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-====Description====
-Equine protozoal myeloencephalitis
-Equine protozoal myeloencephalitis is caused by the protozoan
-Sarcocystis neurona and has only been seen in the
-UK in horses imported from the Americas. S neurona produces
-signs relating to diffuse, focal and multifocal lesions
-of the white and grey matter of the spinal cord and brain.
-Horses may present with ataxia or paresis of one or more
-limbs, manifest as stumbling, falling, knuckling and toe
-dragging. Sacrococcygeal involvement can result in signs
-of involvement of the cauda equina, thus mimicking
-polyneuritis equi. In addition, signs relating to involvement
-of the cranial nerves may be evident, producing signs such
-as loss of tongue tone, loss of sensation to the face and unilateral
-facial paralysis. With brain involvement, dysphagia,
-circling, head tilt or recumbency may be noted.
-At present, diagnosis is based on clinical signs and a
-previous history of importation from the Americas. With
-the recent isolation of the causative organism, laboratory
-diagnostic tests on serum and spinal fluid will become
-available in the future. Treatment involves the administration
-of trimethoprim/sulphadiazine (15 mg/kg orally
-twice daily) in combination with pyrimethamine (0-25
-mg/kg orally once daily), both for at least six weeks. The
-prognosis is dependent on the severity and duration of
-neurological signs.(EPM 3)
-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
-, 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
-). 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
-), 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)
-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)
-First descrobed 1964 by Dr. Jim Rooney, called segmental myelitis, focal myelitis encephlaitis, toxoplasma-like encephalitis. 1976 Dubey suggested caused by Sarcocystis member.  S.neurona was eventually cultured form spinal cord of affected horse and so namedbecuase it developed within neurons.  This and similar organsism have been cultured form several ataxic horses, zebra, domestic cat, Canadian lynx, sea otter, straw-nekced ibis, mink, raccoon and sunk. (Furr)
-The disease is considered rare, though recently, an increasing number of cases have been reported. Research at the University of Kentucky has labeled the opossum as the definitive host of the disease. (Wikipedia)
-Neospora hughesi has recently been shown to also cause EPM in the horse but is probably reltively unimportant.(Furr)
-====Aetiology and Epidemiology====
-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)
-The average incidence of EPM according ot the United Sattes Department of Agroiculture is around 14 cases per 10,000 horses per year.  The true incidecne is porbbaly underestimated due to the complexity of the clincial dx and difficulty in finding conclusive CNS lesions.  Racing and showing animals have been shown to be at higher risk than beeding and pleasure horses.  EPM is a disease of the Western Hemisphere, with cases outside of the Americas havign spendt time in endemic regions.  The diseas ehas been reporetd in England among horses imported from the Eastern US an din an Arbaian horse in South Africa imported from the US.  The cases demonstarte the porbbaility of persitent, subcliicsal, latent infections.  But a few reports exist of neurological horses with consistent cx, positivew immunoblot test results and no hx of travel in the American continent.  This may be due to cross-reactign Ags.  TBs, SBs and Quarterhorses are most commonly affected across the US and Canada.  this may refelct managemetn, env or use of these breeds rather than an innate breed charcterisitic.(Furr)
-Most cases of EPM are caused by an Apicomplexan protozoan, [[Sarcocystis|Sarcocystis neurona]] . Horses are infected by ingestion of S neurona sporocysts in contaminated feed or water. The organism is assumed to undergo early asexual multiplication (schizogony) in extraneural tissues before parasitizing the CNS. Because infectious sarcocysts are not formed, the horse is considered an aberrant, dead-end host for S neurona . All Sarcocystis spp have an obligate predator-prey life cycle. The definitive (predator) host for S neurona is believed to be the opossum ( Didelphis virginiana ). Opossums are infected by eating sarcocyst-containing muscle tissue from an infected intermediate (prey) host and, after a brief prepatent period (probably 2−4 ωκ), infectious sporocysts are passed in the feces. Nine-banded armadillos, striped skunks, raccoons, sea otters, Pacific harbor seals, and domestic cats have all been implicated as intermediate hosts; however, the importance in nature of each of these species is unknown. A few cases of EPM, both in the Americas and Europe, are associated with Neospora hughesi , an organism that is closely related to S neurona . The natural host(s) of this organism have not yet been identified. (Merck)
