cholecalciferol and Poultry-Diseases

Several excellent reviews regarding nutrition and skeletal disorders have appeared in the last 20 yr. This review will cover several areas of vitamin D research, the area of feed deprivation, and bone abnormalities, because there has been considerable interest in these areas during the past 10 yr. Studies indicate that the quantitative requirement for cholecalciferol (D3) for broiler chickens is much greater than previously thought. Ascorbic acid may play a role in stimulating 1-hydroxylation of 25-hydroxycholecalciferol [25-(OH)D3], but the evidence is not clear under exactly what conditions this relationship is important in practical prevention of tibial dyschondroplasia. Studies indicate that dietary supplementation with 1,25-dihydroxycholecalciferol [1,25(OH)2D3] will reduce the incidence of tibial dyschondroplasia in three different strains of broilers bred to develop a high incidence of the disease. But it did not prevent the disease totally in the strains, unless high enough levels of 1,25-(OH)2D3 were fed to reduce growth rate. These studies indicate that these high tibial dyschondroplasia strains have a defect(s) in vitamin D metabolism. Studies continue to elucidate the role of ultraviolet light in preventing leg abnormalities. Only a few studies have been conducted on the efficacy of various vitamin D3 derivatives to prevent tibial dyschondroplasia. Feed deprivation continues to be an intriguing method of preventing tibial dyschondroplasia, and examination of exactly how this prevents the bone abnormality could open avenues for explaining the disease.

Topics: Animal Nutritional Physiological Phenomena; Animals; Bone Diseases; Cholecalciferol; Food Deprivation; Nutritional Requirements; Osteochondrodysplasias; Poultry Diseases; Rickets; Tibia; Ultraviolet Rays

Turkey osteomyelitis complex (TOC) is defined by the US Food Safety Inspection Service (FSIS) to include normal-appearing processed turkey carcasses that contain lesions including green discoloration of the liver, arthritis/synovitis, soft-tissue abscesses, and osteomyelitis of the proximal tibia. The lesions are associated with many different opportunistic organisms, mainly Staphylococcus aureus and Escherichia coli, suggesting that TOC incidence may be influenced more by deficiencies in the host immune response rather than by the virulence of any one organism. This syndrome is primarily a disease of adolescent male turkeys, and birds with TOC lesions have decreased indices of cell-mediated immunity, leading to the hypothesis that defects in the immune response of individuals within flocks of male turkeys may be responsible for the occurrence of these opportunistic infections. We have developed an experimental model for this disease in which treatment with dexamethasone (DEX), either with or without air sac inoculation with Escherichia coli, produces all of the lesions associated with TOC. These studies suggest that TOC is a result of stress-induced immunosuppression in a subpopulation of male turkeys that respond to the stressors in modern poultry production in a detrimental manner. Supplemental vitamin D3 treatment protected male turkeys from the immunosuppression induced by multiple treatments with DEX and resulted in decreased incidence of mortality, TOC, green liver, and isolation of bacteria from tissues, lower air sacculitis scores, and lower heterophil to lymphocyte ratios than nonsupplemented controls. Vitamin D3 also protected BW; relative weights of the liver, heart, spleen, and bursa; and clinical chemistry values from the effects of DEX treatment. The ability of vitamin D3 supplementation to protect turkeys from the immunosuppressive effects of severe stress emphasizes its role as a prohormone that affects health and disease resistance in turkeys and suggests that variation in the vitamin D receptor genotype may be involved in this disease process. This model has potential value in the identification of other nutritional and physiological immunomodulators that can decrease TOC incidence and will provide a means for the divergent selection of birds more resistant to the stressors of turkey production. In addition, this model will provide justification for management options designed to minimize stress.

Topics: Animals; Cholecalciferol; Dexamethasone; Escherichia coli Infections; Female; Glucocorticoids; Immunosuppression Therapy; Male; Osteomyelitis; Poultry Diseases; Staphylococcal Infections; Turkeys

A study was conducted to evaluate the effects of varying dietary vitamin D3 and stocking density on growing performance, carcass characteristics, bone biomechanical properties, and welfare responses in Ross (308) broilers. Experimental diets, containing 1, 10, or 20 times the NRC recommended level of vitamin D3 (200 IU/kg), were formulated with low, medium, or high vitamin D3 levels for 3 growing phases. Two stocking densities were 10 and 16 birds/m(2). One-day-old hatchlings (1,872 males) were randomly assigned to 6 pens in each treatment. Results showed that high stocking density decreased the feed intake, BW gain (P < 0.01), breast muscle yield (P = 0.010), and tibial development (P < 0.01), whereas increasing feed conversion ratio (P < 0.001), and the scores of gait, footpad and hock burn, and abdominal plumage damage (P < 0.01), particularly toward the age when birds attained their market size. Increasing dietary vitamin D3 improved the birds' walking ability and tibial quality (P < 0.05), and reduced the development of footpad or hock dermatitis and abdominal plumage damage (P < 0.01), some aspects of which were age-dependent and appeared to vary with stocking density. These data indicate that increasing supplemental vitamin D3 has a favorable effect on walking ability and welfare status of high stocking density birds, but not on performance.

Topics: Animal Feed; Animal Husbandry; Animal Nutritional Physiological Phenomena; Animal Welfare; Animals; Biomechanical Phenomena; Blood Chemical Analysis; Bone and Bones; Bone Development; Calcium; Chickens; Cholecalciferol; Diet; Dietary Supplements; Dose-Response Relationship, Drug; Lameness, Animal; Male; Phosphates; Population Density; Poultry Diseases; Spectrophotometry, Atomic; Walking

A study was conducted to evaluate four different cholecalciferol levels (NRC; modified), using diets supplemented with 200 (control), 1500, 2500 or 3500 IU/kg of cholecalciferol (VIT-D3). Each treatment was assigned to 3 pens of 17 broiler chicks of a commercial strain grown in an open-sided house with sidewall curtains. At 21 and 42 days, BW and feed conversion (FCR) were determined. At 42 days, five birds per pen were slaughtered to evaluate tibia and toe ash of the right leg, and incidence and severity of tibial dyschondroplasia (TD) of the left tibia and also measured dressing percentage and breast meat yield. Serum calcium and phosphorus concentrations were also determined. Haemagglutination inhibition antibody titre against Newcastle disease virus and lymphoid organs weight/body weight ratio were also determined. At both 21 and 42 days, the BW of birds fed 1500 IU/kg to 3500 IU/kg of VIT-D3 was significantly greater than birds fed 200 IU/kg. Similarly, better FCR was observed in birds those fed diets of high level of VIT-D3. No significant difference was observed for mortality at any age. Better dressing percentage and breast meat yield were noted in birds fed diets containing 2500 or 3500 IU/kg VIT-D3. Both tibia and toe ash contents were increased (p < 0.05) progressively with increased concentrations of cholecalciferol in feed. The incidence of TD (percentage of birds having TD scores greater than zero) was significantly (p < 0.05) influenced by level of 3500 IU VIT-D3/kg at 42 days. The severity of TD in birds fed diets containing 200 IU/kg VIT-D3 was apparently higher than birds fed diets with higher levels of VIT-D3. Concentrations of calcium and phosphorus minerals in the serum increased progressively with the high level of VIT-D3 supplementation to birds at both 21 and 42 days of age. Feeding levels of 1500 or 3500 IU of vitamin D3 did positively affect the immune system within the parameters measured. It may be concluded that performance, bone mineralization, blood chemistry and immunity against disease in broilers could be maintained when supplementing high level of VIT-D3 incorporated in broiler diets.

Topics: Animal Feed; Animal Nutritional Physiological Phenomena; Animals; Chickens; Cholecalciferol; Diet; Dietary Supplements; Dose-Response Relationship, Drug; Osteochondrodysplasias; Poultry Diseases

Two trials were conducted to determine if thiram-induced tibial dyschondroplasia (TD) in chickens was linked to a vitamin D deficiency and calcium homeostasis dysregulation, and whether feeding vitamin D fortified diets may prevent it. Day-old chickens were given grower diets containing different vitamin D products throughout the experiment until necropsy on day 16. Half of the birds in each feed group received thiram at levels of 100 ppm (trial 1) or 50 ppm (trial 2) between days 7-9 to induce TD. The birds were weighed, bled, and euthanized to determine TD incidences and severity by examining the growth plates. Tibial bones were used to measure biomechanical strength and ash content. Blood concentrations of 25-hydroxyvitamin D, Ca, P, alkaline phosphatase, and creatine kinase were measured in serum that showed no differences between different groups. Thiram reduced body weight and induced TD regardless of any vitamin D treatment to the same extent as untreated birds.

Topics: Animal Feed; Animal Nutritional Physiological Phenomena; Animals; Body Weight; Bone and Bones; Calcitriol; Chickens; Cholecalciferol; Diet; Dietary Supplements; Dose-Response Relationship, Drug; Minerals; Osteochondrodysplasias; Poultry Diseases; Thiram; Vitamin D

Four experiments were conducted using Ross x Ross chicks hatched from broiler breeder hens fed various levels of cholecalciferol (vitamin D3; 0 to 4,000 IU/kg of diet) to determine the effect of the maternal diet on the performance and leg abnormalities of the progeny. Chicks hatched from eggs laid by the hens at different ages were used in experiments 1 to 4. The studies were conducted in an ultraviolet light-free environment as split plot designs, with Ca levels or 25-hydroxycholecalciferol (25-OHD3) in the chicks' diet as the whole plot, and vitamin D3 in the maternal diet as a subplot. Chicks in experiments 1 and 2 were fed 2 levels of Ca (0.63% or 0.90%) and chicks in experiments 3 and 4 were fed 6 levels of 25-OHD3 (0 to 40 microg/kg of diet). Significant increases in body weight gain (BWG) of the progeny were observed in experiments 1, 2, and 4 as the vitamin D3 level in the maternal diet increased. Chicks hatched from eggs laid by hens fed the highest levels of D3 had the highest tibia ash. Significant reductions in Ca rickets incidence (experiments 1 and 2) and tibial dyschondroplasia (TD) incidence (experiment 1) were observed as the level of vitamin D3 in the maternal diet increased. Chicks fed lower levels of Ca had lower BWG and tibia ash and higher incidences of TD and Ca rickets than chicks fed higher levels of Ca. Increasing the level of 25-OHD3 in the chicks' diet significantly improved BWG, tibia ash, and plasma Ca and reduced TD and Ca rickets incidence. An overall evaluation of the study indicates that chicks from hens fed the highest levels of vitamin D3 and fed high levels of Ca or 25-OHD3 had the highest BWG, tibia ash, and plasma Ca, and the lowest incidences of TD and Ca rickets.

