Equine degenerative myeloencephalopathy in Lusitano horses

Background

Equine degenerative myeloencephalopathy (EDM) is a neurodegenerative disorder that has been previously associated with low vitamin E concentrations.

Objective

To describe the clinical, electrophysiologic, and pathologic features of EDM in a group of related Lusitano horses.

Animals

Fifteen Lusitano horses.

Procedures

Neurologic examinations were conducted, and serum vitamin E concentrations were measured. Three neurologically abnormal horses were further evaluated by ophthalmologic examination, electroretinography, electroencephalography, muscle and nerve biopsies, and post‐mortem examination.

Results

Six horses appeared neurologically normal, 6 were neurologically abnormal, and 3 had equivocal gait abnormalities. Abnormal horses demonstrated ataxia and paresis. An inconsistent menace response was noted in 4 neurologically abnormal horses and in 1 horse with equivocal findings. All horses had low serum vitamin E concentrations (<1.5 ppm). Ophthalmologic examinations, electroretinograms, electroencephalograms, and muscle and peripheral nerve biopsies were unremarkable in 3 neurologically abnormal horses. At necropsy, major neuropathological findings in these horses were bilaterally symmetric, severe, neuro axonal degeneration in the gracilis, cuneatus medialis, cuneatus lateralis, and thoracicus nuclei and bilaterally symmetric axonal loss and demyelination mainly in the dorsolateral and ventromedial tracts of the spinal cord. A diagnosis of EDM was made based on these findings. Pedigree analysis identified 2 sires among the affected horses.

Conclusions and Clinical Relevance

Equine degenerative myeloencephalopathy is a neurodegenerative disorder that causes ataxia and, in severe cases, paresis, in young Lusitano horses. The disease appears to have a genetic basis, and although vitamin E deficiency is a common finding, low serum vitamin E concentrations also may occur in apparently unaffected related individuals.     

Evaluation of the risk of motor neuron disease in horses fed a diet low in vitamin E and high in copper and iron

OBJECTIVE: To determine whether equine motor neuron disease (EMND) could be induced in adult horses fed a diet low in vitamin E and high in copper and iron. ANIMALS: 59 healthy adult horses. PROCEDURE: Horses in the experimental group (n = 8) were confined to a dirt lot and fed a concentrate low in vitamin E and high in iron and copper in addition to free-choice grass hay that had been stored for 1 year. Control horses (n = 51) were fed a concentrate containing National Research Council-recommended amounts of copper, iron, and vitamin E. The hay fed to control horses was the same as that fed to experimental horses, but it had not been subjected to prolonged storage. Control horses had seasonal access to pasture, whereas experimental horses had no access to pasture. Horses that developed clinical signs of EMND were euthanatized along with an age-matched control horse to determine differences in hepatic concentrations of vitamin E, vitamin A, copper, iron, and selenium. RESULTS: 4 experimental horses developed clinical signs of EMND. Plasma concentrations of vitamin E decreased in all 8 experimental horses. There were no significant changes in plasma concentrations of vitamin A, selenium, and copper or serum concentrations of ferritin. There were no significant differences in those analytes between experimental horses with EMND and experimental horses that did not develop EMND. No control horses developed EMND. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that lack of access to pasture, dietary deficiency of vitamin E, or excessive dietary copper are likely risk factors for EMND.     

Assessment of the influence of dietary vitamin E on sows and offspring in three parities: reproductive performance, tissue tocopherol, and effects on progeny