-EPM is caused by the parasite Sarcocystis neurona. In order to complete its life cycle this parasite needs two hosts, a definitive and an intermediate. In the laboratory, raccoons, cats, armadillos, skunks, and sea otters have been shown to be intermediate hosts. The oppossum is the definitive host of the disease. Horses most commonly contract EPM from grazing or watering in areas where an opossum has recently defecated. However, horses cannot pass the disease among themselves. That is, one horse cannot contract the disease from another infected horse. The horse is the dead-end, or aberrant, host of the disease.[1](Wikipedia)
-====Life Cycle====
-====Pathogenesis====
-The actual method by which the Sarcocystis neurona infects a horse is still unknown, however it is thought to preferentially infect leukocytes (white blood cells) in order to cross the blood brain barrier. (Wikipedia)
-====Signalment====
--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====
-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
-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)
-Postmortem diagnosis is confirmed by demonstration of protozoa in CNS lesions. An immunoblot (Western blot) test for S neurona is used as an aid to antemortem diagnosis. In horses with neurologic signs, demonstration of specific antibody in CSF (by immunoblot) is highly suggestive of EPM. A positive immunoblot test in serum only indicates exposure to S neurona . Conversely, a negative immunoblot result, in either serum or CSF, tends to exclude the diagnosis of EPM. In a few horses with EPM, CSF analysis reveals abnormalities such as mononuclear pleocytosis and increased protein concentration.  (merck)
-Depending on the clinical signs, differential diagnoses may include cervical stenotic myelopathy, trauma, aberrant metazoan parasite migration, equine degenerative myeloencephalopathy, myeloencephalopathy caused by equine herpesvirus 1, equine motor neuron disease, neuritis of the cauda equina, arboviral (Eastern or Western equine, West Nile) encephalomyelitis, rabies, bacterial meningitis, and leukoencephalomalacia. (Merck)
-Equine protozoal myeloencephalitis (EPM) is a commonly
-diagnosed, and sometimes devastating neurological disease of
-horses in North America. The most common cause is
-Sarcocystis neurona, although other protozoal species, such as
-Neospora hughesi, have also been identified in the spinal cord
-of horses (Dubey et al. 2001). Ante mortem diagnosis is
-considered presumptive, as definitive diagnosis requires post
-mortem examination and confirmation of S. neurona infection
-via microscopic identification, immunohistochemistry, culture,
-or polymerase chain reaction (PCR) (Furr et al. 2002). Several
-serological tests have been developed to aid in the
-presumptive diagnosis of EPM, but test interpretation is
-complicated; many horses develop antibodies against S.
-neurona in the absence of neurological disease. The oldest
-and most well-established test is the Western blot (WB)
-(Granstrom et al. 1993). An indirect fluorescent antibody test
-(IFAT) later became available (Duarte et al. 2003), and an
-enzyme-linked immunosorbent assay test for an S. neurona
-surface antigen (SAG-1 ELISA; Ellison et al. 2003) has recently
-become commercially available. Evidence to support the use of
-these tests will be reviewed.Specialists appear to agree that the basis of EPM diagnosis
-should be the presence of compatible neurological signs and
-the exclusion of other potential diseases (Furr et al. 2002).
-When additional supportive evidence is desired, 3 main types
-of testing are commercially available: the WB1,2,3, the IFAT4
-and the SAG-1 ELISA5. The SAG-1 ELISA as designed by Ellison
-et al. has the least amount of evidence to support its use and
-Commercial tests to diagnose Sarcocystis neurona infection
-an accurate assessment of its sensitivity and specificity has not
-appeared in peer-reviewed literature. Although another group
-(Hoane et al. 2005) described the SAG-1 ELISA as having the
-lowest sensitivity and specificity out of all the SAG ELISAs,
-those values were obtained using Hoane’s group’s tests and
-not Antech’s SAG-1 ELISA. However, those results do suggest
-that critical review of the SAG-1 ELISA is necessary before
-recommending its use.
-Both the WB and the IFAT appear to have similar
-sensitivities, approaching 90%. Estimates of WB specificity
-vary from 44–89%, while estimates of IFAT specificity range
-from 97–100%. Results vary depending on the sample set and
-whether serum or CSF is used. Therefore, available evidence
-suggests that either test is appropriate if high sensitivity (and
-therefore high negative predictive value) is desired. If high
-specificity (and therefore high positive predictive value) is
-desired, the IFAT may be the better choice. Furthermore, blood
-contamination of CSF appears to have a more detrimental
-effect on WB testing than on IFAT testing. However, infection
-with S. fayeri may cause false-positive IFAT results without
-causing false-positive WB results. The clinical importance of
-this cross-reactivity has yet to be elucidated.
