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| − | Also known as: '''''EPM — Equine protozoal myelitis — Equine protozoal encephalomyelitis
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| − | ==Introduction== | + | ====Description==== |
| − | A progressive, infectious,<ref name="Pasq">Pasquini, C, Pasquini, S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''' (Third edition), ''SUDZ Publishing'', 245-250.</ref>neurological disease of horses, endemic in the USA<ref name="EPM8">Gray, L.C, Magdesian, K.G, Sturges, B.K, Madigan, J.E (2001) Suspected protozoal myeloencephalitis in a two-month-old colt. ''Vet Rec'', 149:269-273.</ref> and only encountered elsewhere in equids that have travelled in the Americas.<ref name="EPM3">Vatistas, N, Mayhew, J (1995) Differential diagnosis of polyneuritis equi. ''In Practice'', Jan, 26-29.</ref> Equine protozoal myeloencephalitis (EPM) is one of the most frequently diagnosed neurological conditions in the Western Hemisphere<ref name="Furr">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.</ref> and the principal differential for multifocal, asymmetric progressive central nervous system (CNS) disease.<ref name="Pasq">Pasquini, C, Pasquini, S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''' (Third edition), ''SUDZ Publishing'', 245-250.</ref> The disease is not contagious.<ref name="Pasq">Pasquini, C, Pasquini, S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''', (Third edition), ''SUDZ Publishing'', 245-250.</ref>
| + | Equine protozoal myeloencephalitis (EPM) is a common neurologic disease of horses in the Americas; 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 |
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| − | ==Aetiology==
| + | Equine protozoal myeloencephalitis, or EPM, is a disease cause by a protozoal infection of the central nervous system of horses. |
| − | EPM results from infection of the CNS by the apicomplexan parasite [[Sarcocystis|''Sarcocystis neurona'']] or, less frequently, its close relative [[Neospora|''Neospora hughesi'']].<ref>Dubey, J.P, Lindsay, D.S, Saville, W.J, Reed, S.M, Granstrom, D.E, Speer, C.A (2001)A review of ''Sarcocystis neurona'' and equine protozoal myeloencephalitis (EPM). ''Vet Parasitol'', 95:89-131. In: Pusterla, N, Wilson, W.D, Conrad, P.A, Barr, B.C, Ferraro, G.L, Daft, B.M, Leutenegger, C.M (2006) Cytokine gene signatures in neural tissue of horses with equine protozoal myeloencephalitis or equine herpes type 1 myeloencephalopathy. ''Vet Rec'', Sep 9:''Papers & Articles''.</ref><ref>Wobeser, B.K, Godson, D.L, Rejmanek, D, Dowling, P (2009) Equine protozoal myeloencephalitis caused by ''Neospora hughesi'' in an adult horse in Saskatchewan. ''Can Vet J'', 50(8):851-3.</ref> These protozoans develop within neurons<ref name="Furr">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.</ref> causing immediate or inflammatory-mediated neuronal damage. The organisms migrate randomly through the brain and spinal cord causing asymmetrical lesions of grey and white matter and thus multifocal lower and upper motor neuron deficits.<ref name="Pasq">Pasquini, C, Pasquini, S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''' (Third edition), ''SUDZ Publishing'', 245-250.</ref>
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| − | ==Epidemiology==
| + | EPM was discovered in the 1960s by Dr. Jim Rooney. 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. |
| − | In endemic areas of the United States, around a quarter of referrals for equine neurological disease are attributed to EPM.<ref>Reed, S.M, Granstrom, D, Rivas, L.J, Saville, W.A, Moore, B.R, Mitten, L.A (1994) Results of cerebrospinal fluid analysis in 119 horses testing positive to the Western blot test on both serum and CSF to equine protozoal encephalomyelitis. In ''Proc Am Assoc Equine Pract'', Vancouver BC, AEEP, Lexington, KY, p199. In: 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.</ref> According to the United States Department of Agriculture, the average incidence is 14 cases per 10,000 horses per year. However, the challenges of obtaining a definitive diagnosis may mean this figure is an underestimate.<ref name="Furr">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.</ref> EPM has been identified in parts of Central and South America, southern Canada and across most of the USA.<ref name="Furr">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.</ref> The disease is noted occasionally in other countries, in horses that have been imported from endemic regions.<ref>Pitel, P.H, Pronost, S, Gargala, G, Anrioud, D, Toquet, M-P, Foucher, N, Collobert-Laugier, C, Fortier, G, Ballet, J-J (2002) Detection of ''Sarcocystis neurona'' antibodies in French horses with neurological signs, ''Int J Parasitol'', 32:481-485. In: 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.</ref><ref>Goehring, L.S (2001) Sloet van Oldruitenborgh-Oosterbaan MM: Equine protozoal myeloencephalitis in the Netherlands? An overview, ''Tijdschr Diergeneeskd'', 126:346-351. In: 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.</ref> It is likely that these animals carried a silent but persistent infection during transportation. There have been reports of EPM in horses that have not travelled to or from endemic regions,<ref name="Furr">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.</ref> although cross-reacting antigens in immunodiagnostic tests may explain this discrepancy. <ref name="Furr">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.</ref>
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| | + | Etiology and Epidemiology: |
| | + | Most cases of EPM are caused by an Apicomplexan protozoan, 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. |
