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Equine Protozoal Myeloencephalitis (view source)
Revision as of 12:12, 15 July 2010
, 12:12, 15 July 2010no edit summary
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)
EQUINE protozoal myeloencephalitis (EPM) is caused by a protozoal
organism, Sarcocystis neurona. Because it is endemic in
the USA, EPM should be included in the differential diagnosis
of any horse that develops neurological signs. The disease may
mimic almost any neurological disease because the parasite can
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)
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)
A case of equine protozoal myeloencephalitis (EPM) was presumptively diagnosed in a sixyear-old ataxic thoroughbred mare
imported from the USA, based on a weak positive result from Western blot analysis of a serum sample.
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)
1-6yr (not foals), standardbreds (most common) & TBs (Pasq)
1-6yr (not foals), standardbreds (most common) & TBs (Pasq)
Although there is no definitive antemortem test for EPM, the
diagnosis was considered likely in this case for several reasons.
The Western blot testing of CSF was positive with very little
iatrogenic blood contamination. The foal improved within
one week after treatment for EPM was started, and an extensive
diagnostic evaluation provided no evidence of other
conditions.(EPM 8)
====Diagnosis====
====Diagnosis====
It can be difficult to diagnose because
of the imperfections of Western blot and PCR testing. Western
blot analysis is used to detect antibodies in the cerebrospinal
fluid (CSF), and PCR detects S neurona DNA in the CSF.(EPM 8)
There is no definitive antemortem test for evaluating
horses suspected of having EPM infection. The Western blot
test can produce false-positive results because even a small
amount of blood contamination of the CSF of horses with
seropositivity can result in S neurona immunoreactivity in the
CSF. In one study, as few as 8 RBCs/jl produced false-positive
results (Miller and others 1999). In the case reported here,
there was only approximately 1 RBC/l1, suggesting that there
was intrathecal production of antibodies to S neurona. The
blood-brain barrier of foals is more permeable than that of
adult horses, and the antibodies detected in the CSF may have
been of maternal origin. However, the fact that the treatment
induced a clinical improvement after two months of progressive
neurological disease provides good evidence that the
foal had an active infection with S neurona. However, a definitive
diagnosis of EPM could not be made because the organism
was not identified in tissue.
The earliest case report of EPM occurred in a two-monthold
foal (Fayer and others 1990). If transplacental transmission
does not occur, the minimum incubation may therefore
be eight weeks (Granstrom and Saville 1998). Cutler and
others (1999) challenged seronegative horses with S neurona
isolated from opossums; the horses seroconverted between
19 and 26 days after the nasogastric tube challenge, and
antibodies were present in the CSF by 40 days.
The colt in the present study developed clinical signs within
two days afterbirth. At two days of age it was reported to have
a droopy lip which became worse over time, and other clinical
signs associated with a dysfunction of cranial nerve VII. The
colt may have acquired the infection in utero, although there
are no reports of transplacental transfer, but if it acquired the
infection after birth it would appear that the incubation period
may be shorter than previously reported. The colt's dam tested
seropositive for S neurona, but its CSF was not tested.This case raises several questions. More research is needed,
first, to determine whether transplacental transmission of
S neurona occurs, secondly, to investigate to what extent the
permeability of the blood-brain barrier influences the infection
in foals, and thirdly, to evaluate the normal MRI findings
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)
Typically normal, although focal muscle atrophy may be observed. (Wikipedia)
Typically normal, although focal muscle atrophy may be observed. (Wikipedia)
====Clinical signs====
====Clinical signs====
The
clinical signs vary widely and can include lameness, abnormalities
of gait, ataxia, muscular atrophy, cranial nerve deficits
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)
====Treatment====
====Treatment====
Treatment
is based on the use of antiprotozoal drugs which inhibit folic
acid synthesis, the most commonly used being pyrimethamine
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)
====Prognosis====
====Prognosis====
Guarded to poor (Pasq)
Guarded to poor (Pasq)
The prognosis depends on the severity and
duration of the CNS involvement. Early diagnosis and prompt
treatment enhance the chance of a clinical resolution, but
relapses can occur. (EPM 8)
====Prevention====
====Prevention====