Vitamin E deficiency depressed fish growth, disease resistance, and the immunity and structural integrity of immune organs in grass carp (Ctenopharyngodon idella): Referring to NF-κB, TOR and Nrf2 signaling.

This study investigated the effects of dietary vitamin E on growth, disease resistance and the immunity and structural integrity of head kidney, spleen and skin in grass carp (Ctenopharyngodon idella). The fish were fed six diets containing graded levels of vitamin E (0, 45, 90, 135, 180 and 225 mg/kg diet) for 10 weeks. Subsequently, a challenge test was conducted by injection of Aeromonas hydrophila. The results showed that compared with optimal vitamin E supplementation, vitamin E deficiency caused depressed growth, poor survival rates and increased skin lesion morbidity in grass carp. Meanwhile, vitamin E deficiency decreased lysozyme and acid phosphatase activities, complement component 3 and complement component 4 contents in the head kidney, spleen and skin of grass carp (P < 0.05). Moreover, vitamin E deficiency down-regulated antimicrobial peptides (Hepcidin, liver-expressed antimicrobial peptide-2A, -2B, ß-defensin), IL-10, TGFß1, IκBα, TOR and S6K1 mRNA levels (P < 0.05) and up-regulated IL-1ß, IL-6, IL-8, IFN-γ2 and TNFα, NF-κB p65, IKKα, IKKß and 4EBP1 (not in the head kidney) mRNA levels (P < 0.05). In addition, vitamin E deficiency caused oxidative damage, decreased superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and glutathione reductase (GR) activities, and down-regulated the mRNA levels of antioxidant enzymes and signaling molecules Nrf2 (P < 0.05). Vitamin E deficiency also induced apoptosis by up-regulating capase-2, -3, -7, and -8 mRNA levels in the head kidney, spleen and skin of grass carp. In conclusion, this study indicated that dietary vitamin E deficiency depressed fish growth, impaired the immune function and disturbed the structural integrity of the head kidney, spleen and skin in grass carp, but optimal vitamin E supplementation can reverse those negative effects in fish. The optimal vitamin E requirements for young grass carp (266.39-1026.63 g) to achieve optimal growth performance and disease resistance based on the percent weight gain (PWG) and skin lesion morbidity were estimated to be 116.2 and 130.9 mg/kg diet, respectively. Meanwhile, based on immune indicator (LA activity in the head kidney) and antioxidant indicator (protection of spleen against MDA), the optimal vitamin E requirements for young grass carp were estimated to be 123.8 and 136.4 mg/kg diet, respectively.

Pigment retinopathy in warmblood horses with equine degenerative myeloencephalopathy and equine motor neuron disease.

OBJECTIVE: A pigment retinopathy has been reported in adult horses with equine motor neuron disease (EMND) arising from chronic α-tocopherol (α-TP) deficiency. A pigment retinopathy has not been identified in horses with neuroaxonal dystrophy/equine degenerative myeloencephalopathy (NAD/EDM) that affects genetically susceptible young horses with α-TP deficiency. The objective of this report is to describe, for the first time, a pigment retinopathy in a family of α-TP-deficient Warmbloods (WB) with clinically apparent NAD/EDM or EMND. ANIMALS AND PROCEDURES: Twenty-five WB horses from one farm underwent complete neurologic and ophthalmic examinations and serum α-TP concentrations were assessed. Two of the most severely ataxic horses were euthanized and postmortem examinations performed. RESULTS: Alpha-TP deficiency was widespread on this farm (22 of 25 horses). Eleven of 25 horses were clinically normal (age range 2-12 years), one had signs of EMND (6 years of age), 10 had signs of ataxia consistent with NAD/EDM (1-10 years), and two of these were postmortem confirmed concurrent NAD/EDM and EMND. A pigment retinopathy characterized by varying amounts of granular dark pigment in the tapetal retina was observed in four clinically apparent NAD/EDM horses (two postmortem confirmed concurrent NAD/EDM and EMND) and one horse with clinical signs of EMND. CONCLUSIONS: A pigment retinopathy can be present in young α-TP-deficient Warmblood horses with clinical signs of EMND as well as those with signs of NAD/EDM.

CONGENITAL NUTRITIONAL MYODEGENERATION (WHITE MUSCLE DISEASE) IN A GIRAFFE ( GIRAFFA CAMELOPARDALIS) CALF.