Sixty crossbred (Yorkshire-Hampshire X Duroc) gilts were fed one of four corn-soybean meal diets fortified with .3 ppm Se and 0, 16, 33, or 66 IU of DL-alpha-tocopheryl acetate/kg. The study was conducted over a three-parity period to evaluate sow reproductive performance and the vitamin E tissue status of both sows and progeny at various time periods postcoitum and(or) postpartum. The basal diet averaged 8.4 mg of alpha-tocopherol/kg and .38 ppm of Se. Although litter size at birth was lowest (P less than .15) when sows were fed the basal diet, a higher incidence of agalactia when sows were fed the lower dietary vitamin E levels resulted in an increased (P less than .05) litter size at 7 d postpartum as dietary vitamin E increased. Sow serum alpha-tocopherol increased (P less than .01) at each measurement period as dietary vitamin E level increased. Colostrum and milk alpha-tocopherol concentrations increased (P less than .01) as dietary vitamin E level increased, and colostrum values were three to five times higher than at later milks. Colostrum alpha-tocopherol declined by parity from sows fed less than or equal to 16 IU/kg but was similar at each parity for sows fed greater than or equal to 33 IU/kg, resulting in a dietary vitamin E x parity interaction (P less than .01). The Se content of sow milk declined with parity but was not affected by dietary vitamin E level. Sow liver tocopherol at weaning (28 d postpartum) increased (P less than .01) as dietary vitamin E increased and increased with parity (P less than .05). Pig serum and liver alpha-tocopherol concentrations were elevated at birth and 7 and 28 d of age as sow dietary level of vitamin E increased. Upon weaning, pigs were fed a torula yeast-dextrose diet that contained 3.0 mg of alpha-tocopherol/kg and .32 ppm Se for a 28-d postweaning period. Liver and serum alpha-tocopherol concentrations declined during the postweaning period. Evidence of the vitamin E deficiency occurred at 28 d postweaning in the progeny from sows fed the basal diet or 16 IU of vitamin E; the incidence was more prevalent in the pigs from Parities II and III. These results suggest that a supplemental level of 16 IU of vitamin E/kg of diet was inadequate for the reproducing sow; higher levels are justified, particularly when females are retained in the herd for several parities.     

A survey of whole blood selenium concentrations of horses in Maryland

We surveyed the whole blood selenium status of a randomly sampled population of horses from 4 contiguous counties in northern Maryland. Two hundred and two horses from 74 farms were sampled. Whole blood selenium levels greater than or equal to 0.100 parts per million (ppm) were considered adequate; blood levels less than 0.100 ppm were considered marginal or deficient. The average blood selenium concentration of the horses sampled was 0.137 ppm, with a standard deviation of 0.041 ppm. Blood selenium concentrations ranged from 0.050-0.266 ppm. Thirty-eight of 202 horses (18.8%) had a selenium level less than or equal to 0.099 ppm. Twenty-one of 74 farms (28.4%) had at least 1 horse with a selenium level less than or equal to 0.099 ppm. Animal husbandry practices had a significant influence on selenium status. Horses were more prone to having an abnormal selenium status if they were either maintained on pasture or used infrequently, or if their diet did not include mineral and vitamin supplements.     

Down-regulation of GPx1 mRNA and the loss of GPx1 activity causes cellular damage in the liver of selenium-deficient rabbits

The effects of 10 weeks of dietary selenium and/or vitamin E deficiency (< 0.03 mg Se and 1.5 mg vitamin E per kg diet) on body Se and vitamin E stores and on the down-regulation of liver cellular glutathione peroxidase (GPx1) and plasma glutathione peroxidase (GPx3) were examined in growing female New Zealand White rabbits in comparison to Se (+ 0.40 mg Se/kg diet) and/or vitamin E (+ 150 I.U./kg diet) supplemented controls. Additionally plasma lactate dehydrogenase (LDH) activity, liver thiobarbituric acid-reactive substances (TBA-RS) and liver protein carbonyls were measured to assess the development of oxidative stress during an alimentary Se and/or vitamin E deficiency. Significantly decreased concentrations of Se and vitamin E in plasma (Se: − 70%; vitamin E: − 87%) and liver (Se: − 90%; vitamin E: − 95%) indicated an efficacious Se and vitamin E depletion of the rabbits within 10 weeks. GPx1 messenger RNA levels (GPx1 mRNA) in the livers of Se-depleted rabbits were down-regulated to 1/3–1/8 of the Se supplemented controls. GPx1 enzyme activity in the livers of Se-deficient rabbits declined to 10% of the Se-supplied control rabbits. A significantly elevated LDH activity in the blood plasma of Se- and vitamin E-deficient rabbits indicated a general impairment of tissues. Markedly increased TBA-RS concentrations and protein carbonyl contents in the livers of Se- and vitamin E-deficient rabbits gave further evidence for severe oxidative damage of cellular lipids and proteins during an alimentary Se and/or vitamin E deficiency. Both a full expresssion of GPx1 attained by dietary Se supplementation and dietary vitamin E supply effected an almost complete protection against oxidative cellular damage of the liver.     