Topics: Animal Feed; Animal Nutritional Physiological Phenomena; Animals; Bone and Bones; Calcifediol; Calcium; Chickens; Cholecalciferol; Diet; Dietary Supplements; Dose-Response Relationship, Drug; Female; Male; Poultry Diseases; Rickets; Weight Gain

Experiments were conducted to determine whether dietary 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] will alleviate a cholecalciferol deficiency induced by low dietary cholecalciferol and no fluorescent lighting and to determine cholecalciferol requirements as influenced by fluorescent lighting or 1,25-(OH)2D3. In each study, nutritionally complete basal diets were fed to broiler cockerels from 1 to 16 d of age. Experiment 1 had a 2 x 2 x 2 factorial arrangement of treatments with 1,25-(OH)2D3 at 0 and 10 micrograms/kg, cholecalciferol at 2.75 and 27.5 micrograms/kg, and fluorescent lights on or off. Experiments 2 to 4 had four levels of dietary cholecalciferol (0, 5.0, 27.5, and 50.0 micrograms/kg) and fluorescent lights on or off (Experiment 2) or 1,25-(OH)2D3 at 0 and 10 micrograms/kg (Experiments 3 and 4). In Experiment 1, fluorescent lighting increased bone ash, and decreased the incidence and severity of rickets at 2.75 micrograms/kg cholecalciferol and 0 microgram/kg 1,25-(OH)2D3 and reduced the severity of TD at both levels of cholecalciferol and 0 microgram/kg 1,25-(OH)2D3. In all cases 1,25-(OH)2D3 improved bone ash. The metabolite also decreased the incidence and severity of TD at both cholecalciferol levels with lights off and decreased the incidence and severity of rickets at 2.75 micrograms/kg cholecalciferol and lights off. In the absence of fluorescent lighting and 1,25-(OH)2D3 27.5 micrograms/kg cholecalciferol reduced the incidence and severity of rickets to levels equivalent to those produced by either fluorescent lighting or 1,25-(OH)2D3 alone (Experiments 2, 3, and 4). However, even 50.0 micrograms/kg cholecalciferol was not as effective as fluorescent lights or 1,25-(OH)2D3 in reducing the incidence and severity of TD.

Topics: Animals; Calcitriol; Calcium; Chickens; Cholecalciferol; Diet; Fluorescence; Food, Fortified; Incidence; Lighting; Male; Minerals; Osteochondrodysplasias; Phosphorus; Poultry Diseases; Rickets; Severity of Illness Index; Tibia

Coccidiosis penalizes calcium (Ca), phosphorus (P), and fat-soluble vitamin status, as well as bone mineralization in broiler chickens. We hypothesized that dietary vitamin D (VitD) supplementation in the form of 25-hydroxycholecalciferol (OHD), compared to cholecalciferol (D3), would improve bone mineralization in broilers receiving marginally deficient Ca/P diets, with more pronounced effects during malabsorptive coccidiosis. In a 2 VitD source × 2 Ca/P levels × 2 levels of infection factorial experiment (n = 6 pens per treatment, 6 birds/pen), Ross 308 broilers were assigned to an Aviagen-specified diet supplemented with 4,000 IU/kg of either OHD or D3 between days 11 and 24 of age. The diet contained adequate (A; 8.7:4.4 g/kg) or marginally deficient (M; 6.1:3.1 g/kg) total Ca and available (av)P levels. At day 12 of age, birds were inoculated with water (C) or 7,000 Eimeria maxima oocysts (I). Pen performance was measured over 12 days post-infection (pi). One bird per pen was assessed for parameters of bone mineralization and intestinal histomorphometric features (day 6 and 12 pi), as well as E. maxima replication and gross lesions of the small intestine (day 6 pi). There was no interaction between infection status and Ca/avP level on bone mineralization. Bone breaking strength (BS), ash weight (AW), and ash percentage (AP) were highest in broilers fed the OHD-supplemented A diets irrespective of infection status. Eimeria maxima infection impaired (P < 0.05) ADG and FCR pi; Ca and P status at day 6 pi; OHD status, BS, AW, and AP at day 12 pi; and intestinal morphology at day 6 and 12 pi. A- compared to M-fed broilers had higher BS, AW, and AP at day 6 pi, and AW at day 12 pi. VitD source affected only OHD status, being higher (P < 0.001) for OHD- than D3-fed broilers at day 6 and 12 pi. In conclusion, offering OHD and adequate levels of Ca and P improved bone mineralization, with no effect on performance. Dietary D3 and OHD supplemented at 4,000 IU/kg had similar effects on coccidiosis-infected and uninfected broilers, which led to the rejection of our hypothesis.

Topics: Animal Feed; Animals; Calcifediol; Calcification, Physiologic; Calcium; Calcium, Dietary; Chickens; Cholecalciferol; Coccidiosis; Diet; Dietary Supplements; Eimeria; Intestines; Phosphorus; Phosphorus, Dietary; Poultry Diseases; Vitamins

Clostridial dermatitis (CD) is a production disease of commercial turkeys that is characterized by sudden mortality in market-aged male birds and by lesions that include fluid and air bubbles under the skin of the thigh, breast, and tail area. We have developed a model for CD using dexamethasone (Dex) injection that suggests this disease may be related to stressors during the last stages of turkey production. Male turkeys were provided with control feed and water or with feed supplemented with a commercial yeast extract (YE) product, water supplemented with vitamin D (VD), or the combination. At 6, 11, and 15 wk of age birds were treated with three intramuscular injections of Dex over a 5-day period. Both YE and VD, but not the combination, decreased early mortality. At week 7 mortality was increased by VD, and cellulitis lesions were seen in 7/8 mortalities. Mortality at week 12 was decreased by both YE and the combination of YE and VD, and cellulitis lesions were seen in 8/17 mortalities. There were no significant differences in mortality at week 16. Total mortality was 66 birds, and 23 of these had cellulitis lesions (38%). There were no YE-treated birds with CD lesions; however, 67% of VD-treated birds had CD lesions. This study suggests that feed supplementation with YE may improve the ability of turkeys to withstand the stressors during late production and provide protection against the development of CD; however, high levels of VD supplementation may be detrimental.

Topics: Animal Feed; Animal Nutritional Physiological Phenomena; Animals; Cholecalciferol; Clostridium; Clostridium Infections; Dexamethasone; Dietary Supplements; Drinking Water; Immunocompromised Host; Immunosuppressive Agents; Male; Poultry Diseases; Skin Diseases, Bacterial; Turkeys; Yeasts

Epididymal lithiasis is a reproductive dysfunction of roosters that is associated with loss of fertility and is characterized by the formation of calcium stones in the lumen of the efferent ductules of the epididymal region. The efferent ductules of birds are responsible for the reabsorption of the fluid coming from the testis as well as luminal calcium. It has been hypothesized that the epididymal stone formation may be related to the impairment of local fluid or calcium homeostasis, which depends on hormones such as estradiol (E(2)). Therefore, this study aimed to investigate possible alterations in the expression of ERα (ESR1) and ERβ (ESR2) in the epididymal region of roosters affected by epididymal lithiasis. The study was performed by immunohistochemistry and western blotting assays. In addition, the concentrations of E(2), vitamin D3, and testosterone, which are also key hormones in maintenance of calcium homeostasis, were determined in the plasma and epididymal region, by ELISA. It was observed that ESR2 expression is increased in all segments of the epididymal region of affected roosters, whereas ESR1 levels are not altered. Moreover, the hormone concentration profiles were changed, as in the epididymal region of roosters with lithiasis the E(2) levels were increased and vitamin D3 as well as testosterone concentrations were significantly decreased. These results suggest that a hormonal imbalance may be involved with the origin and progression of the epididymal lithiasis, possibly by affecting the local fluid or calcium homeostasis.

Topics: Animals; Chickens; Cholecalciferol; Epididymis; Estradiol; Estrogen Receptor beta; Gene Expression; Genital Diseases, Male; Immunohistochemistry; Lithiasis; Male; Models, Biological; Poultry Diseases; Testosterone

Epididymal lithiasis is a dysfunction characterized by formation of calcium-rich stones in the epididymal region of roosters, associated with decreased serum testosterone and loss of fertility. The segment most affected by the lithiasis is the efferent ductules, which, in birds, are responsible for reabsorption of calcium and luminal fluid. Therefore, we postulated that epididymal lithiasis could result from local impairment of calcium or fluid homeostasis, culminating in initiation of stone formation. Transepithelial calcium transport depends on vitamin D3 and vitamin D3 receptor (VDR). Based on the fact that VDR are present in efferent ductules, possible changes in the pattern of VDR in roosters affected by the epididymal lithiasis was investigated, to start to gain an understanding of the molecular mechanisms involved in the development of calcium stones. To evaluate the potential impact of androgen reduction, changes in androgen receptor (AR) were also investigated. Both VDR and AR were increased in specific segments of the epididymal region, whereas no alterations were found in the testes of affected animals. The increase in VDR was most likely due to an increase in the number of VDR-positive mononuclear leukocyte infiltrates found in the connective tissue followed by an increase in epithelial receptors. The AR were increased, however, mainly in the epididymal duct epithelium. These results suggest that the vitamin D3 and androgen responsive system may be directly/indirectly involved in the development of the disease.

Topics: Animals; Chickens; Cholecalciferol; Epididymis; Immunohistochemistry; Lithiasis; Male; Poultry Diseases; Receptors, Androgen; Testicular Diseases; Testis

Tibial dyschondroplasia is a skeletal abnormality characterized by an avascular plug of cartilage in the metaphysis of the long bones of rapidly growing birds. An avascular, thickened growth plate also occurs in vitamin D/calcium-deficient rickets. This research was conducted to evaluate tibial dyschondroplasia and rachitic tissue for factors shown to be important in normal growth plate vascularization. Immunohistochemical analysis demonstrated the presence of vascular endothelial growth factor, its receptor Flk-1, and matrix metalloproteinases MMP-9 and MMP-13 to be present in all tissues examined. In most cases, immunostaining was intracellular, except near blood vessels where the matrix was also stained. The results suggest that, for the four proteins examined, disruption of their expression is not a key factor in the development of these avascular cartilage lesions in avians. The relationship of these observations to the pathology of tibial dyschondroplasia is discussed.

