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  Discussion on Research Summary: How EPM Causes Disease
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DrO

Posted on Friday, Oct 26, 2007 - 7:53 am:

Hello All,
Here we present the summaries from two hallmark papers on the pathogenesis of Sarcocystis neurona infection in horses or what we call Equine Protozoal Myelitis (EPM). How and why the organism caused disease in some horses while the large majority of exposed horses do not become sick has been a big question. Here they find the immune cells of individuals who are sick are immune suppressed when compared to those exposed but clinically normal. Whether this specific relative suppression is present before the infection or caused by the infection remains a key questions that needs answering. The next paper finds the S. neurona organism can invade the Wbc of horses and conjectures that in a Trojan Horse like scenario, the parasite sneaks unimpeded into the central nervous system, leave the WBC, and then set up housekeeping. How appropriate for October, it sounds a bit like many of the "Alien" movies I have seen. These results suggest that we might have the potential to identify those horses at risk and/or find mechanisms to help protect horses from this organism.
DrO


Vet Parasitol. 2006 Jun 15;138(3-4):200-10.
Immune response to Sarcocystis neurona infection in naturally infected horses with equine protozoal myeloencephalitis.

Yang J, Ellison S, Gogal R, Norton H, Lindsay DS, Andrews F, Ward D, Witonsky S.
Department of Large Animal Clinical Sciences, Phase II, Duck Pond Dr., Virginia-Maryland Regional College of Veterinary Medicine, Virginia Tech, Blacksburg, 24061, USA.

Equine protozoal myeloencephalitis (EPM) is one of the most common neurological diseases of horses in the United States. The primary etiologic agent is Sarcocystis neurona. Currently, there is limited knowledge regarding the protective or pathophysiologic immune response to S. neurona infection or the subsequent development of EPM. The objectives of this study were to determine whether S. neurona infected horses with clinical signs of EPM had altered or suppressed immune responses compared to neurologically normal horses and if blood sample storage would influence these findings. Twenty clinically normal horses and 22 horses with EPM, diagnosed by the presence of S. neurona specific antibodies in the serum and/or cerebrospinal (CSF) and clinical signs, were evaluated for differences in the immune cell subsets and function. Our results demonstrated that naturally infected horses had significantly (P<0.05) higher percentages of CD4 T-lymphocytes and neutrophils (PMN) in separated peripheral blood leukocytes than clinically normal horses. Leukocytes from naturally infected EPM horses had significantly lower proliferation responses, as measured by thymidine incorporation, to a non-antigen specific mitogen than did clinically normal horses (P<0.05). Currently, studies are in progress to determine the role of CD4 T cells in disease and protection against S. neurona in horses, as well as to determine the mechanism associated with suppressed in vitro proliferation responses. Finally, overnight storage of blood samples appears to alter T lymphocyte phenotypes and viability among leukocytes.


Vet Parasitol. 2006 Jun 15;138(3-4):371-6.
Penetration of equine leukocytes by merozoites of Sarcocystis neurona.

Lindsay DS, Mitchell SM, Yang J, Dubey JP, Gogal RM Jr, Witonsky SG.
Department of Biomedical Sciences and Pathobiology, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Tech, 1410 Prices Fork Road, Blacksburg, 24061-0342, USA. lindsayd@vt.edu

Horses are considered accidental hosts for Sarcocystis neurona and they often develop severe neurological disease when infected with this parasite. Schizont stages develop in the central nervous system (CNS) and cause the neurological lesions associated with equine protozoal myeloencephalitis. The present study was done to examine the ability of S. neurona merozoites to penetrate and develop in equine peripheral blood leukocytes. These infected host cells might serve as a possible transport mechanism into the CNS. S. neurona merozoites penetrated equine leukocytes within 5 min of co-culture. Infected leukocytes were usually monocytes. Infected leukocytes were present up to the final day of examination at 3 days. Up to three merozoites were present in an infected monocyte. No development to schizont stages was observed. All stages observed were in the host cell cytoplasm. We postulate that S. neurona merozoites may cross the blood brain barrier hidden inside leukocytes. Once inside the CNS these merozoites can egress and invade additional cells and cause encephalitis.
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