Serum IgM concentrations in normal,fit horses and horses with lymphoma or other medical conditions

The purposes of this study were to (1) prospectively establish serum IgM and IgG concentrations in normal, fit, adult horses over time and (2) determine the accuracy of serum IgM concentrations for diagnosing lymphoma. Serial IgM and IgG concentrations were measured with a radial immunodiffusion assay in 25 regularly exercised horses at 6-week intervals. Horses had serum IgM concentrations ranging from 50 to 242 mg/dL over 5 months, with 20% of horses having IgM < or = 60 mg/dL. The normal range for IgM in fit horses should be considered 103 +/- 40 mg/dL and a cut-point for an IgM deficiency, < or = 23 mg/dL. IgG concentrations ranged from 1,372 to 3,032 mg/dL. Retrospectively, medical records of adult horses (n = 103) admitted to the Cornell University Hospital for Animals for which serum IgM was measured were examined. Horses were categorized as "lymphoma negative" (n = 34) or "lymphoma positive" (n = 18). The sensitivity and specificity of a serum IgM concentration (< or = 60 mg/dL) for detecting equine lymphoma was 50 and 35%, respectively. At the new cut-point (< or = 23 mg/dL), the sensitivity was low at 28% and the specificity improved to 88%. The negative predictive values at various population prevalences indicate that a horse with a high serum IgM (> 23 mg/dL) is unlikely to have lymphoma, whereas the positive predictive value (70%) does not allow for reliable determination of lymphoma in a horse with serum IgM < or = 23 mg/dL. Therefore, serum IgM concentrations should not be used as a screening test for equine lymphoma.     

Serum Vitamin E Concentration of Horses on Different Vitamin E Supplementation Levels

Abstract

The influence of vitamin E supplementation on blood serum vitamin E concentration as well as the seasonal variation of serum vitamin concentration was investigated. Forty horses were divided into a control and three vitamin E supplementation (experimental) groups. The levels of the vitamin E supplementation in the three experimental groups were 1, 3 or 5 mg/kg body weight (bwt) per day. The vitamin was dosed orally. The supplementation was started either at the beginning or in the middle of the indoor (winter) feeding period. There was seasonal variation in the serum vitamin E content; the serum vitamin concentration increased during the grazing and decreased during the indoor feeding period. The basal feeding and a daily supplement of 1 mg/kg bwt were not adequate to maintain or increase the serum vitamin E concentration during the indoor feeding period in an exercising horse. The minimum daily intake of vitamin E would seem to be greater than 1.5 mg/kg bwt. It is suggested that a daily supplement of 3 to 5 mg/kg bwt may be required by horses in training to increase the serum vitamin E levels. This amounts to 1500–2500 mg/day for a horse weighing 500 kg. Supplementation should be started at the beginning of the indoor feeding period.     

The vitamin A and vitamin E status of horses raised in Alberta and Saskatchewan.

The purpose of the study was to determine normal baseline levels of vitamin A and vitamin E in clinically normal horses under typical field conditions in Saskatchewan and Alberta. Heparinized blood samples were collected from approximately 400 clinically healthy horses selected from 24 locations in Alberta and Saskatchewan during a two-year period. For each horse, historical information including feed type, vitamin supplementation, time of year, sex, and age were recorded. From each blood sample, the plasma vitamin A (all-transretinol) and vitamin E (alpha-tocopherol) levels were measured using high pressure liquid chromatography. Normal baseline plasma vitamin A and vitamin E concentrations recorded during the study were 0.70 mumol/L and 7.65 mumol/L, respectively. The plasma vitamin concentrations were lower in the younger horses. The plasma vitamin levels were higher from May to August, as compared to other times of the year. Horses grazing fresh pasture exclusively during the summer months had plasma vitamin A and vitamin E concentrations that were 27% and 63% greater than horses fed harvested or stored feeds during the same time period. Sex-related differences were not evident in the study. A number of factors may influence the baseline plasma vitamin A and vitamin E levels in horses. Consequently, it is unadvisable to use a single evaluation to assess vitamin status. Multiple sampling from individual horses or sampling from many horses within a herd may reduce the variability and improve the ability to monitor vitamin status from plasma submissions.     