It is well known that vitamin E and selenium deficiencies in domestic ruminants can lead to white muscle disease. After a clinically normal gestation period at Ouwehand Zoo in the Netherlands, a newborn giraffe ( Giraffa camelopardalis) calf showed clinical signs of white muscle disease almost immediately after birth. The calf was rejected by the mother and was euthanized 3 days later because of deterioration of clinical signs. At necropsy, pulmonary edema and pallor of skeletal and heart muscles was noted. Histologically, there was hyaline degeneration of skeletal muscle myocytes and pulmonary edema. Blood concentrations of vitamin E were ≤ 0.7 mg/L. Based on clinical, biochemical, and gross and microscopic pathological findings, congenital nutritional myodegeneration was diagnosed. This case of neonatal white muscle disease is particularly remarkable given that the diet of the dam contained more than the recommended amount of vitamin E.

Acute phase response elicited by experimental bovine diarrhea virus (BVDV) infection is associated with decreased vitamin D and E status of vitamin-replete preruminant calves.

Studies in young animals have shown an association between vitamin deficiencies and increased risk of infectious disease; however, there is a paucity of information regarding the effect of acute infection on the vitamin status of the vitamin-replete neonate. To characterize the effects of acute infection on vitamin D and E status of the neonate, 6 vitamin-replete preruminant Holstein bull calves were experimentally infected with bovine viral diarrhea virus (BVDV; strain BVDV2-1373). Six mock-inoculated calves served as controls. Sustained pyrexia, leukopenia, and asynchronous increases in serum haptoglobin and serum amyloid A characterized the response of calves to infection with BVDV. Infection was also associated with increased serum IFN-γ, IL-2, and IL-6 concentrations. During the last 8 d of the 14-d postinoculation period, serum 25-hydroxyvitamin D and α-tocopherol concentrations in infected calves decreased by 51 and 82%, respectively. The observed inverse association between vitamin D and E status and serum amyloid A in infected calves suggests that the infection-induced acute phase response contributed to the reduced vitamin status of these animals. Additional studies are necessary to determine if the negative effect of infection on status are unique to this specific infection model or is representative of preruminant calf's response to acute infection. Studies are also needed to characterize mechanisms underlying infection-related changes in vitamin D and E status and to determine whether additional vitamin D or E supplementation during an acute infection diminishes disease severity and duration in the young animal.

Effect of replacing dietary vitamin E by sage on performance and meatiness of spent hens, and the oxidative stability of sausages produced from their meat.

A total of 3960 hens (half ISA Warren and half Dekalb White) were housed in 18 compartments with 220 hens each. The effect of replacing dietary vitamin E by sage on productivity, meat yield and oxidative stability of sausages was studied. One third of all animals received either a vitamin E deficient diet (negative control) or diets supplemented with 30 mg/kg α-tocopherylacetate (positive control) or 25 g sage leaves/kg. At slaughter, meat yield was assessed and sausages were produced (n = 12 per treatment). The omission of vitamin E did not impair the oxidative stability of the raw sausage material or the spiced sausages in comparison to the positive control. Sage supplementation improved oxidative stability after 7 m of frozen storage, but not after 1, 4 and 10 m. Spice addition during meat processing had an antioxidant effect regardless of dietary treatment. Diet supplementation of any type did not affect laying performance and sausage meat yield. Feeding antioxidants to spent hens seemed to be not as efficient as in growing chickens, while seasoning with spices during sausage production proved to be a feasible way to delay lipid oxidation.

Current insights into equine neuroaxonal dystrophy/equine degenerative myeloencephalopathy.