Topics: Animal Feed; Animals; Cartilage; Chickens; Cholecalciferol; Diet; Disulfiram; Epiphyses; Gene Expression Regulation; Immunohistochemistry; Male; Matrix Metalloproteinase 13; Matrix Metalloproteinase 9; Osteochondrodysplasias; Poultry Diseases; Rickets; Tibia; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factor Receptor-1

Six experiments were conducted using Ross x Ross chicks hatched from eggs laid by broiler breeder hens fed various levels of vitamin D3 (0 to 4,000 IU/kg of diet) to determine the effects of vitamin D3 level in the maternal diet on the performance and leg abnormalities of their progeny. Chicks hatched from eggs laid when hens were 27, 41, 29, 36, 45, and 52 wk of age were used in experiments 1, 2, 3, 4, 5, and 6, respectively. The studies were conducted in a ultraviolet (UV)-light-free environment. Experiments 1 and 2 were conducted as complete randomized designs with the maternal diets as the treatments, and experiments 3, 4, 5, and 6 were conducted as split plot designs, with vitamin D3 in the chick diets as the whole plot and vitamin D3 in the maternal diet as a subplot. Chicks in experiments 1 and 2 were fed a vitamin D3-deficient diet, whereas chicks in experiments 3 and 4 were fed 4 levels of vitamin D3 (0 to 400 IU/kg of diet), and chicks in experiments 5 and 6 were fed 6 levels of vitamin D3 (0 to 3,200 IU/kg of D3). The highest body weight gains and tibia ash were observed in chicks hatched from hens fed the highest levels of vitamin D3 in all experiments. Reductions in the incidence of Ca rickets were observed in experiments 3 and 6, whereas increases in tibia ash were observed in experiments 2 and 6 as the level of vitamin D3 in the maternal diet increased. Body weight gain and tibia ash increased and Ca rickets incidence decreased as the vitamin D3 level in chick diets increased. An evaluation of the study indicates that chicks hatched from eggs laid by hens fed 2,000 or 4,000 IU of D3/kg as the maximum level of vitamin D3 had the highest body weight gains, and chicks fed 3,200 IU had the highest body weight and tibia ash and the lowest TD and Ca rickets incidences.

Topics: Aging; Animals; Bone and Bones; Chick Embryo; Chickens; Cholecalciferol; Diet; Dietary Supplements; Female; Poultry Diseases; Weight Gain

In the hen, heat stress (HS) disrupts shell calcification and reproductive processes, including hormone synthesis and egg production. Two studies were conducted to investigate palliative effects of exogenous estrogen or dietary vitamin D3 on Ca homeostasis and reproductive physiology during HS. Study 1: Hy-Line W36 hens were randomly assigned to thermoneutral (TN) or HS treatments and to 1 of 7 estrogen treatments: zero (control) or one Compudose 200 implant given 1, 2, 3, 8, 9, or 10 d before onset of HS. With no implant, HS reduced plasma estradiol (E2) and total Ca absorbed (CaT) by duodenal cells (P < 0.05). In TN hens with implants, plasma E2 tripled within 24 h (P < 0.05) and remained elevated (P < 0.05) through d 9. In HS hens with implants, plasma E2 rose 6-fold (P < 0.05) to equal TN+E2 concentrations and remained elevated through d 10. In TN and HS hens with implants, the rate of Ca absorption (CaTR) and CaT increased dramatically; the responses were quadratic and essentially identical. Study 2: Hy-Line W36 hens were provided diets formulated either according to NRC requirements (NRC, 1994), or with the addition of 22,000 IU/kg vitamin D3 (+VD hens). A 24-h HS episode was imposed 2 wk after initiation of the dietary regimen. Duodenal samples were collected for Ca absorption assays after the 24-h HS episode. Both CaTR and CaT in +VD hens were approximately 3-fold higher than in hens in the NVD group (P = 0.102). The results lead to the conclusion that exogenous estrogen, high levels of dietary vitamin D, or both, before a HS episode, are efficacious in alleviating at least some of the effects of HS and should be further investigated.

Topics: Animals; Biological Transport; Calcium; Chickens; Cholecalciferol; Drug Implants; Duodenum; Estradiol; Female; Hot Temperature; Poultry Diseases; Stress, Physiological

1. Two experiments were carried out to investigate responses in performance and bone compositional and structural characteristics in broilers fed diets containing 4 concentrations of vitamin D3 (5, 20, 125 and 250 microg cholecalciferol/kg) at different concentrations of calcium, available phosphorus and vitamin A. 2. In experiment 1, body weight and tibia breaking strength were maximised at 14d with 250 microg vitamin D3/kg, tibia ash was maximised with 125 microg vitamin D3/kg. A high incidence of tibial dyschondroplasia (TD) was decreased to very low levels with 125 microg vitamin D/kg. 3. At 42d, performance and bone characteristics showed no response to vitamin D3 concentrations above 20 microg/kg. 4. Dietary vitamin A within the range 2-4 to 4.5 mg retinol/kg did not show any interaction with vitamin D3 status at either age. 5. In experiment 2, responses to vitamin D3 were strongly influenced by dietary calcium/available phosphorus. With 13 g calcium and 5 g available phosphorus/kg, performance and bone characteristics responded to vitamin D3 concentrations up to 125 microg/kg but more was needed at less optimal concentrations of calcium and available phosphorus. TD incidence was minimised with 250 microg/kg. 6. This study shows that high dietary concentrations of vitamin D3 can prevent TD. It is concluded that the vitamin D3 requirement of broilers up to 14 d of age at optimal dietary calcium and available phosphorus concentrations may be in the range 35 to 50 microg/kg for cortical bone quality and up to 250 microg/kg for prevention of TD. The vitamin D3 requirement for cortical bone quality after 14 d is not higher than 20 microg/kg. These requirements are much higher than earlier estimates and may be related to higher calcium requirements of modern broiler genotypes. Current regulations limiting maximum vitamin D3 concentrations in broiler starter diets may need to be reviewed.

Topics: Animals; Biomechanical Phenomena; Body Weight; Bone and Bones; Calcium, Dietary; Chickens; Cholecalciferol; Diet; Drug Interactions; Growth Plate; Male; Minerals; Nutritional Requirements; Organ Size; Osteochondrodysplasias; Phosphorus, Dietary; Poultry Diseases; Tibia; Vitamin A

Six experiments were conducted to study the effects of exposure of young chickens to u.v. radiation. Chickens were fed a cholecalciferol (D3)-deficient diet and exposed to u.v. radiation from fluorescent lights giving total radiance (285-365 nm) at 0.15 m of 99.9 mJ/s per m(2). In Expt 1, chickens had increased body weight, bone ash and plasma Ca and decreased incidence of rickets and tibial dyschondroplasia (TD) when exposed to fluorescent light radiation 24 h per d, 24 h every 2 d, or 24 h every 3 d starting with exposure on day 1 after hatching. However, when not exposed on day 1, but on days 4, 7, 10, 13 and 16, the bone ash was reduced, and the incidence of TD and rickets was increased, compared with chickens exposed on day 1 after hatching. When chickens were exposed at 1 d of age to radiation from two lamps, each of which gave a radiance (285-365 nm) at 0.26 m of 856 mJ/s per m(2), both the length of time of radiation and location of the lamps (above or below the chicken) influenced the response as measured by body weight, bone ash, plasma Ca and incidence of rickets. When chickens that received a TD-inducing diet were exposed to 30 min u.v. radiation from below at 1 d of age they developed significantly less TD than did those not exposed when fed either 27.5 or 55.0 microg D3/kg diet.

Topics: Animals; Chickens; Cholecalciferol; Dose-Response Relationship, Radiation; Male; Osteochondrodysplasias; Poultry Diseases; Rickets; Tibia; Time Factors; Ultraviolet Rays

Three experiments were conducted with broiler chicks that were divergently selected for low or high incidence of tibial dyschondroplasia (LTD and HTD, respectively) to determine if the expression of intestinal calbindin-28 kD mRNA and protein differed between the 2 strains. In addition, levels of intestinal vitamin D receptor mRNA and plasma thyroid hormone concentrations were also examined. In experiment 1, LTD and HTD chicks were fed a corn-soybean meal diet that was adequate in all nutrients except cholecalciferol (D3), which was titrated to 5 or 40 microg/kg diet in a completely randomized 2 x 2 factorial arrangement. At 4 and 8 d of age, HTD chicks fed 5 microg of D3/kg of diet had a lower (P < 0.05) expression level of calbindin-28 kD mRNA than the LTD chicks fed the same diet. At 4 and 8 d of age, HTD chicks fed 5 microg of D3 had the lowest intestinal expression of calbindin-28 kD protein. Expression of vitamin D receptor mRNA did not differ for broiler strains at either level of D3 supplementation. In experiment 2, there was no significant difference in the expression of calbindin-28 kD mRNA or vitamin D receptor mRNA between day-of-hatch LTD, HTD, and commercial broiler chicks. Experiment 3 was similar in design to the first experiment except that the birds were fed for 18 d. Calbindin-28 kD and vitamin D receptor mRNA expression levels at 18 d were similar to those observed in experiment 1. Plasma triiodothyronine and free-triiodothyronine concentrations were greater for LTD chicks, regardless of dietary D3 supplementation levels. These results suggest that divergent selection of broilers for LTD or HTD alters the physiological response to nutritionally inadequate levels of dietary D3.

Topics: Animals; Calbindins; Chickens; Cholecalciferol; Diet; Gene Expression; Genetic Predisposition to Disease; Intestines; Osteochondrodysplasias; Poultry Diseases; Receptors, Calcitriol; RNA, Messenger; S100 Calcium Binding Protein G; Selection, Genetic; Thyroid Hormones; Tibia

Two experiments were conducted using a corn-soybean meal diet that meets or exceeds the NRC (1984) requirements for all nutrients except cholecalciferol (D3) to determine the effectiveness of 1-alpha-hydroxycholecalciferol (1alpha-OHD3) as a substitute for D3 in the diet of young broilers. Ross x Ross mixed-sex, 1-d-old chicks were reared in Petersime battery brooders not exposed to ultraviolet light with feed and water supplied ad libitum for 16 d. In Experiment 1, D3 was fed at 0, 2.5, 5, 10, 20, and 40 microg/kg and one source of 1alpha-OHD3-(Hoffmann-LaRoche, Inc.; HLR) was fed at 0.625, 1.25, 2.5, 5, and 10 microg/kg of diet. In Experiment 2, the D3 was fed at 0, 2.5, 5, and 10 microg and two sources of 1alpha-OHD3-[HLR and Majestic Research Inc. (MRI)] were fed at 0, 0.625, 1.25, and 5 microg/kg of diet. Slope ratio analysis of data from the measurement of 16-d body weight, plasma Ca, rickets, and bone ash indicated bioavailability of the 1alpha-OHD3 as compared to D3 from 1.88 to 21.2. Percentage bone ash gave the most precise values in both experiments. Considering all the data from both experiments, the 1alpha-OHD3 appears to be approximately eight times as effective as D3 for satisfying the requirements of several criteria in two experiments with broiler chickens.

