Sarcocystis neurona: parasitemia in a severe combined immunodeficient (SCID) horse fed sporocysts

Long, Maureen T.; Mines, Melissa T.; Knowles, Donald P.; Tanhauser, Susan M.; Dame, John B.; Cutler, Timothy J.; MacKay, Robert J.; Sellon, Debra C.

doi:10.1016/s0014-4894(02)00012-7

Cited by 20 publications

(16 citation statements)

References 14 publications

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“…Prior to infection, sporocysts were identified as S. neurona by a PCR protocol which differentiates S. neurona from the closely related organism Sarcocystis falcatula (27). Horses were infected orally with 5 ϫ 10 5 sporocysts of S. neurona as previously described (16). For i.v.…”

Section: Methodsmentioning

confidence: 99%

“…For i.v. infections, merozoites of the previously described WSU-1 strain of S. neurona were harvested from culture (16). Merozoites were washed and resuspended in medium, and 5 ϫ 10 8 were injected i.v.…”

Section: Methodsmentioning

confidence: 99%

“…IC horses were anesthetized as described above after infection to obtain CSF for Western blotting to detect an antibody response to S. neurona. To assess parasitemia and seroconversion, blood for culture and Western blotting, respectively, was obtained by jugular venipuncture (16). Horses were monitored for development of neurologic abnormalities.…”

Section: Methodsmentioning

confidence: 99%

“…In order to assess the presence and duration of parasitemia and determine the tissue distribution of parasites, blood and tissue samples were obtained for PCR and culture as previously described (16). Samples were frozen at Ϫ70°C until processed for extraction of DNA, and PCR was performed to identify S. neurona as previously described (27).…”

Section: Methodsmentioning

confidence: 99%

“…In a preliminary experiment, we infected an Arabian horse with SCID (19,28) with sporocysts of S. neurona. The infected horse became parasitemic, and S. neurona merozoites were isolated from the blood on postinfection day (PID) 21 (16). This isolate was designated the WSU-1 strain of S. neurona.…”

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Infection of Immunodeficient Horses withSarcocystis neuronaDoes Not Result in Neurologic Disease

Sellon

Knowles

Greiner

et al. 2004

Clin Vaccine Immunol

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Equine protozoal myeloencephalitis (EPM) is one of the most common neurologic disorders of horses in the Americas. Although there are occasional reports of neurologic disease in horses due to Neospora hughesii, EPM is most frequently associated with infection with the apicomplexan parasite Sarcocystis neurona (9). Despite recent advances in our understanding of the life cycle of S. neurona (1, 2, 10), very little is known about the pathogenesis of infection in horses (9). S. neurona can parasitize all regions of the equine central nervous system (CNS). The route of migration of the parasite from the time of ingestion of sporocysts to neuroinvasion is unknown. Studies of gamma interferon (IFN-␥) knockout (GKO) mice, which develop fulminant neurologic disease after infection, suggest that S. neurona may initially multiply in visceral tissues (6, 8).The major goal of our laboratory is to investigate the pathogenesis of S. neurona infection in horses by determining steps in the progression of infection and the role of innate and adaptive immunity in the control of infection and neuropathology. GKO mice develop profound neurologic disease when they are infected with S. neurona (6,8), suggesting that IFN-␥ is crucial in the elimination of that infection in mice. IFN-␥ is produced by lymphocytes during an adaptive Th1 immune response, and adaptive immune responses are presumed to be important in the protection of horses from S. neurona. However, in the absence of adaptive immune responses, mice are protected from Toxoplasma gondii infection, presumably through the production of IFN-␥ by cells of the innate immune system (5, 13). Similarly, two mice with severe combined immune deficiency (SCID) experimentally infected with S. neurona did not develop neurologic disease (18). In a preliminary experiment, we infected an Arabian horse with SCID (19, 28) with sporocysts of S. neurona. The infected horse became parasitemic, and S. neurona merozoites were isolated from the blood on postinfection day (PID) 21 (16). This isolate was designated the WSU-1 strain of S. neurona. Although this SCID horse did not exhibit convincing neurologic deficits, S. neurona DNA was detectable by PCR after long-term culture of brain tissue obtained at necropsy.In the present study, we further investigate the pathogenesis of S. neurona infection in SCID and immunocompetent (IC) horses. Horses were infected orally with sporocysts isolated from the feces of opossums or intravenously (i.v.) with merozoites of the WSU-1 strain of S. neurona. Parasitemia was monitored after infection by collection of blood samples for culture and PCR. Horses were monitored for the development of neurologic abnormalities. At the time of necropsy, tissues were collected for culture, PCR, immunohistochemistry (IHC), and histopathology to determine the presence of S. neurona and associated inflammatory lesions in peripheral tissues or the CNS. MATERIALS AND METHODSExperimental animals. All horses were obtained from the Arabian herd at Washington State College of Veterinary...

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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