Equine neuroaxonal dystrophy/equine degenerative myeloencephalopathy (eNAD/EDM) is an inherited neurodegenerative disease associated with vitamin E deficiency in the first year of life. It is the second most common cause of spinal ataxia in horses euthanized for neurologic disease. Equine NAD/EDM is characterized by neurologic signs including a symmetric proprioceptive ataxia (> grade 2/5) and a wide-base stance at rest. There are currently no antemortem tests for eNAD/EDM in any breed. Conclusive diagnosis requires postmortem histologic evaluation of the brainstem and spinal cord at necropsy. Research studies on antemortem biomarkers and genetic testing are ongoing. The development of a genetic test for eNAD/EDM would have widespread impact, even if it were breed specific. Currently, the best approach to eNAD/EDM is to focus on preventing cases by providing pregnant mares and foals with access to pasture. Alternatively, dams' diets can be supplemented with high doses of water-soluble RRR-α-tocopherol during the last trimester of gestation, with continued supplementation of foals through the first two years of life. It is important to measure horses' baseline serum vitamin E levels prior to supplementing. While considered generally safe, oversupplementation of vitamin E is possible and can lead to coagulopathies.

Equine neuroaxonal dystrophy/degenerative myeloencephalopathy in Gypsy Vanner horses.

BACKGROUND: Equine neuroaxonal dystrophy/degenerative myeloencephalopathy (eNAD/EDM) is a neurodegenerative disease that primarily affects young, genetically predisposed horses that are deficient in vitamin E. Equine NAD/EDM has not previously been documented in Gypsy Vanner horses (GVs). OBJECTIVES: To evaluate: (1) the clinical phenotype, blood vitamin E concentrations before and after supplementation and pedigree in a cohort of GV horses with a high prevalence of neurologic disease suspicious for eNAD/EDM and (2) to confirm eNAD/EDM in GVs through postmortem evaluation. ANIMALS: Twenty-six GVs from 1 farm in California and 2 cases from the Midwestern U.S. METHODS: Prospective observational study on Californian horses; all 26 GVs underwent neurologic examination. Pre-supplementation blood vitamin E concentration was assessed in 17- GVs. Twenty-three were supplemented orally with 10 IU/kg of liquid RRR-alpha-tocopherol once daily for 28 days. Vitamin E concentration was measured in 23 GVs after supplementation, of which 15 (65%) had pre-supplementation measurements. Two clinically affected GVs from California and the 2 Midwestern cases had necropsy confirmation of eNAD/EDM. RESULTS: Pre-supplementation blood vitamin E concentration was ≤2.0 µg/mL in 16/17 (94%) of GVs from California. Post-supplementation concentration varied, with a median of 3.39 µg/mL (range, 1.23-13.87 µg/mL), but only 12/23 (52%) were normal (≥3.0 µg/mL). Normalization of vitamin E was significantly associated with increasing age (P = .02). Euthanized horses (n = 4) had eNAD/EDM confirmed at necropsy. CONCLUSIONS AND CLINICAL IMPORTANCE: GVs could have a genetic predisposition to eNAD/EDM. Vitamin E supplementation should be considered and monitored in young GVs.

Depleted serum vitamin E concentrations precede left displaced abomasum in early-lactation dairy cows.

Cows with left displaced abomasum (LDA), a costly disease occurring primarily in multiparous dairy cows during early lactation, have been reported to have 40% lower circulating concentrations of vitamin E. It is unknown, however, whether the lower circulating α-tocopherol concentrations precede LDA or remain after LDA. Using a nested case-control design, blood samples taken at d -21, -14, -7, -3, -1, 0, 1, 3, 7, 14, 21, 28, 35, 42, and 49 postpartum from 7 multiparous Holstein cows diagnosed with LDA between d 6 and 32 postpartum and 10 healthy Holstein cows from the same herd were analyzed for serum concentrations of α-tocopherol and indicators of energy and nutrient status and inflammation. In addition to indicators of negative energy balance and inflammation, lower serum α-tocopherol concentrations preceded LDA and persisted after LDA correction. At the last blood sampling before LDA diagnosis, cows had serum α-tocopherol concentrations 45% lower (5.0 ± 0.9 vs. 9.1 ± 0.9 µM) and α-tocopherol to cholesterol molar ratios 39% lower (1.90 ± 0.19 vs. 3.09 ± 0.26) than those of healthy cows. Serum α-tocopherol concentrations remained lower (<10 vs. ~15 µM) up to d 49 postpartum in cows that had LDA. These findings indicate that lower serum α-tocopherol concentrations are a potential early indicator for the development of LDA in multiparous cows.

Evidence of oxidative injury of the spinal cord in 2 horses with equine degenerative myeloencephalopathy.

