Clinical, viral, and genetic evaluation of equine degenerative myeloencephalopathy in a family of Appaloosas.
- Journal Article
- Research Support
- Non-U.S. Gov't
Summary
The research conducted an extensive study over four years on a group of Appaloosa horses that exhibited a high incidence of clinical ataxia and showed signs of equine degenerative myeloencephalopathy. The study looked into clinical, viral, hematologic, and genetic factors of the condition.
Clinical Evaluation
- The researchers observed that the main consistent trait among the affected horses was marginally low to deficient levels of serum vitamin E (alpha-tocopherol) and blood selenium. These elements are crucial for maintaining good health and their deficiency could lead to various health issues.
- All horses in the study had access to pasture grasses, indicating that the health issues weren’t due to lack of access to food or malnutrition, but perhaps the quality of nutrients in their diet could be a factor.
Viral and Genetic Examination
- The genetic examination displayed normal chromosomal karyotypes in the 11 affected and/or related horses tested. This suggests that the disease is not related to a genetic mutation or abnormality, although further studies are needed to confirm this.
- The study also tested for viral causes and found Equine herpesvirus type 2 in 4 of the horses. However, the researchers found no evidence that equine herpesvirus type 2 was directly linked to the manifestation of the equine degenerative myeloencephalopathy. Thus, it seems to rule out the possibility of the disease being caused by this particular virus.
Role of Environment and Antioxidant Deficiency
- The fact that the group of Appaloosa horses, all descendants of a clinically normal mare, were raised in three different environments does bring environment-related factors into the frame. However, the research does not clearly identify if, and how, the different environmental conditions contributed to the disease.
- The role of antioxidant deficiency (as suggested by low levels of vitamin E and selenium) in the manifestation of this neurologic dysfunction among these horses is mooted. Although the correlation is noted, the study acknowledges that its role as a causative agent for equine degenerative myeloencephalopathy remains speculative.
In conclusion, the research conducted an extensive analysis of possible factors underlying the high incidence of equine degenerative myeloencephalopathy among a family of Appaloosa horses. It examined and observed facts but couldn’t conclusively identify the pathogenesis or the primary cause of the disease. Further studies are likely required to better understand the etiology of this condition.
Cite This Article
Publication
Researcher Affiliations
- College of Veterinary Medicine, Oregon State University, Corvallis 97331-4802.
MeSH Terms
- Animals
- Ataxia / genetics
- Ataxia / veterinary
- Breeding
- Central Nervous System Diseases / genetics
- Central Nervous System Diseases / veterinary
- Female
- Horse Diseases / genetics
- Horses
- Karyotyping / veterinary
- Male
- Pedigree
- Selenium / blood
- Selenium / deficiency
- Vitamin E Deficiency / blood
- Vitamin E Deficiency / veterinary
Citations
This article has been cited 10 times.- Powers A, Peek SF, Reed S, Donnelly CG, Tinkler S, Gasper D, Woolard KD, Finno CJ. Equine neuroaxonal dystrophy/degenerative myeloencephalopathy in Gypsy Vanner horses. J Vet Intern Med 2024 May-Jun;38(3):1792-1798.
- Palmisano M, Kulp J, Bender S, Stefanovski D, Robinson M, Johnson A. Measurement of 8-hydroxy-2'-deoxyguanosine in serum and cerebrospinal fluid of horses with neuroaxonal degeneration and other causes of proprioceptive ataxia. J Vet Intern Med 2024 Mar-Apr;38(2):1207-1213.
- Hales EN, Aleman M, Marquardt SA, Katzman SA, Woolard KD, Miller AD, Finno CJ. Postmortem diagnoses of spinal ataxia in 316 horses in California. J Am Vet Med Assoc 2021 Jun 15;258(12):1386-1393.
- Burns EN, Finno CJ. Equine degenerative myeloencephalopathy: prevalence, impact, and management. Vet Med (Auckl) 2018;9:63-67.
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