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| − | The route of infection remains unconfirmed,<ref name="Pasq">Pasquini, C, Pasquini, S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''' (Third edition), ''SUDZ Publishing'', 245-250.</ref> but there is an increased risk associated with a young age (1-4 years)<ref>Saville, W.J.A, Reed, S.M, Granstrom, D.E, Morley, P.S (1997) Some epidemiologic aspects of equine protozoal myeloencephalitis. ''Proceedings of the Annual Convention of the AAEP'', 43:6-7.</ref>and autumn months.<ref name="NAHMS">NAHMS (2000): ''Equine protozoal myeloencephalitis in the US'', Ft Collins, CO, USDA:APHIS:VS, CEAH, National Animal Health Monitoring System. In: 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.</ref> The reported age range for EPM cases is currently 2 months<ref name="EPM8">Gray, L.C, Magdesian, K.G, Sturges, B.K, Madigan, J.E (2001) Suspected protozoal myeloencephalitis in a two-month-old colt. ''Vet Rec'', 149:269-273.</ref> to 24 years.<ref>MacKay, R.J, Davis, S.W, Dubey, J.P (1992) Equine protozoal myeloencephalitis, ''Compend Contin Educ Pract Vet'', 14:1359-1367. In: 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.</ref> Thoroughbreds, Standardbreds and Quarterhorses are most frequently affected across the US and Canada.<ref>Fayer, R, Mayhew, I.G, Baird, J.D, Dill, S.G, Foreman, J.H, Fox, J.C, Higgins, R.J Higgins, Reed, S.M, Ruoff, W.W, Sweeney, R.W, Tuttle, P (1990) Epidemiology of equine protozoal myeloencephalitis in North America based on histologically confirmed cases, ''J Vet Intern Med'', 4:54-57. In: 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.</ref> This may relate to a breed predispostion or alternatively, managemental factors associated with these breeds.<ref>Boy, M.G, Galligan, D.T, Divers, T.J (1990) Protozoal encephalomyelitis in horses: 82 cases (1972-1986), ''J Am Vet Med Assoc'', 196:632-634. In: 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.</ref> Showing and racing have been linked to a greater risk of clinical disease.<ref>Saville, W.J.A, Reed, S.M, Morley, P.S (1999) Examination of risk factors for equine protozoal myeloencephalitis. ''Proceedings of the Annual Convention of the AAEP'', 45:48-49.</ref> Increasing age and environmental temperature have been associated with an increased seroprevalence of ''S. neurona''.<ref>Tillotson, K, McCue, P.M, Granstrom, D.E, Dargatz, D.A, Smith, M.O, Traub-Dargatz, J.L (1999) Seroprevalence of antibodies to ''Sarcocystis neurona'' in horses residing in northern Colorado, ''J Equine Vet Sci'', 19:122-126. In: 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.</ref> Seroprevalence for this species is typically higher than for ''N. hughesi''.<ref name="Furr">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.</ref>Other risk factors for EPM include the presence of opossums, rats, mice and woodland, increased population density of humans and horses, bedding horses on shavings or wood chips and the use of purchased grain.<ref name="Furr">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.</ref>Case clustering may operate where all the risk factors occur, but the majority of cases appear in isolation.<ref name="Furr">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.</ref>
| + | 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] |
| | + | ====Signalment==== |
| | + | ====Diagnosis==== |
| | + | Diagnosis: |
| | + | 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. |
| | + | 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. |
| | + | ====Clinical Signs==== |
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| − | ==Life Cycle==
| + | Variability in signs reflects random distribution of lesions in nervous system. Clinical exam usually normal but may see focal muscle atrophy. History or slowly progressive ataxia. Occassionally acute and rapidly porgressive disease - may be associated with brainstem disease. Neurogenic gait deficits assymmetrical, sinlge or multiple limbs. 3 charcaterisitc As of EPM - ataxia, asymmetry, atrophy - suggetss multifocal or diffuse disease, but not pathognomonic. Less commonly get disease of cerbellum, cereburm or brasintem resultign in cranial nerve deifcits - headtilt, dysphagia, tongue or master paralysis, or masseter atrophy. A small number of horses may have only seizures. Visual deficts including abnormal ,menace and behavoural abnormalities have been observed in some, possibly head shaking |
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| − | [[Image:Equine_Protozoal_Myeloencephalitis_life_cycle.jpg|600px|thumb|centre|''' Life cycle diagram of ''Sarcocystis neurona''. Created by the ''Agricultural Research Service, the research agency of the United States Department of Agriculture'', July 2005. ''Sourced from the USDA Agricultural Research Service page on EPM/Sarcocystis neurona, located via WikiMedia Commons.'' ''']]
| + | Clinical Findings: |
| | + | Because the protozoa may infect any part of the CNS, almost any neurologic sign is possible. The disease usually begins insidiously but may present acutely and be severe at onset. Signs of spinal cord involvement are more common than signs of brain disease. Horses with EPM involving the spinal cord have asymmetric or symmetric weakness and ataxia of one to all limbs, sometimes with obvious muscle atrophy. When the caudal spinal cord is involved, there are signs of cauda equina syndrome. EPM lesions in the spinal cord also may result in demarcated areas of spontaneous sweating or loss of reflexes and cutaneous sensation. The most common signs of brain disease in horses with EPM are depression, head tilt, and facial paralysis. Any cranial nerve nucleus may be involved, Without treatment, EPM often progresses to cause recumbency and death. Progression to recumbency occurs over hours to years and may occur steadily or in a stop-start fashion. |
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| − | Infective sporocysts are passed in the faeces of the definitive host and must be ingested by the horse for infection to occur. See [[Sarcocystis|the ''Sarcocystis'' page]] for further details of the life cycle of ''S.neurona''.