The cervical spinal cords of 2 horses with equine degenerative myeloencephalopathy (EDM) were evaluated for evidence of oxidative damage to the central nervous system (CNS) using immunohistochemical staining for 3-nitrotyrosine (3-NT) and 4-hydroxynonenol (4-HNE). Neurons of the CNS from horses with EDM had positive immunohistochemical staining, whereas control samples did not, thus supporting the theory that oxidative damage is a potential underlying factor in horses with EDM. In addition, serum vitamin E concentration was low in both EDM-affected horses, and vitamin E concentration was also deficient in the cerebrospinal fluid in 1 EDM horse, further supporting the association between low vitamin E concentrations and oxidative damage to the CNS. Continued research is necessary to further define the pathophysiologic mechanisms of EDM.

Oral vitamin E absorption in English Cocker Spaniels with familial vitamin E deficiency and retinal pigment epithelial dystrophy.

BACKGROUND: Retinal Pigment Epithelial Dystrophy (RPED) with neuroaxonal degeneration in English Cocker Spaniels (ECS) is associated with systemic vitamin E deficiency in the absence of dietary insufficiency. OBJECTIVE: To evaluate the ability of ECS with RPED to absorb orally administered vitamin E and establish a basis for vitamin E supplementation in affected dogs. ANIMALS STUDIED: 8 RPED-affected ECS and five clinically normal dogs. PROCEDURES: An oral vitamin E tolerance test (OVETT) was conducted in each dog. Blood samples were obtained prior to and at 3, 6, 9, 12, 24, 120, and 240 h following oral administration of 90 iu/kg of RRR-α-tocopherol. Plasma alpha tocopherol (αTOC) content was measured by normal phase, high-performance liquid chromatography, and indices of vitamin E absorption calculated. RESULTS: There was marked variation in OVETT results between individuals. In RPED-affected ECS, mean peak plasma αTOC concentration (17.87 ± 13.21 µg/mL), attained after administration of a large oral dose of the vitamin, was significantly lower than the mean peak plasma αTOC concentration attained in normal dogs (47.61 ± 17.17 µg/mL; P < 0.005). However, the plasma concentrations achieved in 7/8 RPED-affected dogs remained within the normal reference range for plasma αTOC in vitamin E-replete dogs, for at least 12 h postdose. CONCLUSIONS: Vitamin E-deficient ECS with RPED are capable of absorbing orally administered vitamin E. Twice daily administration of 600-900 iu tocopherol is likely to restore plasma vitamin E concentrations to the normal range in most affected dogs.

Vitamin E Deficiency Disrupts Gene Expression Networks during Zebrafish Development.

Vitamin E (VitE) is essential for vertebrate embryogenesis, but the mechanisms involved remain unknown. To study embryonic development, we fed zebrafish adults (>55 days) either VitE sufficient (E+) or deficient (E-) diets for >80 days, then the fish were spawned to generate E+ and E- embryos. To evaluate the transcriptional basis of the metabolic and phenotypic outcomes, E+ and E- embryos at 12, 18 and 24 h post-fertilization (hpf) were subjected to gene expression profiling by RNASeq. Hierarchical clustering, over-representation analyses and gene set enrichment analyses were performed with differentially expressed genes. E- embryos experienced overall disruption to gene expression associated with gene transcription, carbohydrate and energy metabolism, intracellular signaling and the formation of embryonic structures. mTOR was apparently a major controller of these changes. Thus, embryonic VitE deficiency results in genetic and transcriptional dysregulation as early as 12 hpf, leading to metabolic dysfunction and ultimately lethal outcomes.

The selenium and vitamin E status of horses in Prince Edward Island.

Serum selenium (Se), vitamin E, and resting thyroid hormone concentrations were measured in 201 horses in Prince Edward Island (PEI). Selenium concentrations were either marginal (0.0053 to 0.1200 ppm) or deficient (< 0.0053 ppm) in 79% of horses based on current reference ranges for Se in serum. Aged and young adult pleasure horses had a higher prevalence of inadequate Se concentrations compared to racehorses and broodmares (82% and 97% versus 45% and 72%, respectively). Overall, 13% of horses had inadequate (< 200 µg/dL) serum vitamin E concentrations; most of these were young pleasure horses. No horses were hypothyroid and, contrary to findings in other species, there was a positive relationship between serum thyroxine and Se concentrations (P < 0.05). We conclude that Se deficiency is widespread in PEI horse populations, especially in pleasure horses, and vitamin E deficiency is more common in young pleasure horses. Micronutrient supplementation practices employed by PEI horse owners appear inadequate to ensure sufficiency.

