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.

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.

Aspectos epidemiológicos e clínico-patológicos de um surto de miopatia nutricional em potros ˗ relato de caso / [Epidemiological and clinical-pathological aspects of an outbreak of nutritional myopathy in young horses ˗ case report]

A miopatia nutricional é uma doença degenerativa que pode afetar os músculos esqueléticos e cardíaco, causada pela deficiência dietética de selênio e/ou vitamina E. Objetivou-se relatar a ocorrência de miopatia nutricional em dois potros Puro Sangue Inglês, criados de forma extensiva, com baixa disponibilidade de forragem e sem suplementação mineral. De um lote de nove animais de diferentes idades (cinco éguas adultas, uma potra lactente de três meses,uma mula e dois potros de 16 e 17 meses), apenas os dois últimos foram afetados. Clinicamente, havia decúbito lateral ou esternal, taquicardia, taquipneia, desidratação e dor à palpação muscular na região dos glúteos.O diagnóstico presuntivo de miopatia nutricional foi realizado por meio da associação dos sinais clínicos aos dados epidemiológicos.O animal 1 foi eutanasiado cinco dias após o atendimento devido à piora gradativa do quadro, e o animal 2 recuperou-se com o tratamento adotado. O diagnóstico foi confirmado com base nos exames complementares, nos achados de necropsia e na dosagem da concentração hepática de selênio. Este relato de caso alerta para o risco da ocorrência de miopatia nutricional em equinos, sobretudo jovens, sem acesso a pastagens ou feno de boa qualidade e sem suplementação mineral adequada.(AU)

Nutritional myopathy is a degenerative disease caused by the dietary deficiency of selenium and/or vitamin E that can affect skeletal and cardiac muscles. The objective of this study was to report the occurrence of nutritional myopathy in two Thoroughbred young horses, raised in pastures with low forage availability and no mineral supplementation. From a herd of nine animals of different ages (five adult mares, one three-month-old nursing foal, one mule and two 16- and 17-month-old horses), only the last two were affected. Clinical signs were lateral or sternal recumbency, tachycardia, tachypnea, dehydration and muscle pain. Presumptive diagnosis of nutritional myopathy was made associating clinical signs and epidemiological data. Animal 1 was euthanized five days after the first evaluation due to clinical signs gets worse, and animal 2 recovered with the established treatment. Diagnosis was confirmed with complementary exams, necropsy findings and levels of hepatic selenium. This paper alerts to the risk of nutritional myopathy occurrence in horses, mainly young animals, which are not ingesting good quality hay or green forage and do not receive appropriate mineral supplementation.(AU)

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.

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.

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.

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.

Chronic vitamin E deficiency impairs cognitive function in adult zebrafish via dysregulation of brain lipids and energy metabolism.

Zebrafish (Danio rerio) are a recognized model for studying the pathogenesis of cognitive deficits and the mechanisms underlying behavioral impairments, including the consequences of increased oxidative stress within the brain. The lipophilic antioxidant vitamin E (α-tocopherol; VitE) has an established role in neurological health and cognitive function, but the biological rationale for this action remains unknown. In the present study, we investigated behavioral perturbations due to chronic VitE deficiency in adult zebrafish fed from 45 days to 18-months of age diets that were either VitE-deficient (E-) or VitE-sufficient (E+). We hypothesized that E- zebrafish would display cognitive impairments associated with elevated lipid peroxidation and metabolic disruptions in the brain. Quantified VitE levels at 18-months in E- brains (5.7 ± 0.1 nmol/g tissue) were ~20-times lower than in E+ (122.8 ± 1.1; n = 10/group). Using assays of both associative (avoidance conditioning) and non-associative (habituation) learning, we found E- vs E+ fish were learning impaired. These functional deficits occurred concomitantly with the following observations in adult E- brains: decreased concentrations of and increased peroxidation of polyunsaturated fatty acids (especially docosahexaenoic acid, DHA), altered brain phospholipid and lysophospholipid composition, as well as perturbed energy (glucose/ketone), phosphatidylcholine and choline/methyl-donor metabolism. Collectively, these data suggest that chronic VitE deficiency leads to neurological dysfunction through multiple mechanisms that become dysregulated secondary to VitE deficiency. Apparently, the E- animals alter their metabolism to compensate for the VitE deficiency, but these compensatory mechanisms are insufficient to maintain cognitive function.