-Unfortunately, none of the currently available diagnostic
-tests are ideal. Development of new serological tests, such as
-the SAG ELISAs (Hoane et al. 2005) and an IgM capture ELISA
-(Murphy et al. 2006) may further improve practitioners’ ability
-to diagnose EPM. However, veterinarians should remain critical
-of new assays until their validity has been documented.(EPM 4)
-====Differential Diagnoses====
-Spinal trauma (Pasq)
-Occiptoi-altanato-axial malfomation
-Herpes myeloencephalopoahty
-Degenrative myeloencephaloapthy
-Verminous myeliopathy
-Cauda equina neuritis
-Wobbler
-Rabies
-Congenital abnormalities
-Spinal tumors
-Sorghum cystitis/ataxia
-Stiff neck - meningitis
-Recumbent - obturaotr n paralysis (Pasq)
-Includes virtually all diseases of the CNS
-Cervical compression (usually symmetrcial gait deficits, worse in pelvic limbs with spasticity and hypermetria, with good retention of strensght and no muscle wasting)
-Follwoibng usually systmeically ill with fevers and changes in leukogram:
-WNV encephalitis - CSF abnormal
-EEE - CSF abnromal
-WEE
-Equine herpesvirus-1 (EHV) - dysuria
-Multifocal diease, ataxia and muscle atrphy also found iwth:
-Polyneuritis equi
-Equine degenrative encephalomyelitis
-Changes in leukogram and CSF seen with:
-Verminous encephaltiis
-Bacterial meningitis
-CNS abscessation (Furr)
-====History====
-Usually an insidious onset ataxia, but the presentation may be acute and severe.(Wikpedia)
-====Clinical exam====
-Typically normal, although focal muscle atrophy may be observed. (Wikipedia)
-====Clinical signs====
-Unlike the incidence of equine protozoal myeloencephalitis
-(EPM), which appears to be increasing, headshaking is an
-uncommon problem for horses in Missouri and the adjacent
-states. Equine protozoal myeloencephalitis was incriminated
-in three horses examined for the treatment of headshaking
-on the basis of a neurological examination, an analysis of
-cerebrospinal fluid and their response to treatment. The
-headshaking and stereotypical behaviour associated with EPM
-was successfully treated with potentiated sulphonamides
-and pyrimethamine.(EPM 7)
-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)
-The protozoa can cause lesions sporadically in any part of the CNS which makes the clinical presentation highly variable. The three characteristic 'As' of EPM (ataxia, asymmetry, atrophy) suggest multifocal or diffuse disease, but are not pathognomonic.   It has been suggested that rapidly progressive presentations reflect brainstem lesions.  Spinal cord signs are most commonly seen and may include:
-*asymmetric or symmetric paresis, spasticity and ataxia of one to four limbs
-*focal or general muscle atrophy
-*apparent lameness
-*upward fxation of the patella
-*back pain
-*loss of condition
-*cauda equina signs
-*focal regions of inappropriate sweating, loss of reflexes or cutaneous anaesthesia
-Lesions of the brainstem, cerebrum or cerebellum are less frequently recognized:
-*depression
-*head tilt
-*dysphagia
-*tongue or massetter paralysis
-*massetter atrophy
-*laryngeal hemiplegia
-*dorsal displacement of the soft palate (DDSP)
-*seizures (may be the only clinical sign)
-*abnormal menace response
-*behavioural abnormalities
-*head shaking
-Without treatment, progression to recumbency and death is likely.  This deterioration may occur smoothly or spasmodically over hours to years. (Merck)
-====Laboratory tests====
-====Radiography====
-====Biopsy====
-====Pathology====
-CNS lesions in the horse often extesnive.  Mutlifocal areas of H+ to light discoloration of brain or spinal cord may be visble on gross exam.  Lesions may be microscopic to several cm wide.   Brasintem and spinal cord affected most often but lesions have been seen in perpheral nerves.  Microscopically lesions are focal to diffuse areas of nonsuppurative inflammation and necrosis with perivascualr infiltration of mononclear cells, including lymphocuytes, macs and plasma cells.  Giant cells, eosinphils and gitter cells are also present in inflamatory infiltrates.  Grey or white matter or both affected.  organsisms have been ofund in neurons, leukocytes and vascualr endothelium, but tend to devlop most often in neurons. (Furr)
-Lesions: There is focal discoloration, hemorrhage, and/or malacia of CNS tissue. Histologically, protozoa are found in association with a mixed inflammatory cellular response and neuronal destruction. Schizonts, in various stages of maturation, or free merozoites commonly are seen in the cytoplasm of neurons or mononuclear phagocytes. Also parasitized are intravascular and tissue neutrophils and eosinophils and, more rarely, capillary endothelial cells and myelinated axons. Merozoites may be found extracellularly, especially in areas of necrosis. In at least 75% of cases, protozoa are not seen on H&E-stained sections, and the diagnosis is made on the basis of characteristic focal or multifocal inflammatory change.(Merck)