Topics: Animal Feed; Animal Nutritional Physiological Phenomena; Animals; Biological Availability; Body Weight; Bone and Bones; Calcium; Chickens; Cholecalciferol; Dose-Response Relationship, Drug; Female; Hydroxycholecalciferols; Intestinal Absorption; Male; Minerals; Nutritional Requirements; Poultry Diseases; Rickets

Three experiments were conducted to determine the effect of dietary vitamin K1 (K1) on selected plasma characteristics and bone ash in poults. In Experiment 1, diets were supplemented with 0, 0.5, 1.0, or 2.0 mg of K1/kg. All diets contained 1,650 IU of vitamin D3 (D3)/kg. Dietary K1 had no effect on tibia ash at 7 d or incidence of a severe, rickets-like condition. Tibia ash of poults fed 2.0 mg of K1/kg, however, was greater at 14 d of age than that of poults fed the basal diet. Dietary inclusion of 0.5 mg of K1/kg was as effective as 1 or 2 mg of K1/kg in reducing plasma prothrombin time. In Experiment 2, a 2 x 4 factorial arrangement was used consisting of 1,650 or 550 IU of D3/kg and 0.1, 0.45, 1.0, and 2.0 mg of K1/kg. Dietary D3 and K1 had no effect on bone ash. Dietary inclusion of 0.1 mg of K1/kg seemed to be enough to minimize plasma prothrombin time. In Experiment 3, dietary treatments consisted of a control (1,650 IU of D3 and 2.0 mg of K1/kg) and K1 concentrations of 0, 0.37, 2.28, or 5.33 mg/kg in diets containing 275 IU of D3/kg. Poults fed the low-D3 diet without K1 consumed less feed, gained less weight, and had increased plasma alkaline phosphatase activity, decreased inorganic phosphorus level, and decreased tibia ash (P < 0.05) compared with those of poults fed the control diet. Feed intake and body weight gain were improved, plasma alkaline phosphatase activity decreased, and plasma inorganic phosphorus increased or tended to increase when poults were fed the low-D3 diet supplemented with 0.37 or 2.88 mg of K1/kg compared with poults fed the low-D3 diet without K1 supplementation. Tibia ash of poults fed the low-D3 diet was not affected by K1 supplementation. The results of this research show that dietary K1 concentration had little, if any, effect on bone development in 1- to 14-d-old turkeys.

Topics: Alkaline Phosphatase; Animals; Antifibrinolytic Agents; Bone and Bones; Cholecalciferol; Male; Phosphorus; Poultry Diseases; Prothrombin Time; Rickets; Time Factors; Turkeys; Vitamin D Deficiency; Vitamin K 1

Male turkeys immunosuppressed by injection with dexamethasone (DEX) were given supplemental vitamin D3 in their drinking water in two experiments. In Experiment 1, vitamin D3 was supplemented at a dosage of either 2,064 IU/kg (low level) or 4,128 IU/kg (high level) in drinking water provided ad libitum only from Days 1 through 5 after hatch. In Experiment 2, vitamin D3 was provided at the low dosage for the first 5 d after hatch, followed by treatment with the high dosage for 12 h before and 12 h after each stressful event, which included weekly weighings and two DEX treatments. In both experiments, at 5 wk of age half of the birds were given intramuscular injections of 2 mg/kg DEX on 3 alternating d. In Experiment 1, 100 cfu of Escherichia coli was inoculated into the left thoracic airsac at the time of the third DEX injection. All mortalities were examined, and 10 birds per pen were necropsied 2 wk after treatment and examined for lesions of airsacculitis and turkey osteomyelitis complex (TOC). Four birds per pen were bled before necropsy, and white blood cell total counts, differential white blood cell counts, and clinical chemistry values were determined. In Experiment 2, healthy surviving birds were grown for an additional 5-wk period, after which the DEX-treated birds were given a second series of DEX injections and were bled and necropsied 2 wk later. There were no significant effects of vitamin D3 treatment in combined general linear models analysis of Experiment 1; however, when birds not treated with DEX or E. coli were compared with those treated with both DEX and E. coli, supplementation with the low level of vitamin D3 significantly decreased TOC incidence. There were no significant effects of vitamin D3 treatment in birds treated with DEX at 5 wk of age in Experiment 2. However, when surviving birds were given a second DEX treatment at 12 wk, vitamin D3 treatment resulted in significantly lower incidence of mortality, TOC, green liver, isolation of bacteria from tissues, and lower airsacculitis scores and heterophil-to-lymphocyte ratios than controls. Vitamin D3 also improved BW, relative weights of the liver and heart, and serum levels of glucose and alanine aminotransferase (ALT) of birds receiving two treatments with DEX. The ability of vitamin D3 supplementation to protect turkeys from the immunosuppressive effects of multiple DEX treatments emphasizes the role of vitamin D3 as a prohormone that affects health and disease resistance in t

Topics: Alanine Transaminase; Alkaline Phosphatase; Animals; Aspartate Aminotransferases; Blood Glucose; Body Weight; Cholecalciferol; Creatine Kinase; Dexamethasone; Escherichia coli; Escherichia coli Infections; Glucocorticoids; Least-Squares Analysis; Leukocyte Count; Linear Models; Liver; Lymphocyte Count; Lymphocyte Subsets; Male; Osteomyelitis; Poultry Diseases; Random Allocation; Stress, Physiological; Turkeys; Uric Acid

Three experiments were conducted to test the potencies of nine sources of cholecalciferol using a chick bioassay. The tested products were compared with a Sigma Reference Standard (SRS). All of the diets fed to the chicks were prepared from corn-soybean meal. Each of the products was in premix form containing cholecalciferol. Their physical characteristics reflected the methods used to produce the premixes. They were categorized as spray-dried or drum-dried in the beadlet or flake form. Basal diets without cholecalciferol were used in all experiments. For Experiments 1 and 2, the designs were a 2 x 3 factorial arrangement using three different cholecalciferol products and two levels of 200 and 400 IU/kg dietary cholecalciferol. For both experiments, three additional SRS levels of 600, 800, and 1,000 IU/kg were included in the studies as positive controls as there is a possibility that the cholecalciferol products being tested may exhibit activity higher than the amount stated. In Experiment 3, a 3 x 4 factorial arrangement was used, which was represented by three cholecalciferol products and four levels of dietary cholecalciferol at 150, 300, 600, and 1,200 IU/kg. By using the slope ratio analysis, the potencies of the products from the three experiments were between 86 and 118%. In Experiment 3, the requirement of chicks for cholecalciferol using the three tested products, as determined by a nonlinear regression model based on bone ash, were 843+/-85, 911+/-106, and 986+/-131 IU/kg of diet as compared with 915+/-82 IU/kg when using the SRS. The results from these studies indicate that the chemical assays used to determine the cholecalciferol activity of these products were very reliable.

Topics: Animal Feed; Animals; Biological Assay; Chickens; Cholecalciferol; Glycine max; Poultry Diseases; Rickets; Zea mays

Three experiments were conducted to determine the effects of high dietary levels of vitamins A and E on the utilization of cholecalciferol by broiler chicks. In Experiment 1, chicks were fed six levels of vitamin A (5,000, 10,000, 20,000, 40,000, 80,000, and 160,000 IU/kg). Cholecalciferol (vitamin D3) was not added to the basal diet but all birds were exposed to ultraviolet (UV) fluorescent light. Body weight was decreased only at levels of vitamin A of 80,000 IU/kg or above. In Experiment 2, birds were exposed to UV fluorescent light or no UV light, two levels of dietary vitamin A (1,500 and 45,000 IU/kg) and three levels of dietary vitamin D3 (0, 500, and 2,500 IU/kg) in a 2 x 2 x 3 factorial arrangement. The high level of vitamin A reduced (P < 0.001) bone ash but only at a marginal level of vitamin D3 (500 IU/kg) and when the birds were not exposed to UV light. In Experiment 3, birds were exposed to UV fluorescent light or no UV light, two levels of dietary vitamin E (10 and 10,000 IU/kg) and three levels of dietary vitamin D3 (0; 500 and 2,500 IU/ kg) in a 2 x 2 x 3 factorial arrangement. The high level of vitamin E significantly (P < 0.05) reduced body weight, bone ash, plasma calcium, and increased rickets but only at 500 IU/kg of vitamin D3. Feeding 2,500 IU/kg of vitamin D3 overcame the effects of the high level of vitamin E, causing a significant (P < 0.05) interaction. Ultraviolet light also prevented the detrimental effects of the high level of vitamin E. The results of these studies indicate that high dietary levels of vitamins A and E negatively affected the utilization of vitamin D3 only when D3 was present at a marginal level (500 IU/kg) in the diet but not when it was synthesized in the bird by exposure to UV light or supplemented at 2,500 IU/kg in the diet.

Topics: Animals; Body Weight; Calcium; Chickens; Cholecalciferol; Cohort Studies; Diet; Dietary Supplements; Dose-Response Relationship, Drug; Incidence; Male; Phosphorus; Poultry Diseases; Rickets; Ultraviolet Rays; Vitamin A; Vitamin E

Three experiments were conducted to determine the influence of vitamin A on the utilization and amelioration of toxicity of cholecalciferol (vitamin D3), 25-hydroxycholecalciferol [25-(OH)D3], and 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] in young broiler chicks. Two levels of vitamin A (1,500 and 45,000 IU/kg or 450 and 13,500 microg) were fed in all experiments. In Experiment 1, chicks were fed six levels of vitamin D3 (0, 5, 10, 20, 40, and 80 microg/kg). High dietary vitamin A decreased bone ash (P < 0.001), and increased the incidence of rickets (P < or = 0.02). Linear and quadratic responses to vitamin D3 levels were significant (P < 0.01) for body weight, bone ash, incidence and severity of rickets, and plasma calcium. In Experiment 2, six levels of 25-(OH)D3 (0, 5, 10, 20, 40, and 80 microg/kg) were added to the basal diet. Adding 25-(OH)D3 increased (P < 0.001) body weight, bone ash, and plasma calcium, and decreased rickets and plasma vitamin A. Adding 25-(OH)D3 overcame the reduction in bone ash produced by high dietary vitamin A showing a significant (P < 0.02) interaction. In Experiment 3, six levels of 1,25-(OH)2D3 (0, 2, 4, 8, 16, and 32 microg/kg) were added to the basal diet. High dietary vitamin A increased (P < 0.01) the incidence and severity of rickets. Adding 1,25-(OH)2D3 increased (P < 0.01) body weight, bone ash, plasma calcium, and reduced rickets and plasma and liver vitamin A. Adding 1,25-(OH)2D3 overcame the reduction in bone ash, and the increase in rickets produced by high vitamin A was significant (P < or = 0.05). These results indicate that high dietary vitamin A (45,000 IU/kg) interferes with the utilization of vitamin D3, 25-(OH)D3 and 1,25-(OH)2D3, increasing the requirement for each of them. Moreover, 45,000 IU/kg of dietary vitamin A ameliorated the potential toxic effects of feeding high levels of vitamin D3, 25-(OH)D3 and 1,25-(OH)2D3 to young broiler chickens. Further work is necessary to find the minimum levels of these vitamins needed to cause these effects.