Effect of dietary selenium and vitamin E on the ultrastructure and ATP concentration of boar spermatozoa, and the efficacy of added sodium selenite in extended semen on sperm motility

Three experiments evaluated the effects of dietary Se and vitamin E on the ultrastructure of spermatozoa, ATP concentration of spermatozoa, and the effects of adding sodium selenite to semen extenders on subsequent sperm motility. The experiment was a 2 x 2 arrangement of treatments in a randomized complete block design. A total of 10 mature boars were fed from weaning to 18 mo of age diets fortified with two levels of supplemental Se (0 or .5 ppm) or vitamin E (0 or 220 IU/kg diet). The nonfortified diets contained .06 ppm Se and 4.4 IU vitamin E/kg. In Exp. 1, the spermatozoa from all boars were examined by electron microscopy. Vitamin E had no effect on structural abnormalities in the spermatozoa. When the low-Se diet was fed the acrosome or nuclei of the spermatozoa was unaffected, but the mitochondria in the tail midpiece were more oval with wider gaps between organelles. The plasma membrane connection to the tail midpiece was not tightly bound as when boars were fed Se. Immature spermatozoa with cytoplasmic droplets were more numerous when boars were fed the low-Se diet, but the occurrence of midpiece abnormalities occurred in boars fed diets with or without Se or vitamin E. Our results suggest that Se may enhance spermatozoa maturation in the epididymis and may reduce the number of sperm with cytoplasmic droplets. In Exp. 2, the concentration of ATP in the spermatozoa was evaluated in the semen of all treatment boars. When the low-Se diet was fed, ATP concentration was lower (P < .01), whereas vitamin E had no effect on ATP concentration. Experiment 3 investigated the effect of diluting boar semen with a semen extender with sodium selenite added at 0, .3, .6, or .9 ppm Se. Three ejaculates from each boar were used to evaluate these effects on sperm motility to 48 h after dilution. Sperm motility declined (P < .01) when Se was added to the extender, and this decline was exacerbated as the concentration of added Se increased (P < .01). The added Se was demonstrated to be tightly adhered to the spermatozoa. Overall, these results suggest that low Se-diets fed to boars resulted in abnormal spermatozoal mitochondria, a lower ATP concentration in the spermatozoa, and a loose apposition of the plasma membrane to the helical coil of the tail midpiece, but no effect from inadequate vitamin E was demonstrated. Adding sodium selenite to the semen extender reduced sperm cell motility.     

Vitamin E status of healthy Swedish cattle

Using high pressure liquid chromatography the serum concentration of vitamin E was measured in dairy cows fed either hay or silage as their main roughage, in calves fed milk-replacer, and in young intensively fed bulls. The concentrates fed to the cows, calves and bulls were supplemented with 5–10, 25 and 5–10 mg DL-α-tocopheryl acetate per kg, respectively, and the milk-replacer for the calves was supplemented with 50 mg DL-α-tooopheryl acetate per kg powder. Cows fed silage as their main roughage had higher serum vitamin E concentrations (: 3.8–5.2 mg/l) than cows fed only hay (: 2.5–4.1 mg/1). Lactating cows had higher vitamin E concentrations than dry cows (: 4.1–5.2 and 2.5–3.8 mg/l, respectively) and calves and bulls had much lower vitamin E concentrations (: 1.4 and 1.2 mg/l, respectively) than cows. Thirty per cent of the calves and 41 % of the bulls had serum vitamin E concentrations less than 1.0 mg/l, suggesting that in these animals the conventional level of supplementation of feeds with DL-α-tocopheryl acetate in Sweden is probably inadequate for the prevention of nutritional muscular degeneration and other negative effects.     

The influence of dietary selenium levels on blood levels of selenium and glutathione peroxidase activity in the horse

Twenty mature geldings, averaging 535 kg, were used to determine the influence of dietary selenium (Se) on the blood levels of Se and Se-dependent glutathione peroxidase (SeGSH-Px) activity in the horse. Horses were randomly assigned within breed to four treatments consisting of five horses each and fed a basal diet containing .06 ppm of naturally occurring Se. Diets were supplemented with .05, .10 and .20 ppm Se, as sodium selenite. Blood was drawn for 2 wk before, and for 12 wk following, the inclusion of supplement Se in the diets. Whole blood and plasma Se concentrations and plasma SeGSH-Px activities were determined from all blood samples. Selenium concentrations in plasma and whole blood increased linearly from wk 1 to wk 5 and 6, respectively, in Se-supplemented horses. After these times, no significant changes in Se concentration were observed in Se-supplemented or in unsupplemented horses throughout the remainder of the 12-wk trial. Plasma Se reached plateaus of .10 to .11, .12 to .14, and .13 to .14 micrograms/ml in horses supplemented with .05, .10 and .20 ppm Se, respectively. Whole blood Se reached plateaus of .16 to .18, .19 to .21, and .17 to .18 micrograms/ml in horses supplemented with .05, .10 and .20 ppm Se, respectively. Plasma SeGSH-Px activity was not significantly affected by dietary treatment. Therefore, this enzyme was not a good indicator of dietary Se in these mature horses.     

