Abstract: 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.
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This research paper involves the development of an equine model for Equine Protozoal Myeloencephalitis (EPM), a disease in horses caused by a specific protozoa called Sarcocystis neurona. The study assesses the role of stress, specifically transport stress, in the progression and severity of the disease.
Objective and Methodology
The primary aim of the research was to enhance the understanding of Equine Protozoal Myeloencephalitis’ pathogenesis, a difficult-to-diagnose and treat disease in horses caused by Sarcocystis neurona.
In order to achieve this, the study evaluates the role of transport stress, which prior epidemiology studies have identified as a risk factor for EPM.
The researchers collected sporocysts from feral opossums and used Interferon-gamma gene knockout mice for bioassay to isolate the Sarcocystis neurona sporocysts. 80,000 viable ones were administered to each participating horse.
Experiment Design
The study included twelve S. neurona antibody-negative horses, segregated into four groups.
The horses in group 1 were administered sporocysts upon their arrival at the study location (thus introducing transport stress), group 2 horses received sporocysts 14 days post-acclimatization, and group 3 horses were given sporocysts and dexamethasone 14 days after acclimatization.
Group 4 consisted of control horses who did not receive sporocysts.
Results
All horses that were given sporocysts (groups 1-3) developed S. neurona antibodies in their blood and cerebrospinal fluid (CSF). They also exhibited clinical signs of neurologic disease, indicating successful infection.
Horses in group 1, subjected to transport stress, displayed the most severe clinical signs, while the least severe signs were observed in horses treated with dexamethasone (group 3).
Post-mortem examinations and the collected brain tissues showed no direct evidence of S. neurona infection. Still, they presented lesions that were compatible with S. neurona infection, indicating the possible cause of the neurologic disease.
Conclusion
The study suggests that stress can play a significant role in EPM’s pathogenesis, and additional factors such as transport stress should be included in creating reliable equine models for this disease.
The results also imply that horses might clear S. neurona naturally over time, potentially explaining why many horses have CSF antibodies against S. neurona but do not develop EPM.
Cite This Article
APA
Saville WJ, Stich RW, Reed SM, Njoku CJ, Oglesbee MJ, Wunschmann A, Grover DL, Larew-Naugle AL, Stanek JF, Granstrom DE, Dubey JP.
(2001).
Utilization of stress in the development of an equine model for equine protozoal myeloencephalitis.
Vet Parasitol, 95(2-4), 211-222.
https://doi.org/10.1016/s0304-4017(00)00421-0