Topics: Animals; Body Weight; Calcifediol; Calcitriol; Chickens; Cholecalciferol; Cohort Studies; Diet; Dietary Supplements; Dose-Response Relationship, Drug; Drug Interactions; Incidence; Male; Poultry Diseases; Rickets; Vitamin A

Three experiments were conducted to test the hypothesis that a vitamin D deficiency alters the immune responses of female broiler chicks. The control diet contained 800 IU of cholecalciferol (vitamin D3)/kg and the deficient diet was the same except without supplemental vitamin D3. The vitamin D deficiency status was established on the basis of a significantly lower blood ionized calcium or total serum calcium (75 to 85% of the control). Vitamin D-deficient chicks also had lower growth rate and bone ash. In Experiment 1 at 8 d of age, and Experiment 2 at 23 d of age, the cutaneous basophil hypersensitivity response as determined by the increase in interdigital skin thickness 20 h after a single injection of 100 microg phytohemagglutinin-P was significantly depressed in vitamin D-deficient chicks (62 to 64% of the control). Thymus weight, adjusted for body weight, was significantly lower in the vitamin D-deficient chicks at 24 d of age (61% of the control). Primary and secondary antibody responses against SRBC in vitamin D-deficient chicks were not different from the control. In Experiment 3, in 17-d-old chicks, vitamin D deficiency decreased the number of abdominal macrophages phagocytizing SRBC in vitro within 45 min from 14.7 to 10.1%. These results indicate that vitamin D deficiency depresses the cellular immune responses in young broiler chicks.

Topics: Animal Feed; Animals; Antibody Formation; Basophils; Cells, Cultured; Chickens; Cholecalciferol; Female; Hypersensitivity; Macrophages, Peritoneal; Nutritional Status; Phagocytosis; Poultry Diseases; Vitamin D Deficiency

A series of experiments was conducted to test the hypothesis that vitamin D utilization may not be as efficient in chicks with tibial dyschondroplasia (TD). The basal diet contained 1.0% Ca and 0.45% available P with no supplemental cholecalciferol (D3). Chicks from low TD (LTD) and high TD (HTD) selected lines were fed diets supplemented with various levels of vitamin D compounds and examined for rickets and TD. When chicks were fed a D3-deficient diet containing only 1.25 micrograms/kg added D3, HTD chicks had a greater incidence of severe rickets than LTD chicks (P < 0.05). The LTD chicks did not exhibit TD when fed a diet containing adequate (20 micrograms/kg) D3. The LTD chicks fed a diet supplemented with 5 micrograms/kg D3, however, had 22% incidence of TD. When HTD chicks were fed diets supplemented with 5 micrograms/kg D3 [control diet that meets NRC (1994) requirement for D3], 20 micrograms/kg D3, 5 micrograms/kg 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] or the combination of both D3 (20 micrograms/kg) and 1,25-(OH)2D3 (5 micrograms/ kg), TD incidence was highest in HTD chicks fed the control diet. When HTD chicks were fed diets with an increased dietary level of 1,25-(OH)2D3 (10 micrograms/kg) further reduction of TD incidence (P < 0.05) occurred. A potentially toxic level (Soares et al., 1983) of 1,25-(OH)2D3 (15 micrograms/kg) fed to HTD chicks resulted in still greater suppression of incidence of TD even though growth and feed intake in HTD chicks was greater than those of LTD chicks. It is concluded that the development of TD in HTD chicks is associated with subnormal ability to metabolize vitamin D.

Topics: Animals; Calcitriol; Calcium; Calcium, Dietary; Causality; Chickens; Cholecalciferol; Incidence; Osteochondrodysplasias; Phosphorus; Phosphorus, Dietary; Poultry Diseases; Random Allocation; Rickets; Severity of Illness Index; Tibia; Vitamin D

Four experiments were conducted to investigate the effects of ultraviolet (UV) light exposure and several cholecalciferol metabolites on the development of tibial dyschondroplasia (TD) and other parameters associated with vitamin D metabolism in chickens selected for high (HTD) and low (LTD) incidence of TD. In Experiment 1, exposure of chickens to UV light reduced the incidence and severity of TD more in LTD chickens than in HTD chickens, as evident by the significant interactions (P < 0.10 and 0.04). In Experiment 2, the addition of cholecalciferol to diets that were deficient in cholecalciferol linearly decreased the incidence of vitamin D rickets and increased bone ash, but increased the incidence of severe TD. The LTD chickens had a higher maximal bone ash of 40.0 +/- 0.7% than did the HTD chickens, which had a maximal bone ash of 37.0 +/- 0.7%. In Experiment 3, the addition of 5 micrograms/kg of 25-hydroxycholecalciferol [25-(OH)D3], 1-alpha-hydroxycholecalciferol, or 1,25- dihydroxycholecalciferol decreased the incidence and severity of TD in the LTD chickens and had no effect on TD in HTD chickens. In Experiment 4, increasing dietary 25-(OH)D3 increased plasma 25-(OH)D3 levels in both lines, but HTD chickens had higher plasma 25-(OH)D3 levels at 20 and 40 micrograms/kg of dietary 25-(OH)D3. The incidence and severity of TD were reduced in the LTD chickens by dietary 25-(OH)D3, but little effect was noted in HTD chickens. The LTD chickens reached a maximal bone ash at 9.7 +/- 1.9 micrograms/kg and HTD chickens reached the same bone ash at 33.0 +/- 7.0 micrograms/kg. These results indicate that UV light and vitamin D metabolites are not effective in preventing TD in HTD chickens, but that altered vitamin D metabolism does exist between HTD and LTD chickens.

Topics: Analysis of Variance; Animals; Calcium; Chickens; Cholecalciferol; Congenital Abnormalities; Dose-Response Relationship, Drug; Female; Food, Fortified; Hindlimb; Incidence; Male; Osteochondrodysplasias; Phosphates; Poultry Diseases; Tibia; Ultraviolet Rays

1. The combined effect of moderate excess dietary vitamin E and marginal amounts of dietary cholecalciferol on the performance and tibia bone ash of young male broiler chicks was evaluated. Vitamin E (alpha-tocopheryl acetate) and cholecalciferol were added to a commercial diet not already supplemented with these vitamins, at concentrations of 0 and 150 mg/kg, and 1.875, 5 and 25 micrograms/kg, respectively, and fed to chicks for 23 d. 2. Vitamin E concentration and its combinations with cholecalciferol did not significantly (P > 0.05) affect food intake, weight gain, food efficiency and bone ash. These variables were significantly (P < 0.001) lower in chicks fed on the diets supplemented with 1.875 micrograms cholecalciferol/kg compared with the values observed with the 2 other concentrations of this vitamin. There were no differences in the effects of 5 and 25 micrograms cholecalciferol/kg diet on the above variables. 3. It was concluded that vitamin E, at a concentration of 150 mg/kg diet, did not aggravate a mild cholecalciferol deficiency.

Topics: Animals; Bone Density; Chickens; Cholecalciferol; Dietary Supplements; Drug Interactions; Male; Poultry Diseases; Vitamin D Deficiency; Vitamin E

Over a short period of time, turkeys of various ages from three flocks were sent in with a history of paralysis. In the first necropsies there were no clear signs of the cause of the paralysis. On clinical examination of the flocks it was noted that the birds staggered as if drunk and that standing caused them pain. It was only with the last case that it became clear that the cause was rickets. Analysis of the feed demonstrated that level of vitamin D3 was too low, possibly even in the premix.

Topics: Animals; Cholecalciferol; Paralysis; Poultry; Poultry Diseases; Rickets; Turkeys; Vitamin D Deficiency

Two experiments were designed to determine the effect of dietary boron on broiler cockerels and four experiments were conducted to determine whether an interaction exists among dietary boron, cholecalciferol, and calcium. The parameters measured were weight gain, feed efficiency, tibia bone ash, rickets, tibial dyschondroplasia, and plasma minerals. All experiments were conducted with tibial dyschondroplasia-inducing basal diets fed to broiler cockerels from 1 to 16 days of age. Experiments 1 and 2 had four levels of dietary boron (0, 20, 40, and 80 mg/kg (Experiment 1) and 0, 5, 10, and 20 mg/kg (Experiment 2). Boron had no effect on weight gain, feed efficiency, or plasma minerals in either experiment. In Experiment 2, increasing levels of boron had no influence on tibial dyschondroplasia but did exert a quadratic effect on bone ash with 5 and 10 mg/kg boron increasing bone ash. In Experiment 1, bone ash and the incidence of tibial dyschondroplasia were unaffected, but the severity of tibial dyschondroplasia linearly increased by increasing boron levels. Experiments 3 to 6 had a 2 x 2 x 2 factorial arrangement of treatments with calcium at .65 and .90%, cholecalciferol at 110 and 1,100 ICU/kg, and boron at 0 and 40 mg/kg (Experiments 3 to 5) or 0 and 3 mg/kg (Experiment 6). The higher levels of calcium and cholecalciferol improved weight gain, decreased the incidence of rickets, and decreased the incidence and severity of tibial dyschondroplasia. Feeding cholecalciferol at 1,100 ICU/kg increased plasma calcium and plasma dialyzable phosphorus and decreased plasma magnesium. Calcium at .90% had no effect on plasma magnesium or plasma dialyzable phosphorus and increased plasma calcium only in Experiment 4. The only response to boron in Experiments 3 to 6 was a boron effect and a boron by cholecalciferol interaction on bone ash in Experiment 3, in which boron reduced bone ash at .65% calcium and 110 ICU/kg cholecalciferol. From these experiments, there is no indication that an interaction among boron, cholecalciferol, and calcium exists in broiler cockerels.