Dietary omega-3 fatty acid supplementation does not impair vitamin E status or promote lipid peroxidation in growing horses

Omega-3 (n-3; ω-3) fatty acids (FA) are often included in the diet for their potential health benefits. However, because oxidative potential is increased with the degree of unsaturation in vitro, polyunsaturated FA such as eicosapentaenoic acid (EPA; 20:5n-3) and docosahexaenoic acid (DHA; 22:6n-3) may be at increased risk of lipid peroxidation. We aimed to determine the effects of dietary n-3 FA supplementation on antioxidant status and lipid peroxidation in yearling horses. Quarter Horses (mean ± SEM; 14.6 ± 0.2 mo) were randomly assigned to receive no n-3 FA supplementation (CON; n = 6) or 60 mg n-3/kg body weight from milled flaxseed (FLAX; n = 6) or encapsulated fish oil (FISH; n = 6). All horses received a basal diet of mixed grain concentrate fed individually at 1.5% body weight (dry matter basis) and ad libitum bahiagrass pasture forage. Blood samples were obtained before and after 70 d of supplementation to evaluate vitamin E, selenium, lipids, antioxidant status, and oxidative stress. Data were analyzed using a mixed model ANOVA with repeated measures. Supplementation with n-3 FA did not reduce serum vitamin E or Se and, in fact, elevated (P ≤ 0.0003) vitamin E status in FISH horses. At day 70, serum triglycerides were lower in FISH and FLAX horses than CON horses (P ≤ 0.02) and F2-isoprostanes were lower in FISH than CON horses (P = 0.0002). Dietary n-3 FA had no effect on cholesterol, reduced and oxidized glutathione, glutathione peroxidase, and thiobarbituric acid-reactive substances. In growing horses fed to meet their vitamin E requirements, supplementation with 60 mg n-3/kg body weight did not negatively affect vitamin E status or promote lipid peroxidation. Elevated vitamin E status in horses fed FISH, coupled with lower serum F2-isoprostanes, further suggest that the longer-chain, highly unsaturated n-3 FA, EPA and DHA, may actually attenuate lipid peroxidation.     

Acute vitamin D3 toxicosis in horses: case reports and experimental studies of the comparative toxicity of vitamins D2 and D3

Acute vitamin D toxicosis was diagnosed in 2 horses fed a grain ration containing 1,102,311 IU of cholecalciferol (vitamin D3)/kg (500,000 IU/lb) for about 30 days. Horse 1 died acutely with extensive mineralization of cardiovascular and other soft tissues. Horse 2, which had severe clinical signs and clinicopathologic changes of toxicosis, was treated with nonsteroidal antiinflammatory drugs and recovered in about 6 months. In an experimental study, the toxicity of ergocalciferol (vitamin D2) and cholecalciferol was compared in 2 horses (No. 3 and 4) given the respective vitamins at a daily dosage of 33,000 IU/kg of initial (day 0) body weight for 30 days. Except for slight loss in body weight (8%) during the 1st few days of treatment, horse 3 remained clinically normal. Horse 4 developed limb stiffness and tachycardia, became anorectic, weak, and recumbent, lost 29% of body weight, and had polydipsia and polyuria. Horses 2, 3, and 4 developed persistent hyperphosphatemia. Horse 2 remained normocalcemic whereas horses 3 and 4 became hypercalcemic by day 28. In horse 3, serum vitamin D2 metabolite concentrations on days 0, 1, 14, and 26 were: vitamin D2 (ng/ml) = less than 5.0, 5.7, 71.4, and 188.0; 25-hydroxy-vitamin D2 (ng/ml) = less than 5.0, less than 5.0, 43.1, and 117.5; and 1,25-dihydroxy-vitamin D (pg/ml) = 19.7, 23.2, 25.0, and 45.7, respectively. In horse 4, serum vitamin D3 metabolite concentrations on the same days were: vitamin D3 (ng/ml) = less than 5.0, 110.0, 1,049.0, and 887.0; 25-hydroxy-vitamin D3 (ng/ml) = less than 5.0, 18.9, 201.0 and 182.0; and 1,25-dihydroxy-vitamin D (pg/ml) = 21.5, 18.9, 25.2, and 21.6, respectively. Urine of horses 2 and 4 became acidic (pH 6). Horses 2, 3, and 4 became hyposthenuric, but the decrease in urine specific gravity (sp gr) in horse 3 occurred only after 3 weeks of treatment and was only moderate (sp gr, 1.018 to 1.021) and nonprogressive. Hyposthenuria was evident in horse 4 on day 4 (sp gr, 1.028), and was progressive and marked (sp gr, days 28 to 32: 1.006 to 1.009). Urine sp gr of horse 2 ranged from 1.002 to 1.007. Fractures were demonstrated radiographically and histologically in the costochondral junctions of horses 3 and 4. Mineralization of cardiovascular and other soft tissues developed in horses 3 and 4, with lesions being more severe and having a wider tissue distribution in horse 4.     