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| − | ==Pathogenesis==
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| − | Immune clearance of ''S.neurona'' must be, in the large part, very effective, since less than 1% of horses exposed to the protozoan suffer from EPM.<ref name="NAHMS">NAHMS (2000): ''Equine protozoal myeloencephalitis in the US'', Ft Collins, CO, USDA:APHIS:VS, CEAH, National Animal Health Monitoring System. In: 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.</ref> Both humoral and cell-mediated immune mechanisms are likely to be significant in the host defence against ''S.neurona''. Antibodies are produced soon after infection and offer some degree of protection.<ref name="Furr">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.</ref> CD8 positive T-cells and their production of IFN-γ are likely to be pivotal in the removal of intracellular stages of the parasite.<ref name="Furr">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.</ref>Factors which promote disease development include parasite dose<ref>Sofaly, C.D, Reed, S.M, Gordon, J.C, Dubey, J.P, Oglesbee, M, Njoku, D, Grover, C, Saville, W.J.A (2002) Experimental induction of equine protozoal myeloencephalitis (EPM) in the horse: effect of ''Sarcocystis neurona'' sporocyst inoculation dose on the development of clinical neurological disease, J Parasitol, 88:1164-1170. In: 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.</ref>and, most probably virulence of the protozoal strain. Stress induced by pregnancy, travel, training and showing<ref name="Saville">Saville, W.J, Reed, S.M, Morley, P.S, Granstrom, D.E, Kohn, C.W, Hinchcliff, K.W, Wittum, T.E (2000) Analysis of risk factors for the development of equine protozoal myeloencephalitis in horses. ''J Am Vet Med Assoc'', 217:1174-1180. In: 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.</ref> may have an immunosuppressive effect that encourages infection. Indeed, it has been shown that stress affects the severity of clinical signs seen in natural infections.<ref>Njoku, C.J, Saville, W.J, Reed, S.M, Oglesbee, M.J, Rajala-Schultz, P.J, Stich, R.W (2002) Reduced levels of nitric oxide metabolites in cerebrospinal fluid are associated with equine protozoal myeloencephalitis, ''Clin Diagn Lab Immunol'', 9:605-610. In: 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.</ref>
| + | The neurologic signs that EPM causes are most commonly asymmetric incoordination (ataxia), weakness and spasticity, although they may mimic almost any neurologic disorder. Clinical signs among horses with EPM include a wide array of symptoms that may result from primary or secondary problems. Some of the signs cannot be distinguished from other problems, such as lameness, which can be attributed to many different causes. Airway abnormalities, such as laryngeal hemiplegia (paralyzed flaps), dorsal displacement of the soft palate (snoring), or airway noise of undetermined origin may result from protozoa infecting the nerves which innervate the throat. Apparent lameness, particularly atypical lameness or slight gait asymmetry of the rear limbs are commonly caused by EPM. Focal muscle atrophy, or even generalized muscle atrophy or loss of condition may result. Secondary signs also occur with neurologic disease. Upward fixation of the patella (locking up of the stifle joint) is among the most common findings among horses with neurologic disease. Another common side effect of EPM is back soreness, which can be severe. 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. |
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| − | The 'Trojan horse' hypothesis suggests that ''S.neurona'' meroziotes traverse the blood brain barrier encrypted within leucocytes that have phagocytosed the parasite in the periphery. Once inside the CNS, eggression and infection of other cells results in encephalitis.<ref>Lindsay, D.S, Mitchell, S.M, Yang, J, Dubey, J.P, Gogal, R.M, Jr, Witonsky, S.G (2006) Penetration of equine leukocytes by merozoites of ''Sarcocystis neurona''. ''Vet Parasitol'', 15:138(3-4):371-6</ref> Other theories include haematogenous spread or direct passage of parasites via the cytoplasm of endothelial cells into the CNS. However, despite extensive histological lesions, few organisms are typically visible in the neural tissues of affected horses. This implies that cytokines may have a considerable role in producing pathological changes.<ref>Pusterla, N, Wilson, W.D, Conrad, P.A, Barr, B.C, Ferraro, G.L, Daft, B.M, Leutenegger, C.M (2006) Cytokine gene signatures in neural tissue of horses with equine protozoal myeloencephalitis or equine herpes type 1 myeloencephalopathy, ''Vet Rec'', 159:341-346.</ref> Although the protozoan may induce some degree of immunosuppression in the host<ref>Spencer, J.A, Ellison, S.E, Guarino, A.J, Blagburn, B.L (2004) Cell-mediated immune responses in horses with equine protozoal myeloencephalitis. ''J Parasitol'', 90(2):428-30.</ref><ref>Yang, J, Ellison, S, Gogal, R, Norton, H, Lindsay, D.S, Andrews, F, Ward, D, Witonsky, S (2006) Immune response to Sarcocystis neurona infection in naturally infected horses with equine protozoal myeloencephalitis. ''Vet Parasitol'', 138(3-4):200-10.</ref>, it is likely that the immune-privilege of the CNS prevents parasite clearance from this site.<ref name="Furr">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.</ref>. The methods by which ''S.neurona'' and ''N.hughesi'' cause EPM is still debated. | + | ====Laboratory tests==== |
| | + | ====Radiography==== |
| | + | ====Biopsy==== |
| | + | ====Pathology==== |