Topics: Animal Feed; Animals; Bone Development; Boron; Calcium; Calcium, Dietary; Chickens; Cholecalciferol; Magnesium; Male; Osteochondrodysplasias; Phosphorus; Poultry Diseases; Rickets; Tibia; Weight Gain

A series of experiments was conducted to investigate interactions of dietary calcium levels with ultraviolet light, cholecalciferol (D3), 1,25-dihydroxycholecalciferol [1,25-(OH)2D3], dietary protein, and a synthetic zeolite on the development of tibial dyschondroplasia in broilers. A basal diet low in calcium, high in phosphorus and chloride, and known to promote a high incidence of tibial dyschondroplasia was used. The chicks received ultraviolet radiation from fluorescent lights in addition to 1,100 ICU/kg (27.5 micrograms/kg) of D3 in the basal diet when these were not experimental variables. Regardless of whether the calcium level was low (.65%) or adequate (.95%), the incidence of tibial dyschondroplasia was significantly lower in chicks receiving ultraviolet radiation or dietary vitamin D3 levels well above the required amounts. The addition of 10 micrograms/kg of 1,25-(OH)2D3 to the diet when calcium levels varied from .45 to .95% resulted in a reduction in the incidence of tibial dyschondroplasia and increased tibial bone ash when dietary protein levels were 18 or 22%. The addition of 1% synthetic zeolite to the diet did not influence the incidence of tibial dyschondroplasia when the diet contained widely varying dietary calcium levels (.65 to 1.81%) and .73% phosphorus.

Topics: Aluminum Silicates; Animals; Calcitriol; Calcium; Chickens; Cholecalciferol; Diet; Dietary Proteins; Male; Osteochondrodysplasias; Phosphorus; Poultry Diseases; Tibia; Ultraviolet Rays; Zeolites

The effect was studied of 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] at various levels of vitamin D3, with adequate or inadequate dietary calcium, on performance and bone development in turkey poults. Two experiments were conducted. Experiment 1 lasted 16 days and was a 4 x 2 factorial arrangement using a low calcium diet (.7%), with dietary levels of vitamin D3 of 450, 900, 1,800, and 3,600 ICU/kg of diet and with or without 10 micrograms of dietary 1,25-(OH)2D3. Experiment 2 lasted 14 wk and was a 2 x 2 x 2 factorial arrangement with vitamin D3 levels of 900 or 2,700 ICU/kg of diet, calcium levels at 58 or 100% of the National Research Council requirement (which varies with age), and with or without 10 micrograms/kg of dietary 1,25-(OH)2D3. In Experiment 1, increasing levels of vitamin D3 and 1,25-(OH)2D3 supplementation significantly increased bone ash. Pairwise contrasts at specific vitamin D3 levels indicated that this effect of 1,25-(OH)2D3 was greater at lower levels of vitamin D3. In Experiment 2, the 2,700-ICU level of vitamin D3 decreased the incidence of rickets at 3 wk and partially ameliorated a calcium deficiency, as indicated by an increase in growth at the 2,700-ICU level of vitamin D3 in calcium-deficient diets from 8 to 14 wk. Vitamin D3 by calcium interactions on rickets at 14 wk of age and bone ash at 3 and 14 wk were similar and indicated also that vitamin D3 partially ameliorated a calcium deficiency. In general, the addition to the diet of 1,25-(OH)2D3 increased bone ash and decreased the incidence of rickets in diets deficient in calcium but high in vitamin D3. There is very little evidence in the present study that indicates that 1,25-(OH)2D3 has any effect on tibial dyschondroplasia.

Topics: Animals; Bone Development; Calcitriol; Calcium, Dietary; Cholecalciferol; Male; Poultry Diseases; Rickets; Tibia; Turkeys

The assessment of avian tibial dyschondroplasia (TD) in many recent studies is based on examination of slices of the proximal tibiotarsus with the naked eye. This study examines the incidence and severity of TD in broilers under four different dietary regimes and compares the efficacy of naked eye assessment with histopathological examination. The diets contained reduced levels of calcium relative to phosphorus with adequate (diet 1) and high (diet 2) levels of vitamin D3 supplementation; a very low calcium diet (diet 3) and a standard diet (diet 4) were also included. Gross examination suggested that TD was present in 80 per cent, 79 per cent and 27 per cent of tibiotarsi from birds on diets 1, 2 and 4, respectively. However, histological examination indicated TD, correspondingly, to be present in 18 per cent, 39 per cent and 6 per cent of tibiotarsi. Some birds on diet 1 exhibited physeal changes consistent with mild hypocalcaemic rickets. Many of the bone extremities which, grossly, were considered dyschondroplastic (diets 1, 2 and 4), histologically were shown to have an extensive hypertrophied zone with poor metaphyseal vessel penetration, but no cellular or matrix changes consistent with TD. This cast doubt on the validity of earlier studies of TD which relied solely on naked eye examination. The birds on diet 3 all demonstrated histopathology considered consistent with severe hypocalcaemic rickets and the present study suggests that in three-week-old broilers a moderately hypocalcaemic diet with a high level of vitamin D3 will not cause rickets but will increase the incidence and severity of TD.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Calcium, Dietary; Chickens; Cholecalciferol; Diet; Incidence; Osteochondrodysplasias; Phosphorus, Dietary; Poultry Diseases; Tibia

Adult laying hens were fed diets deficient in phosphorus, calcium, calcium and phosphorus, and vitamin D3 to determine their effects on bone histology and parathyroid gland size. The phosphorus deficient diet caused an insignificant decrease in parathyroid size while the other diets caused significant increases. A considerable amount of individual variation in medullary bone volume and osteoid seam width was observed in all groups but, despite this, the calcium, calcium and phosphorus and vitamin D3 deficient diets clearly resulted in increased osteoid. Birds receiving diets deficient in calcium and phosphorus, and in vitamin D3 for longer periods were observed to have partially or completely resorbed medullary bone. Osteodystrophia fibrosa was noted in vitamin D3 deficient birds which had no follicular activity.

Topics: Animals; Calcium; Chickens; Cholecalciferol; Female; Femur; Osteoporosis; Oviposition; Parathyroid Glands; Phosphorus; Poultry Diseases

Studies were conducted to evaluate several cholecalciferol (D3 metabolites: 1,25-dihydroxycholecalciferol [1,25-(OH)2D3], 1,24R,25-trihydroxycholecalciferol [1,24R,25-(OH)3D3], 1 alpha-hydroxy-cholecalciferol (1 alpha-OHD3), 24R,25-dihydroxycholecalciferol [24R,25-(OH)2D3], 1,25-dihydroxy-26,27 hexadeuterium cholecalciferol (1,25-(OH)2-26,27[2H]6D3) and 1,25-dihydroxy-24R-fluorocholecalciferol [1,25-(OH)2-24R-FD3] for their activity in preventing the development of tibial dyschondroplasia in broilers. The basal diet used is low in calcium, high in phosphorus and chlorine and is known to promote a high incidence of tibial dyschondroplasia. The chicks received ultraviolet radiation from fluorescent lights in addition to 1100 ICU/kg (27.5 micrograms/kg) of D3 in the basal diet. Supplementation of the diet with 10 micrograms/kg of all the metabolites except 24R,25-(OH)2D3 significantly lowered the incidence and severity of tibial dyschondroplasia and increased bone ash when compared to birds receiving the basal diet. None of the active D3 metabolites was effective when fed at 0.1 or 1.0 micrograms/kg of diet. Two active compounds tested [1,25-(OH)2D3 and 1,24R,25-(OH)3D3] at 5 micrograms/kg of diet were effective in reducing either the incidence or severity of tibial dyschondroplasia.

Topics: 24,25-Dihydroxyvitamin D 3; Analysis of Variance; Animals; Calcitriol; Calcium; Chickens; Cholecalciferol; Hydroxycholecalciferols; Male; Osteochondrodysplasias; Poultry Diseases; Tibia

Four experiments were conducted to determine the effect of dietary cholecalciferol (vitamin D3), 25-hydroxycholecalciferol (25-OHD3) and 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) on the changes in growth, feed efficiency and bone ash, and the incidence, severity and number of #3 scores of tibial dyschondroplasia caused by the addition of disulfiram to the diet. The basal diet used was low in calcium and high in phosphorus and chlorine and known to promote a high incidence of tibial dyschondroplasia in broiler chickens. The chickens in all experiments received enough ultraviolet radiation from fluorescent lights in the pens to nearly satisfy their need for vitamin D. The addition of disulfiram to the diet caused an increase in most of the measurements indicating development of tibial dyschondroplasia in all of the experiments, and caused a decrease in bone ash in two of the experiments and a decrease in growth and gain:feed in one experiment. The addition of D3 to a diet containing no D3 caused higher bone ash and lower incidence of tibial dyschondroplasia in the absence or presence of disulfiram. The effects of the addition of 25-OHD3 to diets containing approximately five times the requirement of D3 in the absence and presence of disulfiram caused variable results. The addition of 1,25-(OH)2D3 to the D3-supplemented diet in the absence or presence of disulfiram caused dramatic increases in bone ash and a decrease in most of the criteria used to measure development of tibial dyschondroplasia. There was no indication of interaction of the effects of D3, 25-OHD3 and 1,25-(OH)2D3 with the action of disulfiram.

Topics: Animals; Body Weight; Bone and Bones; Calcifediol; Calcitriol; Calcium; Chickens; Cholecalciferol; Diet; Disulfiram; Male; Minerals; Osteochondrodysplasias; Poultry Diseases; Tibia

Seven experiments were conducted to test the influence of dietary supplementary ascorbic acid on the development of tibial dyschondroplasia in broiler chickens. Ascorbic acid supplementation significantly reduced the incidence and number of birds with a large mass of cartilage in the tibia in the first experiment but not in the two subsequent experiments. Because environmental temperature, microbial infection, and vitamin D3 status had been reported in the literature to influence ascorbic acid metabolism in the chicken, experiments were conducted to see if these variables could influence supplemental ascorbic acid effects on development of tibial dyschondroplasia. Results of the experiments indicated that none of these factors influenced the effect of ascorbic acid on the development of tibial dyschondroplasia. The presence of vitamin D3 in the diet significantly influences the incidence of this disorder.

Topics: Animals; Ascorbic Acid; Chickens; Chlortetracycline; Cholecalciferol; Male; Osteochondrodysplasias; Poultry Diseases; Temperature; Vitamin D Deficiency; Weight Gain

46 one day old chickens, divided into five groups, were fed an alternately composed vitamin D3 ration during 36 days. In the group depleted of vitamin D3 the typical rickets were found. When treated with a standard ration (2000 I.U. vit. D3/kg food) after 15 days depletion of vitamin D3 the chickens showed control-group parameters within 3 weeks. Using 60,000 I.U. vitamin D3 after a period of 15 days depletion evoked rather an abrupt beginning of healing tendency accompanied by signs of intoxication which were enhanced in those chickens treated with 120,000 I.U. vitamin D3: increase in number of osteoblasts, calcification of osteoblastic mitochondrial membranes and endothelial cell membranes, as well as degeneration of osteoblasts together with a strong reaction of eosinophils. There did not occur necrosis of osteocytes or of bone structure. Erythrocytes, being embedded in ground substance without endothelial surrounding, was a common finding in every group.