Effects of feeding two RRR-α-tocopherol formulations on serum, cerebrospinal fluid and muscle α-tocopherol concentrations in horses with subclinical vitamin E deficiency.

BACKGROUND: Alpha-tocopherol (α-TP) supplementation is recommended for the prevention of various equine neuromuscular disorders. Formulations available include RRR-α-TP acetate powder and a more expensive but rapidly water-dispersible liquid RRR-α-TP (WD RRR-α-TP). No cost-effective means of rapidly increasing serum and cerebrospinal fluid (CSF) α-TP with WD RRR-α-TP and then sustaining concentrations with RRR-α-TP acetate has yet been reported. OBJECTIVES: To evaluate serum, CSF and muscle α-TP concentrations in an 8-week dosing regimen in which horses were transitioned from WD RRR-α-TP to RRR-α-TP acetate. STUDY DESIGN: Non-randomised controlled trial. METHODS: Healthy horses with serum α-TP of <2 µg/mL were divided into three groups and followed for 8 weeks. In the control group (n = 5), no α-TP was administered. In the second group (Group A; n = 7), 5000 IU/day RRR-α-TP acetate was administered. In the third group (Group WD-A; n = 7), doses of 5000 IU/day of WD RRR-α-TP were administered over 3 weeks, followed by a 4-week transition from WD RRR-α-TP to RRR-α-TP acetate, and a final 1 week of treatment with RRR-α-TP acetate. Serum samples were obtained weekly; muscle biopsies were obtained before, at 2.5 weeks and after supplementation. CSF samples were obtained before and after the 8-week period of supplementation. RESULTS: Serum α-TP increased significantly in Group WD-A at week 1 and remained significantly higher than in Group A and the control group throughout the transition, with inter-individual variation in response. Serum α-TP increased significantly by week 7 in Group A. CSF α-TP increased significantly in Group WD-A only. Muscle α-TP concentrations did not differ significantly across groups. Serum and CSF α-TP were closely correlated (r = 0.675), whereas serum and muscle-α-TP concentrations were not correlated. MAIN LIMITATIONS: The study duration was short and data on pre-transition CSF was lacking. CONCLUSIONS: The administration of 5000 IU/day of water-dispersible RRR-α-TP rapidly increases serum α-TP. Serum and CSF α-TP concentrations are sustained with a gradual transition to 5000 IU/day of RRR-α-TP acetate. Periodic evaluation of serum α-TP concentrations is recommended because responses vary among individuals.

Prevalence of the Novel Torque Teno Sus Virus Species k2b from Pigs in the United States and Lack of Association with Post-Weaning Multisystemic Wasting Syndrome or Mulberry Heart Disease.

The family Anelloviridae includes a number of viruses infecting humans (Torque teno viruses, TTV) and other animals including swine (Torque teno sus viruses, TTSuV). Two genetically distinct TTSuV species have been identified from swine thus far (TTSuV1 and TTSuVk2), although their definitive association with disease remains debatable. In 2012, a novel TTSuV species was identified from commercial swine serum and classified in the genus Kappatorquevirus as TTSuVk2b. The other Kappatorquevirus species, TTSuVk2a, has been associated with post-weaning multisystemic wasting syndrome (PMWS) when coinfected with porcine circovirus type 2 (PCV2). Therefore, in this study, we initially amplified a portion of TTSuVk2b ORF1 and, subsequently, assessed the molecular prevalence of the virus in pigs in the United States. A total of 127 serum and 115 tissue samples were obtained from pigs with PMWS or mulberry heart disease (MHD) in six states and tested by PCR for the presence of TTSuVk2b DNA. Approximately 27.6% of the serum and 21.7% of tissue samples tested positive for TTSuVk2b DNA, and the positive products were confirmed by sequencing. However, we did not detect a correlation between TTSuVk2b infection and PMWS or MHD. The near full-length genomic sequence of US TTSuVk2b was determined, and sequence analysis revealed that the US TTSuVk2b isolates were 95% identical to the TTSuVk2b isolate from Spain, with most of the variations clustering in ORF1. We conclude that the novel TTSuVk2b species is present in pigs in the United States and its potential association with a disease warrants further investigation.

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.

