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.     

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.     

Ultrastructure of parathyroid glands of growing chickens with vitamin D deficiency rickets

Ultrastructural studies were conducted on the parathyroid glands (PTG) of 2- to 7-week-old nontreated control growing broiler chickens (group A, 6 chickens); the same aged chickens with experimentally induced vitamin D deficiency rickets (18 morbid chickens each from groups B, C, and D); and in 4- to 9-week-old chickens naturally affected with rickets (group E, 8 chickens). Four types of principal cells were classified in the PTG of clinically normal birds and in PTG of birds with secondary hyperparathyroidism as follows: Type I cell (small cell in the resting phase); type II cell (medium-sized cell with well-developed rough-surfaced endoplasmic reticulum in the synthesizing phase); type III cell (large cell with well-developed Golgi apparatus and cytoplasmic organelles in the packaging and secretory phase); and type IV cell (medium-sized cell with poor cytoplasmic organelles in the involuting phase). Many coated vesicles were observed in type II and type III cells. In young control chickens, principal cells of the PTG were considered in the resting phase; in older control chickens, there were increased numbers of cells in the synthesizing phase. In the vitamin D deficiency groups, principal cells were in the synthesizing and packaging and secretory phases. In birds with naturally occurring rickets, principal cells were in packaging and secretory phases, with a small number of cells in the involuting phase. The ultrastructural changes of the PTG from the initial to final phases in growing chickens with secondary hyperparathyroidism were demonstrated.     

生长猪低磷日粮添加植酸酶和有机酸以及维生素D_3的研究

本试验通过添加植酸酶、有机酸(柠檬酸、抗坏血酸)和维生素D3、木聚糖酶来减少无机磷的添加量,提高饲料中植酸磷的利用率,降低磷的排泄量。选择30 kg左右的"斯格"纯种猪70头,随机分成7组:常磷组、低磷日粮组(NC)、NC+600 U/kg植酸酶组、NC+600 U/kg植酸酶+10 g/kg的柠檬酸、NC+600 U/kg植酸酶+10 g/kg的柠檬酸+200 mg/kg抗坏血酸、NC+600 U/kg植酸酶+10 g/kg的柠檬酸+200 mg/kg抗坏血酸+100μg/kg的维生素D3、不添加磷酸氢钙。所有日粮中都添加50 mg/kg木聚糖酶。结果表明:低磷日粮添加植酸酶、有机酸(柠檬酸、抗坏血酸)和维生素D3,平均日采食量无显著影响(P0.05),日增重显著提高(P0.05),料重比显著降低(P0.05);养分消化率均显著提高;血液指标着中,白蛋白显著降低(P0.05),碱性磷酸酶、总蛋白、谷草、谷丙转氨酶无影响(P0.05)。     

Response to dietary phosphorus deficiency is affected by genetic background in growing pigs

Concern over the environmental effect of P excretion from pig production has led to reduced dietary P supplementation. To examine how genetics influence P utilization, 94 gilts sired by 2 genetic lines (PIC337 and PIC280) were housed individually and fed either a P-adequate diet (PA) or a 20% P-deficient diet (PD) for 14 wk. Initially and monthly, blood samples were collected and BW recorded after an overnight fast. Growth performance and plasma indicators of P status were determined monthly. At the end of the trial, carcass traits, meat quality, bone strength, and ash percentage were determined. Pigs fed the PD diet had decreased (P < 0.05) plasma P concentrations and poorer G:F (P < 0.05) over the length of the trial. After 4 wk on trial, pigs fed the PD diet had increased (P < 0.05) plasma 1,25(OH)(2)D(3) and decreased (P < 0.05) plasma parathyroid hormone compared with those fed the PA diet. At the end of the trial, pigs fed the PD diet had decreased (P < 0.05) BW, HCW, and percentage fat-free lean and tended to have decreased LM area (P = 0.06) and marbling (P = 0.09) and greater (P = 0.12) 10th-rib backfat than pigs fed the PA diet. Additionally, animals fed the PD diet had weaker bones and also decreased (P < 0.05) ash percentage and increased (P < 0.05) concentrations of 1alpha-hydroxylase and parathyroid hormone receptor mRNA in kidney tissue. Regardless of dietary treatment, PIC337-sired pigs consumed more feed and gained more BW than their PIC280-sired counterparts (P < 0.05) during the study. The PIC337-sired pigs also had greater (P < 0.05) HCW, larger (P < 0.01) LM area, and tended to have (P = 0.07) greater dressing percentage. Meat from the PIC337-sired pigs also tended to have greater (P = 0.12) concentrations of lactate but decreased (P = 0.07) concentrations of total glucose units 24 h postslaughter. Although plasma 1,25(OH)(2)D(3) concentrations were elevated (P < 0.05) in all the animals fed the PD diet, this elevation due to P deficiency tended (P = 0.09) to be greater in the PIC337-sired pigs after 12 wk on the treatment. The PIC337-sired pigs had stronger (P < 0.01) bones with greater ash percentage than the PIC280-sired pigs. The difference in the strength of the radii between the PIC337-sired pigs fed the PA and PD diets was greater than their PIC280-sired counterparts, which resulted in sire line x treatment interactions (P < 0.05). These data indicate differing mechanisms of P utilization between these genetic lines. Elucidating these mechanisms may lead to strategies to increase efficiency of growth in a more environmentally friendly manner.     