| | + | ====Treatment==== |
| | + | Treatment and Control: |
| | + | 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. |
| | + | 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. |
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| − | ==Signalment==
| + | 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. |
| − | Mostly Standardbreds and Thoroughbreds aged 1-6years.<ref name="Pasq">Pasquini, C, Pasquini, S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''' (Third edition), ''SUDZ Publishing'', 245-250.</ref> Foal infection may be possible.<ref name="EPM8">Gray, L.C, Magdesian, K.G, Sturges, B.K, Madigan, J.E (2001) Suspected protozoal myeloencephalitis in a two-month-old colt. ''Vet Rec'', 149:269-273.</ref>
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| − | ==Clinical Signs==
| + | 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. |
| − | The disease onset may be acute, peracute or chronic. An insidious onset ataxia is most typical and with such cases, the clinical examination may reveal a bright, alert horse, perhaps with some focal muscle atrophy.<ref name="Furr">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.</ref> In all cases, the clinical signs are referable to diffuse focal and multifocal lesions of the white and grey matter of the spinal cord and brain.<ref name="EPM3">Vatistas, N, Mayhew, J (1995) Differential diagnosis of polyneuritis equi. ''In Practice'', Jan, 26-29.</ref> The three characteristic 'As' (ataxia, asymmetry, atrophy) suggest multifocal or diffuse disease, but are not pathognomonic for EPM.<ref name="Furr">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.</ref>
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| + | ====Prognosis==== |
| − | | '''Lesion Location'''
| + | ====References==== |
| − | | '''Clinical signs'''
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| − | |'''Spinal cord'''
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| − | *Ataxia, paresis or spasticity of one or more limbs, often asymmetrical, signs usually worse in hindlimbs, may see stumbling, falling, knuckling, toe dragging, circumduction, crossing over, tetraparesis - areflexia, hyporeflexia (LMN) or hyperreflexia (UMN) depending on site of lesion
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| − | *Loss of reflexes or cutaneous anaesthesia
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| − | *Apparent lameness, particularly atypical or slight gait asymmetry of hindlimbs (not alleviated by local anaesthesia)
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| − | *Abnormal placing reactions
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| − | *Focal muscle atrophy of individual muscle groups<ref name="Pasq">Pasquini, C, Pasquini, S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''' (Third edition), ''SUDZ Publishing'', 245-250.</ref>, especially gluteal muscles, often asymmetrical
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| − | *Generalized muscle atrophy or loss of condition
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| − | *Localized sensory deficits and 'strip sweating' of dermatomes
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| − | *Sacrococcygeal involvement will produce signs that mimic ''polyneuritis equi''
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| − | |-
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| − | |'''Peripheral nerves'''
| |
| − | |
| |
| − | *Upward fixation of the patella
| |
| − | *Exertional rhabdomyolysis
| |
| − | *Back pain
| |
| − | *Gait abnormality
| |
| − | |-
| |
| − | |'''Brainstem''' (cranial nerve signs)
| |
| − | |
| |
| − | *Atrophy of ''temporalis'' and ''masseter'' muscles, loss of facial sensation (V)
| |
| − | *Facial (VII) and vestibulocochlear (VIII) nerve deficits often seen together:
| |
| − | **VIII - vestibular signs: nystagmus, head tilt, base-wide stance (peripheral or central vestibular disease)
| |
| − | **VII - unilateral facial paralysis: muzzle deviation, ptosis, ear droop
| |
| − | *Loss of tongue tone (XII)
| |
| − | *Dysphagia (V, VII, IX, X, XII)
| |
| − | *Dorsal displacement of the soft palate (IX, X)
| |
| − | *Laryngeal hemiplegia (X)
| |
| − | *Abnormal menace response (II, VII)
| |
| − | *Headshaking<ref>Moore, L.A, Johnson, P.J, Messer, N.T, Kline, K.L, Crump, L.M, Knibb, J.R (1997) Management of headshaking in three horses by treatment for
| |
| − | protozoal myeloencephalitis ''Vet Rec'' 141:264-267.</ref>
| |
| − | *Blindness with or without abnormal pupillary reflexes,<ref name="Pasq">Pasquini, C, Pasquini, S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''' (Third edition), ''SUDZ Publishing'', 245-250.</ref>
| |
| − | |-
| |
| − | |'''Cerebrum, basal nuclei, cerebellum'''
| |
| − | |
| |
| − | *Abnormal menace response
| |
| − | *Circling
| |
| − | *Seizures (may be the only clinical sign)<ref>Dunigan, C.E, Oglesbee, M.J, Podell, M 'et al.' (1995) Seizure activity associated with equine protozoal myeloencephalitis, ''Prog Vet Neurol'', 6:50-54. In: 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.</ref>
| |
| − | *Abnormal electroencephalogram (EEG)
| |
| − | *Asymmetrical central blindness
| |
| − | *Facial hypoalgesia
| |
| − | *Cerebellar ataxia
| |
| − | *Altered behavior
| |
| − | *Depression
| |
| − | *Narcolepsy-like syndrome
| |
| − | |}
| |
| | | | |