Influence of specific management practices on blood selenium, vitamin E, and beta-carotene concentrations in horses and risk of nutritional deficiency.

BACKGROUND: Selenium or alpha-tocopherol deficiency can cause neuromuscular disease. Beta-carotene has limited documentation in horses. OBJECTIVE: To evaluate the effect of owner practices on plasma beta-carotene concentration and risk of selenium and alpha-tocopherol deficiencies. ANIMALS: Three-hundred and forty-nine adult (≥1 year), university and privately owned horses and mules. METHODS: Cross-sectional study. Whole blood selenium, plasma alpha-tocopherol, and plasma beta-carotene concentrations were measured once. Estimates of daily selenium and vitamin E intake, pasture access, and exercise load were determined by owner questionnaire. Data were analyzed using t tests, Mann-Whitney tests, parametric or nonparametric analysis of variance (ANOVA), Kruskal-Wallis test, Spearman's correlation and contingency tables (P < .05). RESULTS: Nearly 88% of the horses received supplemental selenium; 71.3% received ≥1 mg/d. Low blood selenium concentration (<80 ng/mL) was identified in 3.3% of horses, and 13.6% had marginal concentrations (80-159 ng/mL). Non-supplemented horses were much more likely to have low blood selenium (odds ratio [OR], 20.2; 95% confidence interval [CI], 9.26-42.7; P < .001). Supplemental vitamin E was provided to 87.3% of horses; 57.7% received ≥500 IU/d. Deficient (<1.5 µg/mL) and marginal (1.5-2.0 µg/mL) plasma (alpha-tocopherol) occurred in 15.4% and 19.9% of horses, respectively. Pasture access (>6 h/d) and daily provision of ≥500 IU of vitamin E was associated (P < .001) with higher plasma alpha-tocopherol concentrations. Plasma beta-carotene concentration was higher in horses with pasture access (0.26 ± 0.43 versus 0.12 ± 0.13 µg/mL, P = .003). CONCLUSIONS AND CLINICAL IMPORTANCE: Suboptimal blood selenium and plasma alpha-tocopherol concentrations occurred in 16.7% and 35.5% of horses, respectively, despite most owners providing supplementation. Inadequate pasture access was associated with alpha-tocopherol deficiency, and reliance on selenium-containing salt blocks was associated with selenium deficiency.

Mulberry Heart Disease and Hepatosis Dietetica in Farm Pigs (Sus scrofa domesticus) in a Research Setting.

Perioperative complications and deaths occurred while developing a novel surgical model of pediatric kyphosis in 10 to 12 kg male farm-raised Yorkshire piglets. All piglets appeared clinically normal preoperatively. Intraoperative complications included tachycardia, respiratory acidosis, and death. Postoperatively, clinical signs included posterior paresis, head pressing, prolonged anesthetic recovery, difficulty rising, and sudden death. Necropsies were performed on all piglets. Some morbidity and mortality were accurately attributed to the spinal surgery. However, the index piglet for this report died suddenly approximately 16 to 18 h after surgery. Necropsy of this animal revealed clear, serosanguineous pleural and pericardial effusions along with myocardial hemorrhage and hepatic lesions, consistent with mulberry heart disease and hepatosis dietetica, respectively. Serum vitamin E and selenium levels from this animal were below age-specific lab reference ranges. Clinical signs of vitamin E and selenium deficiency are most common in fast-growing weaner piglets. The added stress of major surgery may exacerbate the condition in young piglets. Resolution of morbidity and mortality in both juvenile and adult pigs occurred upon the use of an alternate vendor able to provide feed analyses meeting industry standards, although serum levels of vitamin E and selenium in similar ages and breed of swine were still occasionally slightly below reference ranges.

Clinical and pathological findings associated with congenital hypovitaminosis A in extensively grazed beef cattle.