Pleuropneumonia caused by Actinobacillus pleuropneumoniae biotype 2 in growing and finishing pigs.

Actinobacillus pleuropneumoniae biotype 2 was isolated in pure culture or as the predominant isolate from the lungs of 9 growing and finishing pigs with pleuropneumonia. Gross and microscopic lesions resembled those caused by A. pleuropneumoniae biotype 1 serotypes (Nos. 1, 5, and 7) traditionally seen in the United States. The overall mortality rate for growing and finishing pigs on this 1,200-sow farrow-to-finish farm ranged from 0.37% to 0.84% per month from July 1990 to February 1991, and mortality due to respiratory disease ranged from 0.17% to 0.52% per month for the same period. This Actinobacillus species did not require V factor (no satellitism on blood agar with a Staphylococcus streak), was strongly beta-hemolytic, and demonstrated restriction fragment length polymorphisms in hybridization studies with A. suis, A. lignieresii, and A. equuli. Biochemically, the isolate most closely resembled A. pleuropneumoniae, and a DNA fragment considered specific for A. pleuropneumoniae biotypes 1 and 2 was demonstrated using polymerase chain reaction. Necrohemorrhagic pleuropneumonia similar to that caused by A. pleuropneumoniae biotype 1 was reproduced experimentally in 2 4-week-old pigs inoculated intratracheally with broth cultures of the A. pleuropneumoniae biotype 2. This study demonstrated the presence of A. pleuropneumoniae biotype 2 in the United States.     

Mitogen stimulation of lymphocytes in pigs with hereditary vitamin C deficiency

Recently an inherited vitamin G deficiency in the pigs presumably based on an autosomal recessive gene was decribed* Homozygotes are in contrast to heterozygotes and normal pigs unable to synthesize ascorbic acid. In an experiment comprising 3 littermate pigs, 2 homozygous and 1 heterozygous for the vitamin C deficiency gene, the influence of ascorbic acid depletion, and repletion on mitogen stimulation of peripheral blood lymphocytes was studied. Ascorbic acid depletion of the vitamin C dependent pigs resulted in a rapid decline in plasma ascorbic acid. Response of lymphocytes to stimular tion with Concanavalin A (Con A) and phytohemagglutinin M (PHA) decreased more slowly reaching a minimum, which coincidedi with the occurrence of the first clinical symptoms of scurvy. Following resupplementation with vitamin C the plasma content of ascorbic acid rapidly returned to normal, while the lymphocyte response to Con A and PHA stimulation only gradually approached the initial values. The repletion with ascorbic acid caused a transitory increase in the response to pokeweed mitogen (PWM) stimulation. The significance of these findings in relation to the cellular immune system in normal pigs is discussed.     

Hypercalcaemia in two dogs caused by excessive dietary supplementation of vitamin D

A three-year-old Border collie was presented with a two-week history of lethargy, stiff gait, polydipsia and polyuria. Biochemical analysis revealed hypercalcaemia. Serum concentrations of 25-hydroxyvitamin D (25[OH]D) and 1,25-dihydroxyvitamin D (1,25[OH]2D) were markedly elevated and parathyroid hormone was undetectable. Subsequent analysis of the dog's diet revealed that the food contained excessive amounts of vitamin D. The hypercalcaemia resolved following treatment with bisphosphonates and dietary change. Hypervitaminosis D was diagnosed in a second unrelated dog, which had been fed the same brand of dog food as case 1. The dog was also hypercalcaemic and had markedly elevated serum concentrations of 25(OH)D and 1,25(OH)2D. Hypervitaminosis D in dogs has been reported to occur secondarily to ingestion of either rodenticides containing cholecalciferol or antipsoriatic ointments that contain vitamin D analogues. Hypervitaminosis D has also been reported following the treatment of hypoparathyroidism. To the authors' knowledge, this is the first report of hypervitaminosis D in dogs following the accidental over supplementation of a commercial diet with vitamin D. While the benefits of adequate dietary vitamin D are well established in dogs, the potential deleterious effects of over supplementation of vitamin D should also be acknowledged.     