| − | Lesions of the brainstem, cerebrum or cerebellum are less frequently recognized than those of the spinal cord. Horses with severe EPM may be unable to stand or swallow and, if left untreated, progress to recumbency within 14 days to 6 months.<ref name="Pasq">Pasquini, C, Pasquini, S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''' (Third edition), ''SUDZ Publishing'', 245-250.</ref> This deterioration may occur smoothly or spasmodically,<ref name="Merck">Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial</ref> but is likely to result in death. It has been suggested that rapidly progressive presentations reflect brainstem lesions.<ref name="Furr">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.</ref>
| |
| | | | |
| − | ==Diagnosis==
| + | |
| | | | |
| − | It is difficult to obtain a definitive antemortem diagnosis of EPM. Certain criteria must be met before such a diagnosis is assigned<ref name="Furr">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.</ref>:
| + | |
| − | *The relevant clinical signs must be attributable to one or more lesions of the CNS<ref name="Johnson">Johnson, A.L (2009) Evidence-based review of diagnosis and treatment of ''Sarcocystis neurona'' infection (Equine Protozoal Myeloencephalitis). ''Proceedings of the Annual Convention of the AAEP'' - Las Vegas, NV, USA, 55:172-176.</ref>
| |
| − | *Immunodiagnostic tests must confirm exposure to the parasite
| |
| − | *Other differentials with similar presentations should be ruled out wherever possible
| |
| − | *The horse should be resident in or have travelled within the Americas<ref name="EPM3">Vatistas, N, Mayhew, J (1995) Differential diagnosis of polyneuritis equi. ''In Practice'', Jan, 26-29.</ref>
| |
| − | The primary step in the diagnostic procedure should be to carry out thorough clinical and [[:Category:Neurological Examination - Horse|neurological examinations]]. <ref name="Johnson">Johnson, A.L (2009) Evidence-based review of diagnosis and treatment of ''Sarcocystis neurona'' infection (Equine Protozoal Myeloencephalitis). ''Proceedings of the Annual Convention of the AAEP'' - Las Vegas, NV, USA, 55:172-176.</ref>
| |
| | | | |
| − | ===Immunodiagnostic tests===
| + | |
| − | All of these tests aim to confirm exposure to the pathogens of EPM by detecting the presence of antibodies to these parasites.<ref name="Furr">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.</ref> None of these tests is considered a gold standard and they are only supportive. Currently, a definitive diagnosis can only be obtained at postmortem.<ref name="Johnson">Johnson, A.L (2009) Evidence-based review of diagnosis and treatment of ''Sarcocystis neurona'' infection (Equine Protozoal Myeloencephalitis). ''Proceedings of the Annual Convention of the AAEP'' - Las Vegas, NV, USA, 55:172-176.</ref>
| |
| − | *'''Immunoblot analysis (Western blot) of serum and CSF''': senstivity around 90%, specificity 48-89%.<ref name="EPM4>Johnson, A.L (2008) Evidence-based clinical question: which is the most sensitive and specific commercial test to diagnose ''Sarcocystis neurona'' infection (equine protozoal myeloencephalitis) in horses?, ''Equine Vet Educ'', 20(3):166-168.</ref> Cultured merozoites are used to detect antibodies versus ''S.neurona''-specific proteins. The blood brain barrier does not prevent the passage of antibodies, thus the CSF concentration of a specific antibody will be directly related to its serum concentration.<ref>Furr, M (2002) Antigen-specific antibodies in cerebrospinal fluid after intramuscular injection of ovalbumin in horses, ''J Vet Intern Med'', 16:588-592. In: 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.</ref> This permeability is likely responsible for many of the weakly false-positive CSF immunoblot tests. Blood contamination during CSF collection or bleeding within the CNS due to trauma or infection might also cause false positives. The CSF titre will be greatly increased during CNS infection as there will be local production of the antibody. One of the difficulties in interpreting immunoblot results is that many horses develop antibodies against ''S.neurona'' in the absence of neurological disease.<ref name="EPM4>Johnson, A.L (2008) Evidence-based clinical question: which is the most sensitive and specific commercial test to diagnose ''Sarcocystis neurona'' infection (equine protozoal myeloencephalitis) in horses?, ''Equine Vet Educ'', 20(3):166-168.</ref> For this reason, testing CSF may be preferable to serum despite the impact that minor blood contamination may have on CSF results.<ref name="Johnson">Johnson, A.L (2009) Evidence-based review of diagnosis and treatment of ''Sarcocystis neurona'' infection (Equine Protozoal Myeloencephalitis). ''Proceedings of the Annual Convention of the AAEP'' - Las Vegas, NV, USA, 55:172-176.</ref> False negative results may arise if horses fail to respond to the specific proteins recognised by the immunoblot. Such cases are rare, so a negative immunoblot result tends to exclude the diagnosis of EPM.<ref name="Merck">Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial</ref> Cases that originally test negative should be re-tesed 14-21 days later. In most instances, owing to a substantial incubation period, detectable levels of IgG are present prior to the emergence of clinical signs.<ref name="Furr">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.</ref>
| |