Status of selenium and vitamin E on Norwegian organic sheep and dairy cattle farms

Herbage selenium (Se) concentration is generally low in Norway. It is unknown whether feeding practices on Norwegian organic farms fulfil the dietary needs of Se and vitamin E for sheep and dairy cattle. Therefore we analysed Se in soil and herbage, and Se and vitamin E in animal blood in the indoor feeding season at 14 organic dairy and 14 organic sheep farms. The herbage Se concentration was low. Approximately 50 and 35% of all samples in the first and second cut, respectively, had Se concentrations below the detection limit of 0.01 mg/kg dry matter (DM). The median (10th, 90th percentile) Se concentrations were <0.01 (<0.01, 0.03) and 0.02 (<0.01, 0.06) mg/kg DM in the first and second cuts, respectively. Whole blood Se concentrations were 0.10 (0.04, 0.15) μg/g in dairy cattle and 0.14 (0.03, 0.26) μg/g in sheep. Vitamin E concentrations were 4.2 (2.7, 8.4) mg/l in dairy cattle and 1.3 (0.9, 2.4) mg/l in sheep. None of the soil or plant variables explained the variation in herbage Se concentration, although Se in soil and plant tended to be correlated. Herbage Se concentration was inadequate to meet the dietary Se requirements. Vitamin E requirement was only met in dairy herds. We recommend Se and vitamin E supplementation to ruminants on organic farms.     

Genetic predisposition of pigs to hypo- and hyperselenemia

A continuing, sporadic incidence of vitamin E-selenium (Se) responsive disease among confinement-reared pigs believed to be fed complete and adequately supplemented diets prompted these studies on the potential genetic influence over vitamin E and Se metabolism in pigs. The initial study revealed a wide range of serum Se and vitamin E concentrations among age-matched, commonly housed and commonly fed growing pigs. Pigs found relatively hyposelenemic (hypo-Se) or hyperselenemic (hyper-Se) early in life retained their relative Se status while commonly reared. The persistence of vitamin E status was poor. Selected matings between identified, relatively hypo-Se gilts and boars and between relatively hyper-Se gilts and boars produced similarly affected baby pigs. In Exp. 2, representative hypo-Se (20) and hyper-Se (20) pigs were identified from a total of 107 baby pigs by 30 d of age. These pigs were allotted to an experiment to compare the responses of these two populations to .1 and .3 ppm supplemental dietary Se through 150 d of age. The difference in mean serum Se of the selected hypo- and hyper-Se pigs fed .1 ppm Se was significant at each sampling time. This difference approximated that observed between pigs (either hypo- or hyperselenemic) fed .1 and .3 ppm Se. The increase in serum Se due to .3 ppm supplemental dietary Se was greater among the selected hypo-Se pigs than among the hyper-Se pigs. Plasma Se-dependent glutathione peroxidase (GSH-Px) was a better indicator of dietary or serum Se status than was erythrocyte GSH-Px. The selected hyper-Se pigs maintained a more rapid rate of growth than did the hypo-Se pigs and were approximately 10 kg heavier at 150 d than the hypo-Se pigs.     

Effects of monensin on selenium status and related factors in genetically hypo- and hyperselenemic growing swine.

