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

Citation
Wja. Saville et al., Utilization of stress in the development of an equine model for equine protozoal myeloencephalitis, VET PARASIT, 95(2-4), 2001, pp. 211-222
Citations number
28
Categorie Soggetti
Veterinary Medicine/Animal Health
Journal title
VETERINARY PARASITOLOGY
ISSN journal
03044017 → ACNP
Volume
95
Issue
2-4
Year of publication
2001
Pages
211 - 222
Database
ISI
SICI code
0304-4017(20010226)95:2-4<211:UOSITD>2.0.ZU;2-V
Abstract
Neurologic disease in horses caused by Sarcocystis neurona is difficult to diagnose, treat, or prevent, due to the lack of knowledge about the pathoge nesis of the disease. This in turn is confounded by the lack of a reliable equine model of equine protozoal myeloencephalitis (EPM). Epidemiologic stu dies have implicated stress as a risk factor for this disease, thus, the ro le of transport stress was evaluated for incorporation into an equine model for EPM. Sporocysts from feral opossums were bioassayed in interferon-gamm a gene knockout (KO) mice to determine minimum number of viable S. neurona sporocysts in the inoculum. A minimum of 80,000 viable S. neurona sporocyst s were fed to each of the nine horses. A total of 12 S. neurona antibody ne gative horses were divided into four groups (1-4). Three horses (group 1) w ere fed sporocysts on the day of arrival at the study site, three horses we re fed sporocysts 14 days after acclimatization (group 2), three horses wer e given sporocysts and dexamethasone 14 days after acclimatization (group 3 ) and three horses were controls (group 4). All horses fed sporocysts in th e 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 (g roup 3). Clinical signs improved in four horses from two treatment groups b y the time of euthanasia (group 1, day 44; group 3, day 47). Post-mortem ex aminations, and tissues that were collected for light microscopy, immunohis tochemistry, tissue cultures, and bioassay in KO mice, revealed no direct e vidence of S. neurona infection. However, there were lesions compatible wit h 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 evid ence to suggest that horses in nature may clear the organism routinely, whi ch may explain the relatively high number of normal horses with CSF antibod ies to S. neurona compared to the prevalence of EPM. (C) 2001 Elsevier Scie nce B.V. All rights reserved.