| − | *'''Whole organism indirect fluorescent antibody test (IFAT)''': sensitivity around 90%, specificity 97-100%.<ref name="EPM4>Johnson, A.L (2008) Evidence-based clinical question: which is the most sensitive and specific commercial test to diagnose ''Sarcocystis neurona'' infection (equine protozoal myeloencephalitis) in horses?, ''Equine Vet Educ'', 20(3):166-168.</ref> Serum titres of more than 1:100 and CSF titres of more than 1:5 indicate an active infection. The IFAT is considered to have slightly improved diagnostic efficiency than the immunoblot test<ref>Duarte, P.C, Daft, B.M, Conrad, P.A, Packham, A.E, Gardner, I.A (2003) Comparison of a serum indirect fluorescent antibody test with two Western blot tests for the diagnosis of equine protozoal myeloencephalitis, ''J Vet Diagn Invest'', 15:8-13. In: 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.</ref> but is unable to distinguish between ''S.neurona'' and other related nonpathogenic organsims such as ''S.fayeri''.<ref>Granstrom, D.E (1995) Equine protozoal myeloencephalitis testing: review of 1993 and 1994. ''Proc Annu Conv Am Assoc Equine Prac, 41:218-219. In: 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.</ref> This can lead to false positive results. Compared with the immunblot test, CSF blood contamination has an insignificant effect on the IFAT.<ref>Finno, C.J, Packham, A.E, Wilson, W.D, ''et al''. (2007) Effects of blood contamination of cerebrospinal fluid on results of indirect fluorescent antibody tests for detection of antibodies against ''Sarcocystis neurona'' and ''Neospora hughesi''. ''J Vet Diag Invest'', 19:286–289. In: Johnson, A.L (2009) Evidence-based review of diagnosis and treatment of ''Sarcocystis neurona'' infection (Equine Protozoal Myeloencephalitis). ''Proceedings of the Annual Convention of the AAEP'' - Las Vegas, NV, USA, 55:172-176.</ref>An IFAT for ''N.hughesi'' is also available from the Universty of California.<ref name="Furr">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.</ref>
| |
| − | *'''ELISA for antibodies to the snSAG-1 protein''': based on an immunodominant surface antigen of ''S.neurona'' (SAG-1).<ref name="Johnson">Johnson, A.L (2009) Evidence-based review of diagnosis and treatment of ''Sarcocystis neurona'' infection (Equine Protozoal Myeloencephalitis). ''Proceedings of the Annual Convention of the AAEP'' - Las Vegas, NV, USA, 55:172-176.</ref> Serum titres more than 1:100 suggest an active infection. False negatives are possible as not all ''S.neurona'' isolates produce the specific protein.<ref>Howe, D, Gaji, R, Marsh, A (2008) Strains of ''S.neurona'' exhibit differences in their surface antigens, including the absence of the major surface antigen SnSAG1. ''Int J Parasitol'', 38:623-631. In: 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.</ref> SAG-5 is an alternative surface antigen of ''S.neurona'' strains, which is mutually exclusive to SAG-1.<ref>Crowdus, C.A, Marsh, A.E, Saville, W.J, ''et al''. (2008) SnSAG5 is an
| |
| − | alternative surface antigen of ''Sarcocystis neurona'' strains that is mutually exclusive to SnSAG1. ''Vet Parasitol'', 158:36–43. In: Johnson, A.L (2009) Evidence-based review of diagnosis and treatment of ''Sarcocystis neurona'' infection (Equine Protozoal Myeloencephalitis). ''Proceedings of the Annual Convention of the AAEP'' - Las Vegas, NV, USA, 55:172-176.</ref> Therefore, the ELISA may only be of use where strains of ''S.neurona'' expressing SAG-1 predominate.<ref name="Johnson">Johnson, A.L (2009) Evidence-based review of diagnosis and treatment of ''Sarcocystis neurona'' infection (Equine Protozoal Myeloencephalitis). ''Proceedings of the Annual Convention of the AAEP'' - Las Vegas, NV, USA, 55:172-176.</ref>
| |
| | | | |
| − | ===Other tests===
| + | |
| − | *'''CSF analysis''': to rule out other conditions as stated below. Most horses with EPM have normal CSF. Rarely, an increased total protein or white blood cell count is seen in severe cases.<ref name="Furr">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.</ref> PCR can be used to detect ''S.neurona'' DNA in CSF.<ref name="EPM8">Gray, L.C, Magdesian, K.G, Sturges, B.K, Madigan, J.E (2001) Suspected protozoal myeloencephalitis in a two-month-old colt. ''Vet Rec'', 149:269-273.</ref>
| |
| − | *'''Diclazuril''': a positive response to treatment with diclazuril would firmly support a diagnosis of EPM, since the drug has no antimicrobial activity.<ref>Bentz, B.G, Dirikolu, L, Carter, W.G, Saville, W.J.A, Williams, N.M, Bernard, W.V, Wulff-Strobel, C, Baker, C.B, McCrillis, S, Reed, S, Harkins, Granstrom, D.E, Tobin, T (2000) Special Article: Diclazuril and equine protozoal myeloencephalitis (EPM): a
| |
| − | clinical report. ''Equine Vet Educ'', 12(4):195-200.</ref>
| |
| − | *'''Blood gene expression biomarkers''': may be sensitive and specific indicators of early and active disease<ref>Eastman, E, Furr, M, McKenzie, H, Saville, W.J, Dubey, J.P (2005) Early diagnosis of Sarcocystis neurona infection using bloodgene expression biomarkers. In: ''51st Annual Convention of the American Association of Equine Practitioners - AAEP'', Seattle, WA, USA.</ref>
| |
| | | | |
| − | ===Differential Diagnoses===
| |
| | | | |
| − | ''S.neurona'' can migrate to any region of the CNS<ref name="EPM8">Gray, L.C, Magdesian, K.G, Sturges, B.K, Madigan, J.E (2001) Suspected protozoal myeloencephalitis in a two-month-old colt. ''Vet Rec'', 149:269-273.</ref>, thus the differential list comprises almost all diseases of this system. | + | **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 |
| | + | **Causes spinal cord dysfunction |
| | + | ***Ataxia and paralysis |
| | | | |
| − | {| cellpadding="10" cellspacing="0" border="1"
| |
| − | | '''Differential'''
| |
| − | | '''Differentiating signs'''
| |
| − | | '''Tests to rule out'''
| |
| − | |-
| |
| − | |Cervical vertebral malformation (CVM, cervical compressive myelopathy, cervical vertebral instability, cervical stenotic myelopathy, cervical spondylomyelopathy, Wobbler's syndrome).