Sheep deficient in vitamin E preferentially select for a feed with a higher concentration of vitamin E.

Given the capacity of ruminants to modify diet selection based on metabolic needs, we hypothesised that, when given a choice, lambs experiencing a vitamin E deficiency would consume more of a vitamin E-enriched feed than lambs not deficient in vitamin E. Fifty-six Dohne Merino lambs were divided into two groups and fed either a vitamin E-deficient diet over 40 days to induce low plasma vitamin E or a vitamin E-enriched diet to induce high plasma vitamin E. The lambs were then offered a choice of vitamin E-enriched and vitamin E-deficient pellets. For half of the animals, the enriched diet was paired with strawberry flavour and the deficient diet was paired with orange flavour, while the reverse pairings were offered to the others. Lamb preference for the diets was measured daily for the following 15 days. There was a three-way interaction between the high and low vitamin E treatment groups×vitamin E content and type of flavour in the feed×time (days). The lambs preferred pellets flavoured with strawberry but this preference changed to orange flavour in vitamin E-deficient lambs if the orange flavour was paired with high vitamin E. Lambs without a deficiency continued to prefer strawberry-flavoured pellets, regardless of the vitamin E concentrations in the pellets. It is possible that self-learning contributed to the low vitamin E group of lambs changing preference to orange flavour in order to consume more vitamin E, presumably to remediate the deficiency.

Effect of feeding peroxidized dried distillers grains with solubles to sows and progeny on growth performance and metabolic oxidative status of nursery pigs.

This experiment evaluated the effects of including peroxidized corn dried distillers grains with solubles (DDGS) in diets for sows and nursery pigs on growth performance, vitamin E (VE), and Se status, and the incidence of mulberry heart disease (MHD) of nursery pigs. Sows (n = 12) were fed corn-soybean meal diets (C-SBM) or C-SBM diets with DDGS (40% and 20% in gestation and lactation, respectively) for 3 parities. In the third parity, 108 weaned pigs (BW = 6.6 ± 0.36 kg) were blocked by BW within litter, assigned to pens (2 pigs/pen; 5 and 4 pens per litter for groups 1 and 2, respectively), and pens were assigned 1 of 3 nursery diets: 1) corn-soybean meal (CON), 2) 30% peroxidized DDGS (Ox-D), and 3) 30% Ox-D with 5 × NRC (1998) level of VE (Ox-D+5VE) for 7 wk, in a 2 × 3 factorial arrangement of sow and nursery diets (n = 9 pens/treatment). The peroxidized DDGS source in nursery diets contained concentrations of thiobarbituric acid reactive substances (TBARS) and peroxide values that were 25 and 27 times greater than a reference corn sample. Sow colostrum, milk, and serum, as well as pig serum and liver samples, were analyzed for α-tocopherol and Se concentrations. Pig serum was analyzed for glutathione peroxidase activity (GPx), TBARS, and sulfur-containing AA (SAA). Pig hearts were evaluated for gross and histopathological lesions indicative of MHD, but none were detected. Pigs from sows fed DDGS tended to have reduced (P = 0.07) VE in serum during lactation and reduced VE at weaning (P < 0.01; 5.6 vs. 6.7 ± 0.1 µg/mL) compared with pigs from sows fed C-SBM. Inclusion of DDGS in sow diets reduced the VE status of pigs during lactation, but not in the nursery when MHD can be a concern. Pigs fed Ox-D+5VE (P = 0.08) tended to have, and those fed Ox-D (P = 0.04) had greater ADFI than pigs fed CON, but ADG was not affected (P > 0.1) by nursery diet. Feeding Ox-D or Ox-D+5VE increased (P < 0.05) serum α-tocopherol compared with CON (2.5, 2.8, and 3.4 ± 0.09 µg/mL, respectively), but TBARS and GPx were not affected by nursery diet. Serum concentration of SAA was 40% to 50% greater (P < 0.01) for pigs fed Ox-D or Ox-D+5VE compared with those fed C-SBM, which was likely due to greater (P < 0.01) SAA intake for pigs fed Ox-D. The antioxidant properties of SAA may have spared VE and Se and masked any effect of Ox-D on metabolic oxidation status. Therefore, increasing the dietary VE concentration was unnecessary in nursery diets containing Ox-D.

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.

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.

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.

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.

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.