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====Description====
 
====Description====
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EQUINE protozoal myeloencephalitis (EPM) is a progressive
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neurological disease of horses caused by infection of the central
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nervous system (CNS) with the apicomplexan parasites
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Sarcocystis neurona or Neospora hughesi (Mayhew and others
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1976, Marsh and others 1996, Dubey and others 2001a).
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Because these protozoa may infect any part of the CNS,
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affected horses may show a range of neurological deficits and
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a definitive diagnosis of EPM is not possible by clinical signs
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alone; furthermore, no consistent abnormalities are observed
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in the cerebrospinal fluid (CSF) (Johnson and Constantinescu
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2001). An important advance in the antemortem diagnosis
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of EPM was the development of an immunoblot assay for
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the detection of antibodies to S neurona in serum and CSF
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(Granstrom and others 1993), but more recently it has been
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shown that a quantitative indirect fluorescent antibody test
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is more useful than the immunoblot assay for predicting the
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likelihood of infection (Duarte and others 2003).However, the
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mechanism of neuropathogenesis associated with EPM is not
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fully understood; few organisms are usually visible in neural
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tissues of affected horses, even when there are extensive histological
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lesions, suggesting that cytokines and/or metabolites
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may be important contributors to the pathological changesThe detection of protozoal cDNA indicated that there
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were viable organisms in the 12 horses with EPM. Only small
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numbers of protozoal stages are often present in the neural
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tissue of affected horses and they can be difficult to locate
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in routinely stained histological sections, despite the presence
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of inflammation (Dubey and others 2001a). The PCR
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could be useful in the postmortem diagnosis of EPM in cases
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in which there are only small numbers of protozoal pathogens.In two of the horses, both apicomplexan pathogens
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were detected. To the authors’ knowledge such a dual infection
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has not previously been reported. The infection with
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N hughesi would have been missed, in the absence of detectable
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agent, by routine histology and by S neurona specific
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immunohistochemistry. Although the risk factors for exposure
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to the two pathogens are different (Duarte and others
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2004), exposure to both of them has been reported on the
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basis of the detection of specific antibodies to both in serum
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(Vardeleon and others 2001).This would suggest
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that the pathophysiology of EPM may be mediated primarily
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by the pathogen rather than being a dysfunctional immune
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response.TNF-α and IFN-γ were commonly expressed in the neural
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tissue of the horses with EPM; TNF-α is produced predominantly
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by CD4+ T cells, whereas IFN-γ is produced in natural
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killer cells, CD8+ T cells and macrophages, and both cytokines
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have multiple, primarily proinflammatory and cell-mediated
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actions. The positive correlation between the relative levels
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of transcription of protozoal cDNA and IFN-γ provides evidence
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that the parasite induces a cell-mediated immunity.The
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results of the present study suggest that horses with EPM are
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not immunocompromised and mount appropriate responses
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to help fight the invading pathogen.L-10, an immunosuppressive cytokine produced mainly
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by Th2 cells, is a potent inhibitor of Th1 cell cytokines. The
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increase in both pro- and anti-inflammatory cytokines in the
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neural tissues of the horses with EPM suggests a generalised
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dysregulation of the inflammatory pathways.(EPM 6)
    
Primary cause of multifocal, asymmetric, progressive CNS disease.  Can mimic any neurologic disease.  Infectious but not contagious disease (Pasq)
 
Primary cause of multifocal, asymmetric, progressive CNS disease.  Can mimic any neurologic disease.  Infectious but not contagious disease (Pasq)
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