Topics: Animals; Bone and Bones; Bone Development; Cartilage; Chickens; Cholecalciferol; Eosinophils; Female; Growth Plate; Osteoblasts; Osteoclasts; Poultry Diseases; Vitamin D Deficiency

In an experiment of 36 days duration 46 one-day-old chicks were divided into 5 groups and fed with different concentrations of vitamin D3. The animals of the group which lacked vitamin D3, showed the typical rachitic lesions. After a 15 days lack of vitamin D3 the chicks of another group were treated with standard food (2000 I.U. vitamin D3/kg food) with the consequence of an approximation of the analyzed parameters to those of the control group within 3 weeks. When fed with 60,000 I.U. of vitamin D3 after a 15 days lack of this vitamin, the animals showed an over-hasty healing process, ending up with signs of intoxication which were even more conspicuous when fed with 120,000 I.U. of vitamin D3. Besides an increasing calcification of osteoblasts and endothelial cell membranes as well as a degeneration of osteoblasts, a clear increase of eosinophilic granulocytes could be noticed. In all groups free erythrocytes within the ground substance were found. There was no evidence of necroses of osteocytes or of bone.

Topics: Animal Feed; Animals; Bone and Bones; Chickens; Cholecalciferol; Microscopy, Electron; Microscopy, Electron, Scanning; Poultry Diseases; Vitamin D Deficiency

1. Seventeen 32-week-old White Leghorn laying hens were induced to become deficient in calciferol or in calcium (laying thin or soft shelled eggs) by withdrawing either cholecalciferol (27.5 micrograms/kg diet) or calcium (31 g/kg diet) supplements from the control diet. 2. The metabolic fate and metabolic clearance rate (MCR) of intravenously injected 3H-oestradiol-17 beta were then monitored for 40 min. 3. In both the calciferol and calcium-deficient groups a major oestrogen sulphate pathway was particularly affected, resulting in a decreased conversion of oestradiol-17 beta-3-sulphate to oestradiol-17 alpha-3-sulphate, with a concomitant reduced MCR of oestradiol-17 beta from plasma. 4. The metabolic defect was corrected by feeding the control diet. 5. Because the metabolic defect observed in calciferol deficiency occurred in Ca deficiency in a more severe form, we conclude that the more immediate cause was calcium rather than calciferol deficiency. To our knowledge, this is the first observation of a calcium-deficient effect on oestrogen sulphate metabolism in vivo.

Topics: Animals; Calcium; Chickens; Cholecalciferol; Estradiol; Female; Oviposition; Poultry Diseases; Vitamin D Deficiency

Thirty-two outbreaks of leg disorders in turkeys were investigated during 1981-1985. Among them, 22 were characterized by a low percentage of bone ash and were considered as field rickets. Most of the field rickets cases exhibited reduced plasma calcium and inorganic phosphorus. Plasma 25-hydroxyvitamin D3 and intestinal calcium-binding protein were lower in the rachitic than in normal turkeys. These symptoms are typical of rickets resulting from vitamin D deficiency. The vitamin D3 equivalence of a diet that had been fed during field rickets outbreaks was assayed biologically and found to be 111 micrograms/kg diet, about eight times the minimal requirement. In two other cases no symptoms of rickets were observed in turkeys fed diets that had been previously consumed during field rickets outbreaks. The results indicate that in some cases of field rickets there was no involvement of dietary factors and confirm a previous suggestion that field rickets may result from defects in metabolism of vitamin D3, or in its expression.

Topics: Animals; Calcifediol; Cholecalciferol; Poultry Diseases; Rickets; Turkeys; Vitamin D

A study was undertaken to determine the effects of maternal and poult nutrition on poult growth and bone development through to market age. Nicholas Large White turkey hens (200) were fed diets with 300, 900, or 2700 IU vitamin D3/kg from day-old to 37 weeks of age. Male poults (649 from Hatch 1 and 555 from Hatch 2) were fed diets containing .6 or 1.2% Ca; .4 or .8% available P; and 300, 900, or 2700 IU vitamin D3/kg to 4 weeks (Hatch 1) or 2 weeks of age (Hatch 2) in a complete factorial design. All Hatch 2 poults were given a "therapeutic" diet from 2 to 4 weeks, followed by normal grower diets from 4 to 24 weeks of age. Increasing the level of vitamin D3 in the hen diet increased weight at hatching and at 2 and 4 weeks, decreased mortality from 0 to 2 weeks, and increased bone ash percent and breaking strength and decreased the severity of rickets score at 2 weeks. Increasing the levels of Ca, P, and vitamin D3 in the poult diet gave reduced mortality from 0 to 2 weeks, increased weight at 2 and 4 weeks, increased bone ash percent and breaking strength, and decreased severity of rickets score at 2 and 4 weeks. Carcass fleshing score at 24 weeks was improved with 1.2% Ca. Conformation score and percent grade A carcasses increased linearly with level of vitamin D3 in the starter diet and were also improved by increasing the vitamin D3 in the breeder diet.

Topics: Animals; Body Weight; Bone Development; Calcium, Dietary; Cholecalciferol; Female; Male; Phosphorus; Poultry Diseases; Rickets; Turkeys

Two hundred Large White turkey hens were fed diets varying in vitamin D3 supplementation (300, 900, or 2700 IU/kg feed) from day-old to 37 weeks of age. Hens receiving 300 IU vitamin D3/kg feed produced fewer eggs, which were lighter in weight and had thinner shells than those laid by hens receiving the higher levels of vitamin D3. Fertility was not affected by treatment; however, hatchability of eggs from hens fed 300 IU vitamin D3/kg feed was reduced by 48% from that of hens fed the two higher levels. A shortened upper mandible, which was detected in embryos during Week 4 of incubation, accounted for approximately 10% of the total embryo mortality and 49.5% of the embryo mortality, during Week 4. It appeared that hens fed the low vitamin D3 did not have adequate amounts of the vitamin to transport to the egg for normal embryonic development.

Topics: Animal Feed; Animals; Beak; Chick Embryo; Chickens; Cholecalciferol; Female; Fertility; Oviposition; Poultry Diseases

The effects of maternal vitamin D3 carry-over to the poult and dietary vitamin D3 on kidney 25-hydroxyvitamin D3-1-hydroxylase (1-hydroxylase) (EC 1.14.13.13) activity were studied in poults from 6 days prehatching to 46 days of age. Large White female turkeys from day-old were fed diets with either 300, 900, or 2700 IU vitamin D3/kg feed. Progeny from each maternal group were fed diets with either 0, 300, 900, or 2700 IU vitamin D3/kg feed. Low maternal vitamin D3 carry-over increased kidney 1-hydroxylase activity in embryos and poults to at least 5 days of age. Low dietary vitamin D3 increased the enzyme activity over that of poults fed higher levels. Kidney 1-hydroxylase activity peaked at about 8 to 18 days to a level similar in all groups. This peak is coincident with the appearance of rickets often noted in the field. Maternal diet did not affect plasma calcium (Ca) but plasma inorganic phosphorus (Pi) decreased with decreasing maternal vitamin D3 up to 14 days of age. Plasma Ca increased at 14 days with higher dietary vitamin D3, as did plasma Pi from day 8. Plasma alkaline phosphatase increased with age to 18 days and then declined. Tibia ash increased with higher maternal vitamin D3 carry-over to 12 days and with higher dietary vitamin D3 after 12 days of age. Body weight was reduced with low maternal vitamin D3 carry-over until at least 2 weeks of age, after which the effect of progeny diet was highly significant; birds receiving 2700 IU vitamin D3/kg feed were almost twice as large as those receiving none. This study shows the importance of adequate maternal carry-over of vitamin D3 and its possible influence on the development of rickets in starting poults.

Topics: 25-Hydroxyvitamin D3 1-alpha-Hydroxylase; Animals; Body Weight; Bone and Bones; Calcium; Cholecalciferol; Diet; Female; Kidney; Male; Minerals; Poultry Diseases; Rickets; Steroid Hydroxylases; Turkeys

Supplemental vitamin D3 (D3) was removed from the diet given to an experimental group of White Leghorn hens, at 227 days of age, while a control group continued to receive a supplemental diet. By 14 days after D3 withdrawal, egg weight, egg specific gravity, shell weight, percent shell, shell thickness, and plasma calcium were lower (P less than .05) in the experimental compared to the control group. At 30 to 37 days after D3 withdrawal, experimental hens had less (P less than .05) jejunal adenosine triphosphatase (ATPase) activity than the control hens. The study indicated that lack of D3 supplementation in laying diets reduced jejunal ATPase activity as well as egg shell quality.

Topics: Adenosine Triphosphatases; Animals; Calcium; Chickens; Cholecalciferol; Egg Shell; Eggs; Female; Jejunum; Poultry Diseases; Vitamin D Deficiency

When fed to chicks rye is rachitogenic as well as growth depressing. The component or components of rye that cause these effects have not been identified. In an attempt to separate the factors, a water extract of rye was fractionated by precipitation with ethanol or ammonium sulfate. The precipitated fractions were fed to chicks. Although there were different responses to growth and bone ash from the ethanol fractions, they were not statistically significant. In another experiment, guar gum, pectin, or gum arabic was fed to chicks as 2% of the diet. Guar gum was both growth depressing and rachitogenic, pectin was only growth depressing, and gum arabic was without effect.

Topics: Animals; Body Weight; Chemical Fractionation; Chickens; Cholecalciferol; Dietary Carbohydrates; Dietary Fiber; Edible Grain; Food Additives; Galactans; Gum Arabic; Mannans; Pectins; Plant Gums; Polysaccharides; Poultry Diseases; Rickets; Secale

A demonstration project is described that proved to be popular with undergraduate students enrolled in a senior level course on animal and poultry nutrition. A total of 100 male, day-old broiler chicks were housed in a Petersime battery brooder and used in a 3-week test. Students were responsible for the management and care of the birds throughout the test. The birds were allotted to 5 groups (4 replicates each of 5 birds per group) and the test involved the omission of calcium, phosphorus, vitamin D3, or sodium chloride from a nutritionally adequate diet for a period of 2 weeks. After that period, one pen of each group was repleted with the control diet. Feed consumption, liveweight, feed conversion efficiency, and tibia bone ash content were measured weekly. Deficiency signs of the nutrients were observed, and it was noted that sodium chloride had the most marked effect on growth. Phosphorus deficiency had the most severe effect on bone development and resulted in a high incidence of rickets. Repletion resulted in a marked response in all parameters measured and was most marked in the group deficient in sodium chloride.

