|Fenger, Clara - UNIV OF KY, LEXINGTON, KY|
|Granstrom, David - UNIV OF KY, LEXINGTON, KY|
|Gajadhar, Aliv - AGRICULTURE CANADA|
|Williams, Neil - UNIV OF KY, LEXINGTON, KY|
|Mccrillis, Shani - UNIV OF KY, LEXINGTON, KY|
|Stamper, Shelby - UNIV OF KY, LEXINGTON, KY|
|Langemeier, John - UNIV OF KY, LEXINGTON, KY|
Submitted to: Veterinary Parasitology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: December 11, 1996
Publication Date: N/A
Interpretive Summary: Sarcocystis neurona is a single celled parasite that causes fatal neurologic disease in the horse in the U.S. Its life cycle is unknown. Opossums are suspected as the main reservoirs of infection. Scientists at the Beltsville Agricultural Research Center and the University of Kentucky, Lexington, KY fed Sarcocystis sporocysts from feces of opossums to parasite free foals. The foals fed Sarcocystis developed neurologic diseases similar (but milder) to the disease seen in naturally infected horses. This is the first experimental induction of neurologic sarcocystosis in the horse. The results will be useful to horse owners and veterinarians.
Technical Abstract: Sarcocystis sp. sporocysts isolated from opossums (Didelphis virginiana) were fed to five foals (foals 2, 3, 4, 5, and 7) and 2 foals were maintained as uninoculated controls (foals 1 and 6). Foal 5 was given 0.05 mg/kg dexamethasone sodium phosphate daily beginning 2 days before inoculation for a total of 2 weeks. Horse sera were tested 3 times per week, and cerebrospinal fluid (CSF) samples were tested biweekly for anti-S. neurona antibodies by western blot analysis. All foals had no S. neurona-specific antibodies by western blot analysis prior to sporocyst ingestion. Seroconversion occurred in foals 3, 5, and 7 by 24 dpi, followed by positive CSF tests on 28 dpi. Foals 2 and 4 seroconverted by 40 dpi. Cerebrospinal fluid from foal 2 tested positive by 42 dpi, but foal 4 remained seronegative throughout the study. Sera and CSF from control foals 1 and 6 remained seronegative. All foals with positive CSF developed neurologic clinical signs. Neurologic disease was evident in foals 2 and 3 by 42 dpi and in foal 7 by 28 dpi. The severity of clinical signs progressed to marked spasticity, hypermetria and ataxia in foal 7 by the end of the trial. Necropsy examination of inoculated foals did not reveal gross lesions, however, microscopic lesions consistent with equine protozoal myeloencephalitis (EPM) were found in foals 2, 3, and 7. Protozoa were not observed in the tissue sections. Microscopic lesions consistent with EPM were not found in foals 4 and 5 or in uninoculated control foal 1 and 6. Foal 5 had unilateral non- inflammatory lesions in cervical and thoracic spinal cord consistent with cord compression. These data indicate that the opossum is a definitive host of S. neurona.