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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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EQUINE protozoal myeloencephalitis (EPM) is caused by a protozoal
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organism, Sarcocystis neurona. Because it is endemic in
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the USA, EPM should be included in the differential diagnosis
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of any horse that develops neurological signs. The disease may
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mimic almost any neurological disease because the parasite can
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localise in any region of the central nervous system (CNS).(EPM 8)
    
Equine protozoal myeloencephalitis, or EPM, is a disease cause by a protozoal infection of the central nervous system of horses. (Merck) EPM is one of the most commonly diagnosed neurological diseases of the Western Hemisphere, accounting for around a qaurter of equine neurological cases admitted to two referrral centres in the United States; it has been reported in most of the contiguous 48 states of the USA, southern Canada, and several countries in Central and South America. In other countries, EPM is seen sporadically. (Furr)  
 
Equine protozoal myeloencephalitis, or EPM, is a disease cause by a protozoal infection of the central nervous system of horses. (Merck) EPM is one of the most commonly diagnosed neurological diseases of the Western Hemisphere, accounting for around a qaurter of equine neurological cases admitted to two referrral centres in the United States; it has been reported in most of the contiguous 48 states of the USA, southern Canada, and several countries in Central and South America. In other countries, EPM is seen sporadically. (Furr)  
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S.neurona, lesion in brain and spinal cord, asymmetric loss of LMN and/or UMN.  Route of infection unknown, organism randomly migrates through spinal cord and brain, white and grey matter damage.  Midwst, NE and S USA (Pasq)
 
S.neurona, lesion in brain and spinal cord, asymmetric loss of LMN and/or UMN.  Route of infection unknown, organism randomly migrates through spinal cord and brain, white and grey matter damage.  Midwst, NE and S USA (Pasq)
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A case of equine protozoal myeloencephalitis (EPM) was presumptively diagnosed in a sixyear-old ataxic thoroughbred mare
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imported from the USA, based on a weak positive result from Western blot analysis of a serum sample.
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The mare initially responded well to treatment, but was euthanased on humane grounds after a relapse (recumbency). Lymphohistiocytic,multifocal, severe meningoencephalomyelitis with intralesional schizonts was revealed.(EPM 9)
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1-6yr (not foals), standardbreds (most common) & TBs (Pasq)
 
1-6yr (not foals), standardbreds (most common) & TBs (Pasq)
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Although there is no definitive antemortem test for EPM, the
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diagnosis was considered likely in this case for several reasons.
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The Western blot testing of CSF was positive with very little
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iatrogenic blood contamination. The foal improved within
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one week after treatment for EPM was started, and an extensive
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diagnostic evaluation provided no evidence of other
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conditions.(EPM 8)
    
====Diagnosis====
 
====Diagnosis====
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It can be difficult to diagnose because
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of the imperfections of Western blot and PCR testing. Western
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blot analysis is used to detect antibodies in the cerebrospinal
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fluid (CSF), and PCR detects S neurona DNA in the CSF.(EPM 8)
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There is no definitive antemortem test for evaluating
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horses suspected of having EPM infection. The Western blot
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test can produce false-positive results because even a small
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amount of blood contamination of the CSF of horses with
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seropositivity can result in S neurona immunoreactivity in the
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CSF. In one study, as few as 8 RBCs/jl produced false-positive
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results (Miller and others 1999). In the case reported here,
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there was only approximately 1 RBC/l1, suggesting that there
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was intrathecal production of antibodies to S neurona. The
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blood-brain barrier of foals is more permeable than that of
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adult horses, and the antibodies detected in the CSF may have
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been of maternal origin. However, the fact that the treatment
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induced a clinical improvement after two months of progressive
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neurological disease provides good evidence that the
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foal had an active infection with S neurona. However, a definitive
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diagnosis of EPM could not be made because the organism
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was not identified in tissue.
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The earliest case report of EPM occurred in a two-monthold
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foal (Fayer and others 1990). If transplacental transmission
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does not occur, the minimum incubation may therefore
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be eight weeks (Granstrom and Saville 1998). Cutler and
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others (1999) challenged seronegative horses with S neurona
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isolated from opossums; the horses seroconverted between
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19 and 26 days after the nasogastric tube challenge, and
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antibodies were present in the CSF by 40 days.
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The colt in the present study developed clinical signs within
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two days afterbirth. At two days of age it was reported to have
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a droopy lip which became worse over time, and other clinical
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signs associated with a dysfunction of cranial nerve VII. The
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colt may have acquired the infection in utero, although there
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are no reports of transplacental transfer, but if it acquired the
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infection after birth it would appear that the incubation period
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may be shorter than previously reported. The colt's dam tested
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seropositive for S neurona, but its CSF was not tested.This case raises several questions. More research is needed,
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first, to determine whether transplacental transmission of
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S neurona occurs, secondly, to investigate to what extent the
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permeability of the blood-brain barrier influences the infection
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in foals, and thirdly, to evaluate the normal MRI findings
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of foals of this age more precisely.(EPM 8)
    
Hx (age), Cx (asymmetric multifocal ataxia & weakness), CNS Cx plus positive Western blot of CSF highly suggestive.  Presumptive: treat and rul out others.  Western blot serological test for CSF and serum, 50% horses positive serum.  CSF taps: normal or maybe increased protien & monocytes (pleocytosis).  Post multiple sections of spinal cord: multifocal & asymmetrci, gross: grey-brown dicsoloration, with H+, swelling & liquefaction, histo: nonsuppurative inflammatory focal malacia & H+, perivasucalr cuffing, gliosis, astrocytosis, neuronal necrosis & gitter cell proliferation, multinucleated giant cells.  Parasite in CNS defintiive, schizonts & merozoites at perhoepry of lesions, but may not be demonstarted (Pasq)
 