| |
| − | |Symmetrical gait deficits, worse in pelvic limbs<ref>Mayhew, I.G, deLahunta, A, Whitlock, R.H, Krook, L, Tasker, J.B (1978) Spinal cord disease in the horse, ''Cornell Vet'', 68(Suppl 8):110-120. In: Hahn, C.N (2010) ''Cervical Vertebral Malformation'' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12.</ref> with spasticity and dysmetria, good retention of strength, no muscle wasting.<ref name="Furr">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.</ref> '''NB: can be concurrent with EPM'''.<ref name="Hahn">Hahn, C.N (2010) ''Cervical Vertebral Malformation'' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12.</ref>
| |
| − | |Plain lateral radiography of C1 to T1<ref name="Hahn">Hahn, C.N (2010) ''Cervical Vertebral Malformation'' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12.</ref>, myelography. <ref name="Seino">Seino, K.K (2010) ''Spinal Ataxia'' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 3.</ref>
| |
| − | |-
| |
| − | |[[West Nile Virus|West Nile encephalitis]]
| |
| − | |Systemically ill, pyrexia. Difficult to differentiate if horse is afebrile and has no excessive muscle fasciculations.<ref name="Long">Long, M.T (2010) ''Flavivirus Encephalitis'' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12.</ref>
| |
| − | |Leukogram, CSF analysis, IgM capture ELISA, plaque reduction neutralization test (PRNT),<ref name="Seino">Seino, K.K (2010) ''Spinal Ataxia'' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 3.</ref>absence of mosquito vectors.<ref name="Johnson">Johnson, A.L (2009) Evidence-based review of diagnosis and treatment of ''Sarcocystis neurona'' infection (Equine Protozoal Myeloencephalitis). ''Proceedings of the Annual Convention of the AAEP'' - Las Vegas, NV, USA, 55:172-176.</ref>
| |
| − | |-
| |
| − | |[[Equine Togaviral Encephalitis|WEE]]
| |
| − | |Systemically ill, pyrexia, abnormal motor function.<ref name="Long">Long, M.T (2010) ''Flavivirus Encephalitis'' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12.</ref>
| |
| − | |Leukogram, ELISA, titres, virus isolation.<ref name="Seino">Seino, K.K (2010) ''Spinal Ataxia'' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 3.</ref>
| |
| − | |-
| |
| − | |[[Equine Togaviral Encephalitis|EEE]]
| |
| − | |Systemically ill, pyrexia, abnormal motor function<ref name="Long">Long, M.T (2010) ''Flavivirus Encephalitis'' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12.</ref>, rapidly progressive.<ref name="Seino">Seino, K.K (2010) ''Spinal Ataxia'' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 3.</ref>
| |
| − | |Leukogram, CSF analysis, ELISA, titres, virus isolation.<ref name="Seino">Seino, K.K (2010) ''Spinal Ataxia'' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 3.</ref>
| |
| − | |-
| |
| − | |[[Equine Togaviral Encephalitis|VEE]]
| |
| − | |Systemically ill, pyrexia.
