplasm were occasionally observed among the hypertrophied C cells. The present ultrastructural findings clarified that C cells synthesize and secrete calcitonin continuously due to prolonged hypercalcemia induced by long-term administration of excessive doses of vitamin D3 in sheep.     

Disorders of the parathyroid glands

The three calcitropic hormones, parathyroid hormone (PTH), 1,25-dihydroxycholecalciferol and calcitonin are together responsible for calcium homeostasis in the mammal. Feline PTH is an 84 amino acid, single chain polypeptide with a molecular weight of 9449, which is secreted by the parathyroid glands. The principle secretagogue for PTH is a low plasma ionised calcium concentration, although both 1,25-dihydroxycholecalciferol and phosphate have significant roles in regulating PTH secretion. The ability to accurately measure circulating PTH in the cat has simplified the evaluation of disorders of calcium metabolism in this species. In primary parathyroid disorders the lesion is located within the parathyroid gland, with parathyroid secretion being inappropriate to the prevailing mineral balance. By contrast, in secondary conditions a pathological state out with the parathyroid gland alters mineral homeostasis and the parathyroid gland responds in an appropriate manner. The measurement of circulating PTH may then be used to determine if PTH secretion is appropriate to the prevailing calcium concentrations to differentiate primary from secondary disorders. Although primary hyper and hypoparathyroidism are generally considered rare endocrine conditions of the cat, the ability to measure PTH has led to their increasing recognition.     

Histomorphometry and vitamin D metabolism of valgus-varus deformity in broiler chickens

Vitamin D metabolite levels and tibiotarsal histomorphometric characteristics were determined in 49-day-old male broilers. Valgus-varus bone deformity was present in 5.2% and tibial dyschondroplasia (TD) in 3% of these broilers, which were raised on floor litter under seemingly normal nutritional, space, and lighting conditions. No significant weight differences were observed between normal and lame broilers. The plasma levels of 25-OH-D were the same in lame and normal broilers. However, 1,25-(OH)2D plasma levels were reduced 28% in broilers with valgus-varus deformities but normal in broilers with TD. Anatomically, there were three different patterns of bone development in the undecalcified mid-diaphyseal sections. The pattern with the least periosteal growth, lowest tetracycline labeling, and smallest marrow cavity was most often seen in valgus-varus deformities. Patterns with greatest periosteal growth, high tetracycline labeling, and larger marrow cavities were more representative of normal broilers. It was hypothesized that defective prostaglandin metabolism reduced 1,25-(OH)2D levels, contributing to the overall reduction in bone formation and bone resorption observed in broilers with valgus-varus bone deformity.     

Pathology of experimental vitamin D deficiency in turkeys and the effects of various vitamin D supplements.

One-day-old poults fed a vitamin D3-deficient diet were examined for clinical, biochemical, and morphological changes at 14 days of age. Changes in these parameters were compared at 15.5 and 17 days of age after one of the following vitamin D-replacement therapies was provided: water-soluble vitamin-mineral packs that contained vitamin D3; vitamin D3 in the feed; or vitamin D, 1,25-dihydroxyvitamin D3 in the feed. The vitamin D3-deficient poults were lame and had significant decreases in weight gain and in longitudinal skeletal growth. None of the therapies alleviated all these changes, but clinical lameness subsided in poults provided 1,25-dihydroxyvitamin D3. Calcium concentrations were significantly improved by all therapies. Treatment with vitamin D3 in the feed and water significantly increased 25-hydroxyvitamin D3 concentrations in vitamin D-deficient poults. The growth plate zones, with the exception of the mineralized hypertrophied zone, were all increased in length and not modified by treatment. However, the mineralized hypertrophied zones in the 1,25-dihydroxy-vitamin D3 group and the group receiving vitamin D3 in the water were comparable to that in the controls on day 15.5.     

维生素E缺乏对雏鸡淋巴细胞膜脂质和通透性的影响

维生素E是机体内具有广泛生理功能的重要脂溶性维生素和营养性抗氧化剂,广泛存在于体内储脂器官和生物膜上,具有免疫调节、阻止自由基对组织攻击和维持膜结构的稳定等重要作用[1].     

Intestinal immunomodulation by vitamin A deficiency and lactobacillus-based probiotic in Eimeria acervulina-infected broiler chickens

In a 2 X 2 factorial study, a broiler starter ration was amended for vitamin A (control, C; deficient, A) and probiotic status (-, P) to investigate their modulatory effects onthe host immune system. Birds were inoculated orally with Eimeria acervulina (EA) oocysts, and disease susceptibility was evaluated by assessment of fecal oocyst shedding. Humoral and local cellular mediated immunity were assessed by evaluation of antibody and cytokine (interferon-gamma [IFN-gamma] and interleukin-2 [IL-2]) levels in sera and intestinal secretions on a 3-day interval after inoculation. Fecal oocyst shedding was highest (P < 0.05) in A- birds, followed by AP, C-, and CP birds. Feeding the probiotic reduced shed oocysts by 20% in A fed birds and by 26% in C fed birds. Intestinal IFN-gamma was relatively constant in all treatment groups except for A-, where it declined steadily and was lower (P < 0.05) from day 6 on. Serum IFN-gamma levels fluctuated within each treatment and over time were not revealing. Intestinal IL-2 was highest in CP birds at 3 and 9 days postinfection (DPI) and lowest in A- birds at 3, 9, and 12 DPI (P < 0.05); no difference between treatments was found at 6 DPI (P > 0.05). Eimeria-specific intestinal antibody (Ab) level was constant (P > 0.05) in C- birds but increased with time (P < 0.05) in A-, AP, and CP birds. Serum Ab levels were also constant in A- and CP birds but increased (P < 0.05) in C- and AP birds after 6 DPI. The data demonstrate for the first time a probiotic-enhanced immunity in vitamin A deficient birds. This study is also the first to demonstrate the probiotic effect on local cell-mediated immunity of chickens, best manifested by apparent lower intestinal invasion and development by EA, on the basis of higher IL-2 secretion and lower EA oocyst production.     