Monensin is an ionophoretic antibiotic, which selectively transports alkali metal cations across biological membranes. In growing swine, monensin toxicosis causes acute, degenerative cardiac and skeletal myopathy resembling vitamin E-selenium deficiency. Selenium is an essential trace element incorporated in glutathione peroxidase (GSH-Px), an antioxidant enzyme system that protects subcellular membranes. In our study, we examined the effects of monensin on body weight, Se balance, antioxidant status, and serum concentrations of selected minerals in growing pigs that were genetically hypo- or hyperselenemic (hypo-Se and hyper-Se, respectively). Three groups of eight 8-week-old pigs, each comprised of 4 hypo-Se and 4 hyper-Se pigs (76.4 +/- 3.0 and 106.3 +/- 10.3 ng of Se/ml of serum, respectively), were fed standard diets containing 0.1 mg of supplemental Se/kg of body weight, and either 0, 200, or 400 mg of monensin/kg for a 77-day period, followed by a 28-day monensin withdrawal period. On days 0, 7, 28, 56, 70, and 98, all pigs were weighed and blood was collected for determination of serum GSH-Px, creatine phosphokinase, and aspartate transaminase values, as well as serum concentrations of vitamin E, Se, Ca, Cu, Fe, K, Mg, Na, P, and Zn. Significance of main effects of monensin treatment, genetic Se status, and their interactions was tested by Fisher's variance ratio test, followed by conditional comparison of treatment means with a Bonferroni test. Signs of monensin toxicosis were not observed and monensin consumption had no effect on body weight, or serum creatine phosphokinase, aspartate transaminase, or Se values. However, pigs consuming monensin had consistently higher serum GSH-Px activities, possibly because of increased synthesis of this adaptive antioxidant enzyme. Interactions were not found between monensin and genetic Se status. Hyperselenemic pigs were heavier and had higher serum Se and GSH-Px values than hypo-Se pigs. Furthermore, hypo-Se and hyper-Se pigs were hypo- and hypercupremic, respectively, suggesting genetic regulation of copper status. It is likely that pigs with inadequate antioxidant status (hyposelenemia, hypocupremia) are more susceptible to diseases associated with cellular membrane damage, such as vitamin E-Se deficiency disease and monensin toxicosis.     

Dose response effects of long-acting injectable vitamin B12 plus selenium (Se) on the vitamin B12 and Se status of ewes and their lambs

AIM: To determine the effect of increasing doses of long-acting injectable vitamin B12 plus selenium (Se) given pre-mating on the vitamin B12 and Se status of ewes and their lambs from birth to weaning. METHODS: Four groups of 24 Poll Dorset ewes each were injected 4 weeks pre-mating with different doses of a long-acting vitamin B12 + Se product, containing 3 mg vitamin B12 and 12 mg Se per ml. The treatment groups received 5 ml (15 mg vitamin B12 + 60 mg Se), 4 ml (12 mg vitamin B12 + 48 mg Se), 3 ml (9 mg vitamin B12 + 36 mg Se), or no vitamin B12 or Se (control). Twelve of the twin-bearing ewes per group were selected for the study. Efficacy of the product was evaluated from changes in the concentrations of vitamin B12 in serum and liver, and of Se in blood, liver and milk in the ewes during gestation and lactation, and in their lambs from birth to weaning. Pasture samples in paddocks grazed by the ewes and lambs were collected at about 2-monthly intervals from 200-m transects. RESULTS: The flock was Se-deficient, as the mean initial concentration of Se in the blood of ewes was 182 (SE 20.3) nmol/L. Compared with untreated controls, all doses significantly (p < 0.01) increased concentrations of Se in the blood of ewes for at least 300 days. Selenium concentrations in milk were likewise increased throughout lactation, as were those in the blood and liver of lambs. The mean concentration of vitamin B12 in the serum of ewes was initially > 1,000 pmol/L, but this decreased within 28 days to < 460 pmol/L. Treatment with the 5-ml and 4-ml doses raised serum vitamin B12 concentrations of ewes for at least 176 days (p < 0.01), while their lambs had significantly greater concentrations of vitamin B12 in serum and liver for less than 37 days after birth. Tissue concentrations and duration of elevation of both vitamin B12 and Se were proportional to the dose administered. The mean concentrations of Se and cobalt (Co) in the pastures were 32 and 74 microg/kg dry matter (DM), respectively. CONCLUSIONS: Injecting ewes from a Se-deficient flock 4 weeks prior to mating with 48 or 60 mg Se and 12 or 15 mg vitamin B12 increased and maintained the Se status of ewes for at least 300 days, and of their lambs from birth to weaning. The vitamin B12 status of ewes was increased for at least 176 days and that of their lambs for less than 37 days. Due to the proportional nature of the response to increasing dosage, the dose rate of the formulation tested can be adjusted according to the severity of Se and Co deficiency in a flock. CLINICAL SIGNIFICANCE: A single subcutaneous injection of vitamin B12 + Se administered pre-mating to Se-deficient flocks is likely to prevent Se deficiency in ewes and their lambs until weaning, as well as increase the vitamin B12 status of ewes and their lambs until 5 weeks after lambing.     