Effect of vitamin E and copper on the vitamin E status and performance of growing pigs

A 13-wk trial was conducted with 32 pigs to determine the effects of dietary Cu (250 ppm) and alpha-tocopheryl acetate (ATA, 22 IU/kg) on the performance, serum enzymes, serum and tissue tocopherols, and antibody production in growing pigs. Pigs were fed corn-soybean meal diets containing 21% CP the first 4 wk and 18% CP during the rest of the trial. All feed was stored a minimum of 14 d before it was fed. The addition of Cu decreased (P less than .01) the concentration of alpha-tocopherol in the feed. alpha-Tocopherol concentrations were less than .01 mg/kg in the starter diet and less than 2 mg/kg in the grower diet after 14 d of storage. Supplemental Cu or ATA had no effect on ADG, feed intake, or gain:feed during the first 4 wk. During wk 5 to 13, the addition of Cu to diets containing no ATA increased daily feed intake and decreased gain:feed, but with ATA addition, feed intake decreased and gain:feed increased, resulting in a Cu x ATA interaction (P less than .05). The addition of Cu or ATA had no effect (P greater than .1) on serum glutathione peroxidase or lactic dehydrogenase activity. Serum tocopherols were reduced (P less than .05) by the addition of Cu during wk 1 to 4, 6 (P less than .01), and 7 (P less than .05) and increased (P less than .01) by ATA addition during the entire experiment. The addition of ATA increased the tocopherol concentrations in bile, ham, heart, pancreas, kidney, spleen, liver, psoas and longissimus muscle (P less than .01), kidney fat, backfat, and adrenal gland (P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

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.     

Mulberry heart disease in young pigs without vitamin E and selenium deficiency

Mulberry heart disease persists among young pigs in Denmark although abundant supplies of selenium and vitamin E are added to feedstuffs for sows and pigs. The concentrations of selenium and vitamin E in the liver and heart tissues of young pigs which had died suddenly, and had the characteristic lesions of mulberry heart disease post mortem, were not significantly different from the concentrations found in pigs of the same age which had died suddenly for other reasons. The concentrations of selenium and vitamin E in the livers (0.3 mg/kg and 4 mg/kg, respectively) appeared to be satisfactory in all the pigs examined.     

Nephrotoxicity in lambs apparently caused by experimental feeding withNarthecium ossifragum

Seven lambs were fed a mixture of bog plants containing 15 g (wet matter)Narthecium ossifragum per kg live weight for 10 consecutive days. Their serum creatinine concentration increased from day 1 to 4 but then fell to normal by day 6 after feeding started. In the same animals, the serum magnesium concentration was increased on days 3, 4 and 5. Histopathological examination of the kidneys of 2 lambs killed after being fed 25 gN. ossifragum per kg live weight for one day revealed tubular epithelial cell degeneration and necrosis. There were no signs of disease or distress in the experimental animals and their appetite remained normal throughout the experimental period. It was concluded thatN. ossifragum is probably nephrotoxic to lambs.Abbreviations ALP alkaline phosphatase - ASAT aspartate aminotransferase - -HBA -hydroxybutyric acid - CK creatine kinase - d.m. dry matter - -GT -glutamyltransferase - GLDH glutamate dehydrogenase - MCV mean cell volume - RBC red blood cells - SEM standard error of the mean - WBC white blood cells - w.m. wet matter     

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.     

Inhaled feed particles in experimental pigs with and without vitamin A deficiency.

An attempt was made to experimentally reproduce an unusual respiratory disease of pigs fed a dusty mixture of finely ground peas, wheat, and barley. Groups of vitamin-A-deficient piglets from this herd were either given dry feed and daily exposure to dust from the feed or were given wet feed. Vitamin-A-fortified pigs of another stock were also given the dry feed and dust exposure. The upper and lower respiratory tracts, renal pelves, and interlobular ducts of salivary glands were studied histologically. The distinguishing features of lungs were starch particles from feed (up to 31.2 mum in diameter) in all lungs (but more in lungs of pigs given dry feed), free alveolar macrophages, giant cell formations, and mild degenerative processes of respiratory epithelium. The epithelium of most renal pelves was marked by mucinous degeneration.