Concurrent Equine Degenerative Myeloencephalopathy and Equine Motor Neuron Disease in Three Young Horses.
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ABSTRACT:
SUBMITTER: Finno CJ
PROVIDER: S-EPMC5089576 | biostudies-literature | 2016 Jul
REPOSITORIES: biostudies-literature
Publications
Concurrent Equine Degenerative Myeloencephalopathy and Equine Motor Neuron Disease in Three Young Horses.
Finno C J CJ Miller A D AD Sisó S S Divers T T Gianino G G Barro M V MV Valberg S J SJ
Journal of veterinary internal medicine 20160614 4
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Project description:ObjectiveA 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 proceduresTwenty-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.ResultsAlpha-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.ConclusionsA 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.
| S-EPMC5292316 | biostudies-literature
Project description:Equine degenerative myeloencephalopathy (EDM) is characterized by a symmetric general proprioceptive ataxia in young horses, and is likely underdiagnosed for 2 reasons: first, clinical signs overlap those of cervical vertebral compressive myelopathy; second, histologic lesions--including axonal spheroids in specific tracts of the somatosensory and motor systems--may be subtle. The purpose of this study was (1) to utilize immunohistochemical (IHC) markers to trace axons in the spinocuneocerebellar, dorsal column-medial lemniscal, and dorsospinocerebellar tracts in healthy horses and (2) to determine the IHC staining characteristics of the neurons and degenerated axons along the somatosensory tracts in EDM-affected horses. Examination of brain, spinal cord, and nerves was performed on 2 age-matched control horses, 3 EDM-affected horses, and 2 age-matched disease-control horses via IHC for calbindin, vesicular glutamate transporter 2, parvalbumin, calretinin, glutamic acid decarboxylase, and glial fibrillary acidic protein. Primary afferent axons of the spinocuneocerebellar, dorsal column-medial lemniscal, and dorsospinocerebellar tracts were successfully traced with calretinin. Calretinin-positive cell bodies were identified in a subset of neurons in the dorsal root ganglia, suggesting that calretinin IHC could be used to trace axonal projections from these cell bodies. Calretinin-immunoreactive spheroids were present in EDM-affected horses within the nuclei cuneatus medialis, cuneatus lateralis, and thoracicus. Neurons within those nuclei were calretinin negative. Cell bodies of degenerated axons in EDM-affected horses are likely located in the dorsal root ganglia. These findings support the role of sensory axonal degeneration in the pathogenesis of EDM and provide a method to highlight tracts with axonal spheroids to aid in the diagnosis of this neurodegenerative disease.
| S-EPMC4831571 | biostudies-literature
Project description:Equine neuroaxonal dystrophy/equine degenerative myeloencephalopathy (eNAD/EDM) is a neurologic disease that has been reported in young horses from a wide range of breeds. The disease is inherited and associated with vitamin E deficiency during the first two years of life, resulting in bilateral symmetric ataxia. A missense mutation (chr3:71,917,591 C > T) within adhesion G protein-coupled receptor L3 (ADGRL3) was recently associated with risk for EDM in the Caspian breed. In order to confirm these findings, genotyping of this missense mutation, along with the three other associated single nucleotide polymorphisms (SNPs) in the genomic region, was carried out on 31 postmortem-confirmed eNAD/EDM cases and 43 clinically phenotyped controls from various breeds. No significant association was found between eNAD/EDM confirmed cases and genotype at any of the four identified SNPs (P > 0.05), including the nonsynonymous variant (EquCab2.0 chr3:71,917,591; allelic P = 0.85). These findings suggest that the four SNPs, including the missense variant in the ADGRL3 region, are not associated with risk for eNAD/EDM across multiple breeds of horses.
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Project description:BackgroundEquine herpesvirus myeloencephalopathy (EHM) is a persistent threat to horses, with unclear risk factors and disease severity.ObjectivesTo evaluate risk factors, effective reproduction rate (Rt), and long-term athletic outcomes of an EHM outbreak.MethodsRetrospective study of the 2021 EHM outbreak in Valencia, Spain, examining associations between risk factors (sex, age, breed, country of origin, and vaccination status) and case fatality rate, EHM development, and odds of returning to competition using odds ratios [95% CI] and Rt via the Robert Kochs Institute method.ResultsAmong 191 horses, 38 (20%) were clinically normal, 13 (7%) were subclinical, and 140 (73%) presented clinical signs (89 EHM, 64%). One hundred sixty horses were isolated at the show, while 47 were treated in hospitals. The mean age was 9.8 ± 3.0 years; 85 (45%) were mares, 79 (41%) geldings, and 27 (14%) stallions. The EHM case fatality rate was 11/89 (12%). Vaccination was associated with EHM development (4.54[2.23-9.27]; OR[95% CI]; p < 0.001) and case fatality rate (3.9[1.1-14.4]; OR[95% CI]; p < 0.043). EHV-1-infected horses without EHM were more likely to return to competition (54/61; 89%) than those recovering from EHM (65/89; 73%; p = 0.024). It was initially 4.2 and decreased to < 1 within 2 weeks of the outbreak.ConclusionsDuring the 2021 EHV-1 outbreak in Valencia, vaccination status appears to be associated with EHM development. Horses recovering from EHM had slightly lower chances of returning to competition than those shedding EHV-1 without EHM. The high Rt value underscores the contagious nature of EHV-1.
