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Equine Protozoal Myeloencephalitis (view source)
Revision as of 13:07, 15 July 2010
, 13:07, 15 July 2010no edit summary
====Description====
====Description====
EQUINE protozoal myeloencephalitis (EPM) is a progressive
neurological disease of horses caused by infection of the central
nervous system (CNS) with the apicomplexan parasites
Sarcocystis neurona or Neospora hughesi (Mayhew and others
1976, Marsh and others 1996, Dubey and others 2001a).
Because these protozoa may infect any part of the CNS,
affected horses may show a range of neurological deficits and
a definitive diagnosis of EPM is not possible by clinical signs
alone; furthermore, no consistent abnormalities are observed
in the cerebrospinal fluid (CSF) (Johnson and Constantinescu
2001). An important advance in the antemortem diagnosis
of EPM was the development of an immunoblot assay for
the detection of antibodies to S neurona in serum and CSF
(Granstrom and others 1993), but more recently it has been
shown that a quantitative indirect fluorescent antibody test
is more useful than the immunoblot assay for predicting the
likelihood of infection (Duarte and others 2003).However, the
mechanism of neuropathogenesis associated with EPM is not
fully understood; few organisms are usually visible in neural
tissues of affected horses, even when there are extensive histological
lesions, suggesting that cytokines and/or metabolites
may be important contributors to the pathological changesThe detection of protozoal cDNA indicated that there
were viable organisms in the 12 horses with EPM. Only small
numbers of protozoal stages are often present in the neural
tissue of affected horses and they can be difficult to locate
in routinely stained histological sections, despite the presence
of inflammation (Dubey and others 2001a). The PCR
could be useful in the postmortem diagnosis of EPM in cases
in which there are only small numbers of protozoal pathogens.In two of the horses, both apicomplexan pathogens
were detected. To the authors’ knowledge such a dual infection
has not previously been reported. The infection with
N hughesi would have been missed, in the absence of detectable
agent, by routine histology and by S neurona specific
immunohistochemistry. Although the risk factors for exposure
to the two pathogens are different (Duarte and others
2004), exposure to both of them has been reported on the
basis of the detection of specific antibodies to both in serum
(Vardeleon and others 2001).This would suggest
that the pathophysiology of EPM may be mediated primarily
by the pathogen rather than being a dysfunctional immune
response.TNF-α and IFN-γ were commonly expressed in the neural
tissue of the horses with EPM; TNF-α is produced predominantly
by CD4+ T cells, whereas IFN-γ is produced in natural
killer cells, CD8+ T cells and macrophages, and both cytokines
have multiple, primarily proinflammatory and cell-mediated
actions. The positive correlation between the relative levels
of transcription of protozoal cDNA and IFN-γ provides evidence
that the parasite induces a cell-mediated immunity.The
results of the present study suggest that horses with EPM are
not immunocompromised and mount appropriate responses
to help fight the invading pathogen.L-10, an immunosuppressive cytokine produced mainly
by Th2 cells, is a potent inhibitor of Th1 cell cytokines. The
increase in both pro- and anti-inflammatory cytokines in the
neural tissues of the horses with EPM suggests a generalised
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)