-====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)
-Antiprotozoals
-Sulphonamide drugs combined with pyrimethamine for synergism
-Sulfadiazine and pyriemthamine PO SID 'Re-Balance' no longer available? - 61.5% improvement by one clinical grade, tx fro 90-270days
-Complications: anaemia, leukopenia, neutropenia - usually self limiting, resolve with cessatrion of tx
-Use of sulfadizine in breeding animals contorverisla but one study showed no effect on preganncy rates or EED
-Sulfamthoxazole and pyrimethaine caused mild ataxia associated with mounting and ejaculation in a grp of pony stallions
-Ponazuril (Marquis, Bayer Animal Health) - 1st FDA-approved drug for EPM, well absorbed PO, achieves steady state theraeutic concentration in 3days in CSF of hroses treated with 5mg/kg (Furr)
-The only FDA-approved treaments for EPM are ponazuril (5 mg/kg, PO, sid for 28 days) and nitazoxanide (50 mg/kg, PO, sid for 28 days), both as paste formulations. An alternative approach is the use of antifolate drugs, eg, sulfadiazine, or sulfamethoxazole (15-25 mg/kg, PO, sid-bid) in combination with pyrimethamine (1 mg/kg, PO, sid). The sulfonamide can be given with or without trimethoprim. Pyrimethamine must be given at least 1 hr before or after hay is fed. Treatment is usually continued for 6 mo. Anemia may develop after prolonged treatment with antifolate drugs and is best prevented by provision of high quantities of green forage. At least 60% of horses improve with treatment, but <25% recover completely. Relapses are common in horses that remain positive on immunoblot and rare in those that become negative. (Merck)
-No proven preventive is available. A conditionally approved vaccine is marketed, and its efficacy continues to be evaluated. There is interest in using antiprotozoal drugs for prevention; however, evidence-based protocols are not yet available. The source of infective sporocysts is probably opossum feces, so it is prudent to prevent access of opossums to horse-feeding areas. Horse and pet feed should not be left out; open feed bags and garbage should be kept in closed galvanized metal containers, bird feeders should be eliminated, and fallen fruit should be removed. Opossums can be trapped and relocated. Because putative intermediate hosts cannot be directly infective for horses, it is unlikely that control of these populations will be useful in EPM prevention.  (Merck)
-This disease is curable if caught soon enough and treated with antiprotozoal drugs. There are currently three antiprotozoal treatments available: potentiated sulfonamide medications such as ReBalance, Marquis (ponazuril), and Navigator.(Wikipedia)
-Control of this disease includes a recently released vaccine against the parasite and control of opposums in an area. The vaccine, however, has only been conditionally approved by the USDA until efficacy tests are available. (Wikipedia)
-====Prognosis====
-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====
-Control difficult becasue of widespread distirbution of parasite and variety of intermediate hosts.  Monitor high risk grousp (young and old horses) closely for evidence of neurologic disease to help dtect EPM early.  Neuro disease in wamrer months suspiciois.  Wildlife such as opossums and pests should be denied access to feed, use rodent-proof contianers, protect forages in enclosed faciltiies.  Early diagnosis aided by close monitoring of brrodmares close to foaling and hoirses that dvelop major illness or injury.  Prophylaxis with pronazuril has reduced the incidence and sevrity of cx in one study.  Probably not financially viable but may vbe useful before and during persistentyl stressful events to redcue risk of illness.  Interval tx may also be an option.(Furr)
-====References====
-Furr, M (2010) Equine Protozoal Myeloencephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) ''Equine Internal Medicine'', Third Edition, Saunders, Chapter 12.
-Pasquini C, Pasquini S, Woods P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''', third edition, SUDZ Publishing, p245-250.
-**Necrotising encephalomyelitis affecting the grey and white matter of the CNS
-**Caused by ''[[Sarcocystis]] neurona''
-**Opossum thought to be the definitive host
-**Horses thought to be accidental hosts
-**Natural intermediate hosts currently unknown
-**Western Blotting shows 50% of horses in the USA are seropositive
-**Risk factors poorly understood

Difference between revisions of "Equine Protozoal Myeloencephalitis"

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