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Project description:Equine herpesvirus-1 is the cause of respiratory disease, abortion, and equine herpesvirus myeloencephalopathy (EHM) in horses worldwide. EHM affects as many as 14% of infected horses and a cell-associated viremia is thought to be central for EHM pathogenesis. While EHM is infrequent in younger horses, up to 70% of aged horses develop EHM. The aging immune system likely contributes to EHM pathogenesis; however, little is known about the host factors associated with clinical EHM. Here, we used the "old mare model" to induce EHM following EHV-1 infection. Peripheral blood mononuclear cells (PBMCs) of horses prior to infection and during viremia were collected and RNA sequencing with differential gene expression was used to compare the transcriptome of horses that did (EHM group) and did not (non-EHM group) develop clinical EHM. Interestingly, horses exhibiting EHM did not show respiratory disease, while non-EHM horses showed significant respiratory disease starting on day 2 post infection. Multiple immune pathways differed in EHM horses in response to EHV-1. These included an upregulation of IL-6 gene expression, a dysregulation of T-cell activation through AP-1 and responses skewed towards a T-helper 2 phenotype. Further, a dysregulation of coagulation and an upregulation of elements in the progesterone response were observed in EHM horses.
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Project description:BackgroundMicroRNAs (miRNAs) are potential biomarkers for equine sarcoids (ES).ObjectivesTo assess eca-miR-331, eca-miR-100, and eca-miR-1 as serum biomarkers for ES disease.AnimalsSixty-eight ES cases (56 horses, 12 donkeys), 69 tumor-free controls (60 horses, 9 donkeys), and 20 horses with other skin tumors.MethodsFor this case-control study, expression of serum eca-miR-331, eca-miR-100, and eca-miR-1 in ES-affected equids was compared to tumor-free age-, sex-, and breed-matched control horses and donkeys with other skin tumors using reverse transcription quantitative PCR (polymerase chain reaction) for relative miRNA quantification. Biological, preanalytical, and clinical variable influences on miRNA expression were examined. Receiver operator characteristic (ROC) curve analyses were used to determine differences in miRNA expression between groups.ResultsThe expression of eca-miR-100 was affected by age (P = .003) and expression of eca-miR-100 and eca-miR-1 were affected by hemolysis (both P < .001). Eca-miR-331 was unaffected by biological variation, hemolysis, ES type, and disease severity. Eca-miR-331 concentrations were higher in ES-affected compared to tumor-free controls (P = .002). The ROC curve analysis indicated an area under the curve of 0.65 (P = .002) with a sensitivity of 60%, specificity of 71%, and positive and negative likelihood ratios of 2.1 and 0.56, respectively, to diagnose ES. Eca-miR-331 expression did not discriminate between horses with ES and other skin tumors. Expression of eca-miR-100 and eca-miR-1 was not different between groups.Conclusions and clinical importanceSerum eca-miR-331 expression is neither sensitive nor specific enough as a single ES biomarker. If combined with other miRNAs, it may be helpful for ES diagnosis.
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Project description:Recumbency is a prerequisite for horses achieving rapid eye movement (REM) sleep and completing a full sleep cycle. An inability to lie down due to environmental insecurities or pain results in REM sleep deficiency, which can cause substantial impairment of welfare and health. Therefore, the present study used wearable automated sensor technology on 83 horses housed in an animal sanctuary to measure and compare the recumbency, locomotion, and standing time budgets of geriatric horses with and without chronic lameness to younger adult sound and lame horses. Recumbency times ranged from 0 to 319 min per day with an overall mean of 67.4 (±61.9) minutes; the time budget for locomotion was 19.1% (±11.2% s.d.) and for standing 75.6% (±13.1 s.d.). Interestingly, neither age nor lameness due to chronic orthopedic disease had a significant influence on recumbency times in this study. Eight horses showed symptoms of REM deficit. These horses had significantly shorter lying times (7.99 ± 11.4 min) and smaller locomotion time budgets than the other horses enrolled in this study (73.8 ± 61.8 min), indicating a general compromise of well-being. Thus, wearable sensor technology can be used to identify horses with low recumbency times at risk for REM sleep deficiency and to assess and monitor equine welfare objectively.
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