OBJECTIVE: To determine the cause of exceptionally high mortality (41.4%) in perinatal calves on a beef cattle property 50 km south-west of Julia Creek in north-western Queensland. DESIGN: Investigations were based on clinical assessment of affected calves and laboratory analysis of pre- and postmortem specimens taken from 12 calves aged from 6 to 36 h of age. METHODS: Associations between gross and histopathological findings and biochemical analyses conducted on serum and tissue samples were examined in relation to clinical observations. RESULTS: Clinical signs varied, but commonly included mild to severe ataxia, difficulty finding a teat and sucking, blindness (partial or complete, as judged by avoidance of obstacles) and depression with prominent drooping of the head. Gross and histopathological findings included herniation of the cerebellar vermis through the foramen magnum, squamous metaplasia of interlobular ducts in the parotid salivary glands and Wallerian degeneration of the optic nerves. Biochemical analysis of serum and liver samples available from four of the calves revealed low or undetectable levels of both vitamin A and vitamin E. CONCLUSION: Although vitamin E is known to have a sparing effect on vitamin A, the role (if any) played by deficiency of this vitamin was uncertain. The combination of clinical signs, postmortem findings, histopathological features and biochemical findings indicate that gestational vitamin A deficiency was highly likely to have been an important contributor to perinatal calf mortalities in this herd.

Investigating the Risk of Equine Motor Neuron Disease in a Brazilian Stable and Successful Intervention.

We carried out an investigation to identify the factors that predispose to the risk of equine motor neuron disease (EMND) and evaluated the long-term impact of an intervention. Data on several biomarkers, including antioxidants (α-tocopherols, ß-carotenes, glutathione peroxidase (GSHPx)), and superoxide dismutase (SOD1), neurofilaments, and other putative risk factors hypothesized to associate with the likelihood of EMND were collected. The data were analyzed for their significance of association with the condition. The EMND outbreak started in 1991 and continued until 1998. A total of 69 EMND cases and 64 control horses met the inclusion criteria and were enrolled in the study. Most cases (74%) occurred in 1996 and 1997. Horses afflicted with EMND had significantly lower plasma levels of vitamin E than control horses (0.381 vs. 1.148 µg/mL). There were no significant differences in the levels of vitamin A, ß-carotenes, GSHPx, or the activities of SOD1 between EMND cases and control horses. Horses afflicted with EMND had significantly higher serum levels of phosphorylated neurofilament heavy than controls (2.85 vs. 0.27 ng/mL). The probability of EMND diagnosis increased above 50% when the serum levels of phosphorylated neurofilament heavy increased beyond 2.54 ng/mL. Mixed and Brazilian breeds had a significantly higher risk of EMND in comparison to Standardbred horse among the study population. In 1997, there was a change in the diet where better quality green hay was used. The incidence of EMND dropped to 0 in 1 year after intervention and remained at that level for the past 20 years.

Impact of alpha-tocopherol deficiency and supplementation on sacrocaudalis and gluteal muscle fiber histopathology and morphology in horses.

BACKGROUND: A subset of horses deficient in alpha-tocopherol (α-TP) develop muscle atrophy and vitamin E-responsive myopathy (VEM) characterized by mitochondrial alterations in the sacrocaudalis dorsalis medialis muscle (SC). OBJECTIVES: To quantify muscle histopathologic abnormalities in subclinical α-TP deficient horses before and after α-TP supplementation and compare with retrospective (r)VEM cases. ANIMALS: Prospective study; 16 healthy α-TP-deficient Quarter Horses. Retrospective study; 10 retrospective vitamin E-responsive myopathy (rVEM) cases . METHODS: Blood, SC, and gluteus medius (GM) biopsy specimens were obtained before (day 0) and 56 days after 5000 IU/450 kg horse/day PO water dispersible liquid α-TP (n = 8) or control (n = 8). Muscle fiber morphology and mitochondrial alterations were compared in samples from days 0 and 56 and in rVEM cases. RESULTS: Mitochondrial alterations more common than our reference range (<2.5% affected fibers) were present in 3/8 control and 4/8 treatment horses on day 0 in SC but not in GM (mean, 2.2; range, 0%-10% of fibers). Supplementation with α-TP for 56 days did not change the percentage of fibers with mitochondrial alterations or anguloid atrophy, or fiber size in GM or SC. Clinical rVEM horses had significantly more mitochondrial alterations (rVEM SC, 13% ± 7%; GM, 3% ± 2%) and anguloid atrophy compared to subclinical day 0 horses. CONCLUSIONS AND CLINICAL IMPORTANCE: Clinically normal α-TP-deficient horses can have mitochondrial alterations in the SC that are less severe than in atrophied VEM cases and do not resolve after 56 days of α-TP supplementation. Preventing α-TP deficiency may be of long-term importance for mitochondrial viability.