Topics: Animals; Body Weight; Bone and Bones; Calcium Carbonate; Calcium Phosphates; Chickens; Cholecalciferol; Diet; Eating; Feeding Behavior; Male; Minerals; Nutrition Disorders; Poultry Diseases; Sodium Chloride

Vitamin D3 is essential for calcification and normal bone development in chicks. In its absence, calcification is reduced but the volume (and mass) of bone increases. In vitamin D3-deficient chicks, this study shows the major defect to be in bone resorption rather than formation. Bone formation measured serially by the apposition of periosteal matrix was normal, whereas bone resorption measured by dissolution at the endosteal surface was dramatically reduced. Bone cells, therefore, would appear to retain their capacity to synthesize a collagenous matrix in the absence of vitamin D3 but lose their capacity to resorb bone. Calcification and its putative dependence on bone resorption (and vitamin D) remain to be elucidated. The vitamin D3-deficient chick provides a convenient and easily quantifiable model in which the morphological and biochemical effects of vitamin D3 can be further studied.

Topics: Animals; Bone Development; Chickens; Cholecalciferol; Microradiography; Poultry Diseases; Tibia; Vitamin D Deficiency

Two experiments were conducted on dietary predisposition to rickets in poults. The first experiment compared fat type (corn oil or tallow), level of added fat (3.5 or 7%), vitamin D3 (900 or 2,400 IU/kg feed), and total calcium (.6, 1.2, or 3%) inclusion in the diet. Poults fed diets supplemented with corn oil had higher percentage tibia ash than poults fed tallow-supplemented diets. Vitamin D3 included at 2,400 IU/kg feed increased body weights significantly by 2 and 4 weeks of age and lowered plasma alkaline phosphatase (AP) at 2 and 4 weeks compared with diets containing 900 IU/kg feed. Tibia ash was significantly greater with the higher vitamin D3 supplementation at 2 weeks. At 2 weeks of age both low (.6%) and high (3%) levels of dietary calcium increased plasma AP, decreased tibia ash, and decreased body weight compared with diets containing 1.2% calcium. By 4 weeks of age, diets containing 1.2 and 3% calcium had no significant effects on body weight and plasma AP; however, tibia ash was significantly greater with these levels than with the .6% calcium diets. The second experiment compared level of dietary tallow inclusion (2.5 or 7%) and supplementary vitamin A (4,000, 16,000, or 44,000 IU/kg feed). The high tallow diets decreased tibia ash at 3 weeks, and the maximum supplementation of vitamin A significantly depressed body weight. Clinical rickets were first noted at 18 days of age. By 26 days of age the higher level of dietary fat and the highest level of vitamin A caused a significant increase in severity of rickets. The results suggested that rickets can be induced by high dietary levels of tallow and vitamin A.

Topics: Alkaline Phosphatase; Animals; Body Weight; Bone and Bones; Calcium; Calcium, Dietary; Cholecalciferol; Dietary Fats; Disease Susceptibility; Male; Phosphorus; Poultry Diseases; Rickets; Turkeys; Vitamin A

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.

Topics: Animals; Bone and Bones; Chickens; Cholecalciferol; Hydroxycholecalciferols; Poultry Diseases; Vitamin D Deficiency

Graded levels of aflatoxin (0, .625, 1.25, 2.5, 5.0, and 10.0 micrograms/g diet) were incorporated into a broiler-starter ration and fed to chicks from 1 day to 3 weeks of age. The tibias and middle toes were removed, and both bone ash and toe ash were determined. Toe ash significantly (P less than .05) increased at the aflatoxin levels of 2.5 ppm and above, while bone ash significantly (P less than .05) deceased at the same aflatoxin levels (2.5 ppm and above). The increase in toe ash could be partially attributed to a significant (P less than .05) decrease in toe lipid levels at the aflatoxin levels of 2.5 ppm and above. The data indicate that aflatoxin inhibits bone mineralization. The data also show that toe ash does not in all experimental designs reflect bone ash and that data interpreted solely on toe ash determination may not accurately reflect bone mineralization.

Topics: Aflatoxins; Animals; Bone and Bones; Chickens; Cholecalciferol; Male; Minerals; Poultry Diseases

Topics: Animals; Chickens; Cholecalciferol; Female; Japan; Male; Poultry Diseases; Rickets

Experiments were conducted to study the effect of gamma irradiation on the rye-vitamin D antagonism in broiler chicks. In an initial study, the irradiated grain was exposed to gamma rays for 6 hr (2 Mrad) and was fed to rachitic chicks for only 12 hr before a single oral dose of vitamin D3. In another trial, birds were fed during the entire experiment (12 days) on the different experimental diets, and the irradiated grain was exposed to gamma rays for 20 hr. Results indicate that the factor in rye that interferes with vitamin D utilization was largely inactivated by exposing this grain to gamma rays for 20 hr. Additional information is reported in this paper related to the alleviation by extraction or antibiotic supplementation on the rachitogenic properties of rye. These studies were conducted by feeding to rachitic chicks the test materials for only a short period of time (12 hr) before a vitamin D3 oral dose and measuring the bone mineralization 48 hr later. Results indicate that the rachitogenic factor in rye is not present in the ash portion of the grain, that it can be largely overcome by water extraction and penicillin supplementation, and that an organic solvent extraction has no effect. Cooked beans which depress growth and increase the growth response to antibiotics are not rachitogenic.

Topics: Animal Feed; Animals; Chemical Fractionation; Chickens; Cholecalciferol; Edible Grain; Female; Gamma Rays; Male; Penicillin G Procaine; Poultry Diseases; Rickets; Secale; Zea mays

Male broiler chicks were fed diets containing either O (control) or 2.5 p.p.m. aflatoxin (toxin) for four weeks. A group of eight birds fed each diet was infected intravenously with radioactive vitamin D3 (D3) and a second group with radioactive 25-hydroxy vitamin D3 (25-OH D3). Plasma was obtained 24 hr. after dosing with D3 and 6 hr. after dosing with 25-OH D3. The vitamin D metabolites were extracted from the plasma an chromatographed on Sephadex LH-20 for separation. The four peaks of radioactivity separated corresponded to D3, 25-OH D3, 24,25-dihydroxy vitamin D3 (24,25-(OH)2D3) and 1,25-dihydroxy vitamin D3 (1,25-(OH)2D3). Percentages of radiation in each peak were (1) controls given D3--6.55, 64.30, 5.94 and 4.04; (2) toxin given D3--10.05, 56.96, 8.95 and 4.68; (3) control given 25-OHD3-2.16, 85.80, 4.11 and 2.04; and (4) toxin given 25-OH D3--1.53, 79.84, 5.56 and 2.14. The only significant differences between the control and toxin groups were in D3 and 24,25-(OH)2D3 in chicks given D3. Even these changes were small and the data would suggest that feeding 2.5 p.p.m. aflatoxin for four weeks does not greatly alter vitamin D metabolism.

Topics: Aflatoxins; Animals; Chickens; Cholecalciferol; Dihydroxycholecalciferols; Hydroxycholecalciferols; Liver; Male; Poultry Diseases

Topics: Animals; Calcium; Cartilage; Chickens; Cholecalciferol; Male; Plants, Toxic; Poultry Diseases; Protein Binding; Rickets; Strontium; Tibia

Topics: Animal Feed; Animals; Body Weight; Bone Resorption; Calcium; Calcium, Dietary; Chickens; Cholecalciferol; Egg Shell; Female; Intestinal Absorption; Intestine, Small; Oviposition; Paralysis; Parathyroid Glands; Phosphorus; Poultry Diseases; Protein Binding; Uterus; Vitamin D Deficiency

Three experiments were conducted with turkey poults to study the effects of the grain component of the diet (corn or rye), added fat, penicillin or extra vitamin D on growth and bone ash. In the first trial, where rye replaced corn in the diet, growth was depressed and the pults were rachitic before two weeks of age. Adding fat or penicillin to the rye containing diets significantly improved growth and increased bone ash. In the second trial, adding extra vitamin D3 or penicillin to a diet with rye increased both growth and bone ash. Diets containing either corn or rye were used in the third trial and the results again showed that extra vitamin D or penicillin markedly improved growth and bone ash when added to the diets with rye but did not significantly increase growth of poults on the diets with corn. Bone ash of turkeys fed the corn diets was significantly increased by a combination of extra vitamin D3 and penicillin.

Topics: Animal Feed; Animal Nutritional Physiological Phenomena; Animals; Cholecalciferol; Dietary Fats; Edible Grain; Female; Growth; Male; Penicillin G Procaine; Poultry Diseases; Rickets; Secale; Turkeys; Zea mays

Three experiments using day-old chicks were conducted in battery brooders to further study the rye-vitamin D antagonism. Birds were fed a vitamin D3-free diet containing corn or rye and submitted to diverse treatments for the first 10 days. At this time the chicks were either continued on the same diet or changed to other grain-type diets. The effect of ultraviolet light exposure on the chicks and of a single oral dose of vitamin D3 was studied, and body weight gain and bone ash were determined after a one-week experimental period. Rachitic chicks on a corn diet responded significantly better than rye-fed chicks to a single oral dose of vitamin D3, based on bone ash of fat-free, dry tibia. This rachitogenic effect of rye was completely overcome by exposing the chicks to ultraviolet light or by water extraction or acid-autoclaving this grain. The results also demonstrate that the interference by rye does not persist after this grain is removed from the diet.

Topics: Administration, Oral; Animal Feed; Animals; Body Weight; Chickens; Cholecalciferol; Edible Grain; Female; Male; Poultry Diseases; Rickets; Secale; Tibia; Ultraviolet Rays; Zea mays

A natural occuring outbreak of aflatoxicosis was observed in Bobwhite quail chicks while on a brooding experiment. A slight reduction in effects was noted for birds which received Tylan in the water from 0-3 days and Terramycin from 0-35 days of age. No symptoms of aflatoxicosis were observed in birds which received a product (FloxAid) containing two antibiotics and eight vitamins from 0-14 days. It is postulated that the primary mode of protection was via the water soluble vitamin D content of the product with possibly some protection from vitamins A, E and K.

Topics: Aflatoxins; Animals; Cholecalciferol; Choline; Folic Acid; Housing, Animal; Leucomycins; Oxytetracycline; Penicillin G Procaine; Poultry Diseases; Pyridoxine; Quail; Streptomycin; Vitamin A; Vitamin B 12; Vitamin E; Vitamin K

Topics: Animals; Bone and Bones; Calcium; Chickens; Cholecalciferol; Eggs; Female; Fertilization; Osteomalacia; Phosphorus; Poultry Diseases

Topics: Animals; Chickens; Cholecalciferol; Deficiency Diseases; Fertility; Insemination, Artificial; Liver; Male; Nutritional Requirements; Poultry Diseases; Reproduction; Riboflavin; Riboflavin Deficiency; Seasons; Semen; Spermatozoa; Testis; Vitamin A; Vitamin A Deficiency

Topics: Animals; Avitaminosis; Cholecalciferol; Food; Poultry Diseases