Hx (age), Cx (asymmetric multifocal ataxia & weakness), CNS Cx plus positive Western blot of CSF highly suggestive.  Presumptive: treat and rul out others.  Western blot serological test for CSF and serum, 50% horses positive serum.  CSF taps: normal or maybe increased protien & monocytes (pleocytosis).  Post multiple sections of spinal cord: multifocal & asymmetrci, gross: grey-brown dicsoloration, with H+, swelling & liquefaction, histo: nonsuppurative inflammatory focal malacia & H+, perivasucalr cuffing, gliosis, astrocytosis, neuronal necrosis & gitter cell proliferation, multinucleated giant cells.  Parasite in CNS defintiive, schizonts & merozoites at perhoepry of lesions, but may not be demonstarted (Pasq)
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Typically normal, although focal muscle atrophy may be observed. (Wikipedia)
 
Typically normal, although focal muscle atrophy may be observed. (Wikipedia)
 
====Clinical signs====
 
====Clinical signs====
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The
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clinical signs vary widely and can include lameness, abnormalities
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of gait, ataxia, muscular atrophy, cranial nerve deficits
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and behavioural changes.(EPM 8)
    
Gait abnormlaitiy (peracute or acute) - 1 or all 4 limbs depending on wehre migrates, asymmetricasl (because multifocal), ataxia, pareiss & spasticity - knuckling, circumduction, crossing oiver, teraparesis - areflexia, hyporefelxia (LMN) or hyperreflexia (UMN) dependng on site of lesion, muscle atrophy of individual muscle groups, localized areas of sensory deficits, 'strip sweating' localized areas (dermatomes, sympathetic whitematter tracts), cerebellar, brain stem (less ocmmon) or cerebral signs, crnaial nn - head titl, facial paralysis, circling, nystagmus, dysphagia, blindness with or without abnral pupillary refelxes, untreated progressive to recumbency in 14days to 6mths (Pasq)
 
Gait abnormlaitiy (peracute or acute) - 1 or all 4 limbs depending on wehre migrates, asymmetricasl (because multifocal), ataxia, pareiss & spasticity - knuckling, circumduction, crossing oiver, teraparesis - areflexia, hyporefelxia (LMN) or hyperreflexia (UMN) dependng on site of lesion, muscle atrophy of individual muscle groups, localized areas of sensory deficits, 'strip sweating' localized areas (dermatomes, sympathetic whitematter tracts), cerebellar, brain stem (less ocmmon) or cerebral signs, crnaial nn - head titl, facial paralysis, circling, nystagmus, dysphagia, blindness with or without abnral pupillary refelxes, untreated progressive to recumbency in 14days to 6mths (Pasq)
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====Treatment====
 
====Treatment====
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Treatment
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is based on the use of antiprotozoal drugs which inhibit folic
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acid synthesis, the most commonly used being pyrimethamine
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and sulphadiazine. (EPM 8)
    
Combo of antifoliate drugs - trimethoprim sulfa (PO q12hrs, 4-8wks) plus pyrimethamine (Darapem(R) malaria drug) (PO q12h, 3 d then PO q24h 4-8wk), blood count eveyr 2wk during therapy because may cause foliate deficiency (leukopenia, thrombocytopenia & anaemia, rare) - discontinue and give folaite, foliate supplemnt - potential toxicity in mares, NSAIDS, no seroids (because of need for cell mediated immunity to control parasites) DMSO IV to decrease inflamation in 5% dextrose - given wihtiut difficulty but casues intravsacualr haemolysis so haemogloniuria or haematuria, variable positive or negaitve response time - insurance reuiqre 6wk before euthanise, montor CBC every 10-14d, folate inhibitors, can get pancytopenia, marked plateelet drop, cut back dose, multiple B vitmain supplement, stall rest, Diclazuril & Toltrazuril: antiprotozoal disease, need testing, euthanzie if dn't repsond. (Pasq)
 
Combo of antifoliate drugs - trimethoprim sulfa (PO q12hrs, 4-8wks) plus pyrimethamine (Darapem(R) malaria drug) (PO q12h, 3 d then PO q24h 4-8wk), blood count eveyr 2wk during therapy because may cause foliate deficiency (leukopenia, thrombocytopenia & anaemia, rare) - discontinue and give folaite, foliate supplemnt - potential toxicity in mares, NSAIDS, no seroids (because of need for cell mediated immunity to control parasites) DMSO IV to decrease inflamation in 5% dextrose - given wihtiut difficulty but casues intravsacualr haemolysis so haemogloniuria or haematuria, variable positive or negaitve response time - insurance reuiqre 6wk before euthanise, montor CBC every 10-14d, folate inhibitors, can get pancytopenia, marked plateelet drop, cut back dose, multiple B vitmain supplement, stall rest, Diclazuril & Toltrazuril: antiprotozoal disease, need testing, euthanzie if dn't repsond. (Pasq)
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====Prognosis====
 
====Prognosis====
 
Guarded to poor (Pasq)
 
Guarded to poor (Pasq)
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The prognosis depends on the severity and
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duration of the CNS involvement. Early diagnosis and prompt
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treatment enhance the chance of a clinical resolution, but
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relapses can occur. (EPM 8)
    
====Prevention====
 
====Prevention====
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