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ARS Home » Research » Publications at this Location » Publication #121658


item Dubey, Jitender

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 8/29/2001
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Sarcocystis neurona is the most important cause of equine protozoal myeloencephalitis (EPM) in the horse. The life cycle of S. neurona is not completely known. Opossums (Didelphis virginiana; D. albiventris) are definitive hosts and they excrete S. neurona sporocysts in feces. Cats can act as experimental intermediate hosts. Horses and several other animal species are considered aberrant hosts. In aberrant hosts, only schizont stages have been identified and are confined to the central nervous system. Gamma interferon gene knock out (KO) mice develop encephalitis after being fed sporocysts from opossums. We have found that the KO mouse model is useful in studying biology and therapy of S. neurona. Parasitemia was demonstrated by bioassay in KO mice 1 through 8 days after feeding sporocysts (DAFS). Sporozoites were seen in histologic sections of all regions of small intestine and in cells in Peyer's patches of a mouse killed 6 hr after feeding sporocysts. At 1 DAFS, organisms were still present in all regions of small intestine and were also seen in mesenteric lymph nodes. At 3 DAFS, organisms had begun to invade extra-intestinal tissues. S. neurona was demonstrated histologically in mouse brain as early as 4 DAFS. First generation of schizogony occurred in visceral tissues. Three weeks post-infection, organisms were confined to the brain, heart, and lungs. All mice fed viable sporocysts died of neural sarcocystosis within 62 days. Diclazuil was found to be an effective prophylactic drug against EPM in KO mice.