Parenteral selenium and vitamin E supplementation of weaned beef calves.

BACKGROUND: The weaning process in beef calves elicits physiological stress responses that can negatively affect performance and health. Supplementation of vitamins and minerals, particularly selenium (Se) and vitamin E, might be warranted. HYPOTHESIS: That parenteral administration of Se or vitamin E would correct or prevent deficiencies of these nutrients in postweaned beef calves during a backgrounding period (42 days after weaning). ANIMALS: One hundred and forty-four weaned steers (200-250 kg) in 3 trials. METHODS: One trial was conducted with cattle on a dry lot fed a total mixed ration and 2 trials were conducted on cattle on pasture. Selenium was administered at 0.05 mg/kg BW (SC) and vitamin E was administered at 1500 IU on days 0 and 28 (SC). RESULTS: A treatment effect attributable to Se or vitamin E supplementation on average daily gain was not detected in any trials. Parenteral supplementation with Se on days 0 and 28 resulted in higher serum Se concentrations as compared with controls on day 42. Parenteral supplementation with Se on days 0 and 28 improved Se status from marginal to adequate in 1 trial. Parenteral supplementation with vitamin E did not improve serum vitamin E concentrations in any experiment. CONCLUSIONS AND CLINICAL IMPORTANCE: Supplementation with vitamin E or Se or a combination of both did not have a significant effect on calf performance during the 42-day backgrounding period.

Field investigation of perinatal mortality in friesian cattle associated with myocardial degeneration and necrosis.

Perinatal mortality and stillbirths were investigated in an extensively managed herd of Friesian cows and heifers calving over a 2-year period: 504 cows were calved and 215 heifers. Cows were bred to Friesian and Jersey bulls using natural service. The perinatal fetal mortality rate was 7.5% for cows and 30% for heifers. An experienced stockman managed these calvings and veterinary assistance was required only on nine occasions. All stillborn fetuses were examined post-mortem by the Veterinary Laboratories Agency, Carmarthen and no infectious agent was identified on any occasion. Thyroid hyperplasia was found in two fetuses. In blood samples taken from 10 late pregnant heifers, mean glutathione peroxidase values were 7.9 +/- 1.7 IU/ml Packed Cell Volume (PCV). Tissues from eight fetuses were submitted to the University of Liverpool for histopathological examination; all presented lesions consistent with myocardial degeneration and necrosis of the left ventricle. Following treatment of 205 late pregnant heifers with sodium selenite and vitamin E, the overall perinatal mortality rate in these cattle fell to below 11%.

Juvenile mortality in captive lesser kudu (Tragelaphus imberbis) at Basle Zoo and its relation to nutrition and husbandry.

Since 1956, when the Basle Zoo (Switzerland) initiated the breeding of lesser kudu (Tragelaphus imberbis), 43% of the lesser kudu juveniles died before reaching an age of 6 mo. In this study, the objective was to obtain the pathological findings, nutritional history, and family tree information in order to evaluate the influence of husbandry on juvenile mortality in these animals. The main cause of death was white muscle disease (WMD), diagnosed in 14 cases (26%) of the deceased juveniles. Although enclosure size had remained constant and animal accessibility to the public was constantly high, both herd size and juvenile mortality had increased from 1956-2004. The diet consumed by the whole group in 2004 had deficient levels of vitamin E and selenium. The increasing linear trend of the mortality rate since the 1960s was significant, and there was a significant correlation between herd size and overall juvenile mortality. In contrast, there was no correlation between herd size and the occurrence of juvenile mortality associated specifically with WMD. Other investigated factors (sex, inbreeding, and season) had no significant effect on overall mortality up to 6 mo of age or on mortality associated with WMD. These results characterize both a dietary and a husbandry problem, and are supported by a lack of similar juvenile mortality in another facility where the diet was supplemented with vitamin E, animal numbers were kept low, and the enclosure structure offered more retreat options for the animals.