Utilization of stress in the development of an equine model for equine protozoal myeloencephalitis

Neurologic disease in horses caused by Sarcocystis neurona is difficult to diagnose, treat, or prevent, due to the lack of knowledge about the pathogenesis of the disease. This in turn is confounded by the lack of a reliable equine model of equine protozoal myeloencephalitis (EPM). Epidemiologic stu...

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Published in:	Veterinary parasitology Vol. 95; no. 2; pp. 211 - 222
Main Authors:	Saville, W.J.A, Stich, R.W, Reed, S.M, Njoku, C.J, Oglesbee, M.J, Wunschmann, A, Grover, D.L, Larew-Naugle, A.L, Stanek, J.F, Granstrom, D.E, Dubey, J.P
Format:	Journal Article
Language:	English
Published:	Netherlands Elsevier B.V 26-02-2001
Subjects:	Animals Blotting, Western - veterinary Dexamethasone - pharmacology Didelphis virginiana Disease Models, Animal Encephalomyelitis - complications Encephalomyelitis - veterinary Equine protozoal myeloencephalitis Horse Diseases - etiology Horse Diseases - parasitology Horses Immunosuppressive Agents - pharmacology Mice Mice, Knockout Opossum Opossums - parasitology Risk Factors Sarcocystis neurona Sarcocystosis - etiology Sarcocystosis - veterinary Sporocysts Stress, Physiological - complications Stress, Physiological - veterinary Transportation Sarcocystis neurona Didelphis virginiana Sporocysts Opossum Equine protozoal myeloencephalitis
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Summary:	Neurologic disease in horses caused by Sarcocystis neurona is difficult to diagnose, treat, or prevent, due to the lack of knowledge about the pathogenesis of the disease. This in turn is confounded by the lack of a reliable equine model of equine protozoal myeloencephalitis (EPM). Epidemiologic studies have implicated stress as a risk factor for this disease, thus, the role of transport stress was evaluated for incorporation into an equine model for EPM. Sporocysts from feral opossums were bioassayed in interferon-gamma gene knockout (KO) mice to determine minimum number of viable S. neurona sporocysts in the inoculum. A minimum of 80,000 viable S. neurona sporocysts were fed to each of the nine horses. A total of 12 S. neurona antibody negative horses were divided into four groups (1–4). Three horses (group 1) were fed sporocysts on the day of arrival at the study site, three horses were fed sporocysts 14 days after acclimatization (group 2), three horses were given sporocysts and dexamethasone 14 days after acclimatization (group 3) and three horses were controls (group 4). All horses fed sporocysts in the study developed antibodies to S. neurona in serum and cerebrospinal fluid (CSF) and developed clinical signs of neurologic disease. The most severe clinical signs were in horses in group 1 subjected to transport stress. The least severe neurologic signs were in horses treated with dexamethasone (group 3). Clinical signs improved in four horses from two treatment groups by the time of euthanasia (group 1, day 44; group 3, day 47). Post-mortem examinations, and tissues that were collected for light microscopy, immunohistochemistry, tissue cultures, and bioassay in KO mice, revealed no direct evidence of S. neurona infection. However, there were lesions compatible with S. neurona infection in horses. The results of this investigation suggest that stress can play a role in the pathogenesis of EPM. There is also evidence to suggest that horses in nature may clear the organism routinely, which may explain the relatively high number of normal horses with CSF antibodies to S. neurona compared to the prevalence of EPM.
Bibliography:	ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2
ISSN:	0304-4017 1873-2550
DOI:	10.1016/S0304-4017(00)00421-0