Normal vitamin D receptor function with increased expression of 25-hydroxyvitamin D(3)-24-hydroxylase in Corriedale sheep with inherited rickets

A likely inherited disease with gross and microscopic features of rickets has been recognised in Corriedale sheep in New Zealand, and a defect in end-organ responsiveness to vitamin D has been proposed as a likely mechanism. The aim of the present study was to characterize the mode of inheritance and determine the disease mechanism. Breeding trials showed that the mode of inheritance was autosomal recessive. Serum chemistry testing using different methodology and studies in cultured skin fibroblasts did not support our previous hypothesis of a defect in end-organ responsiveness. The studies revealed normal serum 1,25-dihydroxyvitamin D concentrations, normal vitamin D receptor function, and the presence of 24-hydroxylase mRNA in cells from affected sheep, even without induction by 1,25-dihydroxyvitamin D₃. In addition, osteocalcin mRNA expression was similar in both affected and control sheep. It was concluded that increased expression of 25-hydroxyvitamin D₃-24-hydroxylase, the enzyme that breaks down vitamin D, may be involved in the pathogenesis of inherited rickets in Corriedale sheep, but its role requires further clarification.     

Effect of vitamin A deficiency on the activity of macrophages in Newcastle disease virus-infected chickens

The effect of vitamin A deficiency on the activity of peritoneal macrophages (PM) was investigated in noninfected and Newcastle disease virus (NDV)-infected chickens. Day-old chickens with limited vitamin A reserves were fed diets containing either marginal (120 retinol equivalents (RE)/kg) or adequate (1200 RE/kg) levels of vitamin A. At 4 weeks of age, half of the chickens in each group were infected with the La Sota strain of NDV and PM were isolated 11 or 12 days later. These were used for counting the uptake of fluorescein isothiocyanate-labeled yeast cells as an indicator of phagocytic activity and for measuring the reduction of nitroblue tetrazolium (NBT), which provides an estimate of oxygen-dependent killing of microorganisms. Vitamin A deficiency impaired NBT reduction and, to a lesser extent, phagocytosis in both infected and noninfected chickens. NDV infection increased phagocytosis and NBT reduction in normal and, to a lesser extent, in vitamin A-deficient chickens.     

Effects of dietary vitamin E and C supplementation on heart failure in fast growing commercial broiler chickens

1. It has recently been shown that oxidative stress is involved in the pathogenesis of congestive heart failure (CHF) in broiler chickens. Vitamins E and C, common antioxidants, have been advocated for the prevention of heart failure in humans. The present study examines the effects of supplementation of these vitamins on incidence of CHF and prevention of oxidative stress in the myocardium.

2. Commercial male broilers were randomly allocated to three experimental groups and, respectively, offered commercial broiler diet (control), commercial diets fortified with vitamin E (960 IU/kg) or vitamin C (400 mg/kg). The broilers were monitored daily for overt signs of heart failure and clinical data including ECG and blood gas analysis were collected periodically. Lipid peroxidation was measured in cardiac tissues from apparently normal broilers and broilers developing CHF in each group using thiobarbituric acid reactive substances (TBARS) assay.

3. Overall, the incidence of CHF in broilers given diets fortified with vitamin E or vitamin C was not significantly different as compared to the control group. The incidence of overt signs of hypoxaemia was lower in the vitamin C group than in the control group. Lipid peroxidation was highest in broilers that developed CHF as compared to apparently normal broilers fed either vitamin E or C fortified diets. Neither vitamin E nor vitamin C was effective in preventing oxidative damage in broilers that developed CHF.

4. In conclusion, the present study confirmed that oxidative stress is involved in the pathogenesis of heart failure in broilers, but dietary supplementation of antioxidant vitamins did not prevent oxidative damage in broilers that developed CHF. Beneficial effects of vitamin C supplementation were evidenced by lower incidence of hypoxaemia, and the tendency to reduce the susceptibility of broilers to heart failure. However, vitamin E did not have any impact on clinical status or the incidence of CHF.     

Amino acid requirements of growing chickens.

1. Using 18% protein diets (N times 6-25), consisting mainly of conventional ingredients of known amino acid composition, the amino acid requirements as percentages of diet and of dietary protein respectively for broiler chickens between 14 and 28 d of age were found to be: threonine 0-50-0-52% of diet (2-8-2-9% of dietary protein); glycine 0-48-0-50 (2-7-2-8); valine 0-69-0-71 (3-8-3-9); methionine+cystine 0-58 (3-2); isoleucine smaller than 0-48 (smaller than 2-7); leucine smaller than 1-05 (smaller than 5-8); tyrosine+phenylalanine 1-09-1-12 (6-1-6-2); lysine 0-87 (4-8); histidine smaller than 0-34 (smaller than 1-9); arginine smaller than 0-76 (smaller than 4-2); tryptophan smaller than 0-14 (smaller than 0-78). 2. Values found were in general lower than those determined using diets consisting entirely of purified amino acids and the reasons for this are discussed.