Effect of selenium on performance, serum selenium concentration and glutathione peroxidase activity in pigs

Pigs from sows fed a diet deficient in Se and low in vitamin E were fed a Torula yeast diet supplemented with 100 IU dl-alpha-tocopheryl acetate/kg of diet. Dietary treatments were levels of supplemental Se of 0, .025, .050, .075 or .100 ppm. Some death loss occurred in pigs receiving no supplemental Se at approximately 5 wk of age. Autopsy revealed liver and heart lesions typical of vitamin E-Se deficiency. Selenium supplement had no significant effect on average daily gain, feed intake or gain to feed ratio for the 4-wk experiment. Selenium status of pigs was determined by serum Se concentration and serum glutathione peroxidase (GSH-Px) activity. Serum Se increased linearly (P less than .01) with increasing supplemental Se. Serum GSH-Px activity increased linearly (P less than .01) and quadratically (P less than .05) with increasing supplemental Se. With time, the level of serum Se and GSH-Px activity decreased in unsupplemental pigs, but increased in pigs fed diets supplemented with Se and resulted in significant interactions (P less than .01) between dietary Se level and time on experiment. The correlation between serum Se concentration and GSH-Px activity was .81 (P less than .01).     

Progression of Femoropatellar Osteochondrosis in Nine Young Horses Clinical, Radiographic and Arthroscopic Findings

The clinical and radiographic progression, and arthroscopic findings for nine young horses (<1 year of age) with femoropatellar osteochondrosis (OCD) are presented. Horses had a 2 to 12 week history of bilateral (8 horses) or unilateral (1 horse) hindlimb lameness. The most consistent clinical signs included femoropatellar joint distention and bilateral hindlimb lameness. At the onset of clinical signs, radiographic lesions were not present (4 horses) or subtle (5 horses), but were easily identified on radiographs taken 4 to 24 weeks later. Arthroscopic surgery was delayed until radiographic changes became obvious. Surgical findings in 20 femoropatellar joints were most commonly osteochondral "flaps" located on the proximal lateral trochlear ridge of the femur and were larger than had been indicated by the radiographs. Eight horses were being used for their intended purpose, which was racing (3 horses were racing and 3 were in race training), dressage (1 horse) or pleasure riding (1 horse). One horse required a second surgery when similar lesions developed in the opposite stifle, and was euthanatized 2 months later because of persistent lameness. Once clinical signs are observed, osteochondrosis lesions of the distal femur can progress in foals younger than 9 months of age and the full extent of the radiographic lesion may take several weeks to develop.     

Horses on pasture may be affected by equine motor neuron disease

REASONS FOR PERFORMING STUDY: Equine motor neuron disease (EMND) was diagnosed in 3 horses maintained on lush, grass-based pasture. This contrasted with North American studies which identified limited or no access to green herbage as an important risk factor for EMND. HYPOTHESIS: Grazing horses that have an apparently adequate intake of pasture herbage to meet normal equine vitamin E requirements can develop EMND. METHODS: Owners of 32 European horses diagnosed with EMND completed a questionnaire regarding intrinsic, managemental, nutritional and environmental factors that could potentially be risk factors for EMND, and also regarding clinical signs, treatments and case outcome. Plasma/serum vitamin E data for these horses were supplied by the veterinarians. No control population was studied. RESULTS: Thirteen of 32 horses (termed the 'grazing' group) had part- or full-time access to grass-based pasture at the onset of EMND (median duration at pasture 12 h/day, range 3-24 h). Five of these horses were at pasture for at least 235 h/day at the onset of EMND, 2 of which were at pasture for at least 23.5 h/day throughout the year. Despite grazing, all these horses had a low vitamin E status. The remaining 19 horses resembled those cases reported from North America, in that they had no or limited access to pasture. CONCLUSIONS AND POTENTIAL RELEVANCE: A diagnosis of EMND should not be discounted on the basis that a horse has access, even full-time, to lush grass-based pasture. Inadequate vitamin E intake was probably not the sole cause of either the EMND or the low vitamin E status in the grazing horses; the latter was probably the result of abnormal bioavailability or excessive utilisation of vitamin E.