| |
| − | |Leukogram, IgM ELISA<ref>Bertone, J.J (2010) ''Viral Encephalitis'' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12.</ref>
| |
| − | |-
| |
| − | |[[Equine Herpesvirus 1|Equine herpesvirus-1 myeloencephalopathy]]
| |
| − | |Sudden onset and early stabilization of neurological signs, multiple horses affected, recent fever, respiratory disease, abortion.<ref>Wilson, W.D, Pusterla, N (2010) ''Equine Herpesvirus-1 Myeloencephalopathy'' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12.</ref> Dysuria not often seen in EPM.<ref name="Furr">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.</ref>
| |
| − | |CSF analysis, buffy coat, nasal swab PCR.<ref name="Johnson">Johnson, A.L (2009) Evidence-based review of diagnosis and treatment of ''Sarcocystis neurona'' infection (Equine Protozoal Myeloencephalitis). ''Proceedings of the Annual Convention of the AAEP'' - Las Vegas, NV, USA, 55:172-176.</ref><ref name="Seino">Seino, K.K (2010) ''Spinal Ataxia'' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 3.</ref>
| |
| − | |-
| |
| − | |[[Rabies]]
| |
| − | |Rapid progression<ref name="Sommardahl">Sommardahl, C.S (2010) ''Rabies'' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12.</ref>, behavioural alterations, depression, seizure, coma.<ref name="Long">Long, M.T (2010) ''Flavivirus Encephalitis'' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12.</ref>
| |
| − | |Post-mortem fluorescent antibody testing of brain required for definitive diagnosis.<ref name="Sommardahl">Sommardahl, C.S (2010) ''Rabies'' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12.</ref>
| |
| − | |-
| |
| − | |''Polyneuritis equi'' (previously ''cauda equina'' neuritis)
| |
| − | |Cranial nerve deficits are peripheral with no change in attitude.<ref>Scaratt, W.K, Jortner, B.S (1985) Neuritis of the cauda equina in a yearling filly. ''Compend Contin Educ Pract Vet'', 7:S197-S202. In: Saville, W.J (2010) ''Polyneuritis equi'' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12.</ref>
| |
| − | |Western blot analysis of CSF.<ref>Granstrom, D.E, Dubey, J.P, Giles, R.C (1994) Equine protozoal myeloencephalitis: biology and epidemiology. In Nakajima, H, Plowright, W, editors: ''Refereed Proceedings'', Newmarket, England, R & W Publications. In: Saville, W.J (2010) ''Polyneuritis equi'' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12.</ref>
| |
| − | |-
| |
| − | |Equine degenerative myeloencephalopathy
| |
| − | |Symmetrical signs.<ref name="Nout">Nout, Y.S (2010) ''Equine Degenerative Myeloencephalopathy'' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12.</ref>
| |
| − | |May get increased CSF creatinine kinase (CK)<ref>Mayhew, I.G, deLahunta, A, Whitlock, R.H, Krook, L, Tasker, J.B (1978) Spinal cord disease in the horse, ''Cornell Vet'', 68(Suppl 8):1-207. In: Nout, Y.S (2010) ''Equine Degenerative Myeloencephalopathy'' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12.</ref> and reduced serum Vitamin E concentrations but these are unreliable for ante mortem diagnosis.<ref name="Nout">Nout, Y.S (2010) ''Equine Degenerative Myeloencephalopathy'' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12.</ref>
| |
| − | |-
| |
| − | |Verminous encephalomyelitis
| |
| − | |Acute onset.
| |
| − | |CSF analysis.<ref>Jose-Cunilleras, E (2010) ''Verminous Encephalomyelitis'' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12.</ref>
| |
| − | |-
| |
| − | |Bacterial meningoencephalitis
| |
| − | |Stiff neck.<ref name="Pasq">Pasquini, C, Pasquini, S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''' (Third edition), ''SUDZ Publishing'', 245-250.</ref>
| |
| − | |CSF analysis and culture. '''NB: CSF collection contraindicated if clinical signs suggest high intracranial pressure'''
| |
| − | |-
| |
| − | |CNS abscessation due to [[Streptococcus equi subsp. equi|'bastard strangles]]'<ref name="Furr">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.</ref>
| |
| − | |History of [[Streptococcus equi subsp. equi|''Streptococcus equi subsp. equi'']] infection.<ref name="Byrne">Byrne, B. A (2010) ''Diseases of the Cerebellum'' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12.</ref>
| |
| − | |CSF analysis (severe, suppurative inflammation), culture of CSF.<ref name="Byrne">Byrne, B. A (2010) ''Diseases of the Cerebellum'' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12.</ref>
| |
| − | |-
| |
| − | |Spinal trauma<ref name="Pasq">Pasquini, C, Pasquini, S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''' (Third edition), ''SUDZ Publishing'', 245-250.</ref>
| |
| − | |History (usually acute onset neurological signs), usually solitary lesion localised by neurological exam.<ref>Smith, P.M, Jeffery, N.D (2005) Spinal shock - comparative aspects and clinical relevance. ''J Vet Intern Med'', 19:788-793. In: Nout, Y.S (2010) ''Central Nervous System Trauma'' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12.</ref>
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| − | |Radiography, myelography, CT, MRI, nuclear scintigraphy, ultrasound, CSF analysis, nerve conduction velocities, EMG, transcranial magnetic stimulation.<ref>Nout, Y.S (2010) ''Central Nervous System Trauma'' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12.</ref>
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| − | |Occipito-atlanto-axial malformation (OAAM)
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| − | |Deficits develop before 6mths in Arabian horse.<ref>Watson, A.G, Mayhew, I.G (1986) Familial congenital occipitoatlantoaxial malformation (OAAM) in the Arabian horse. ''Spine'', 11:334-339. In: Seino, K.K (2010) ''Spinal Ataxia'' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 3.</ref>
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| − | |Radiography.<ref name="Seino">Seino, K.K (2010) ''Spinal Ataxia'' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 3.</ref>
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| − | |Spinal tumor
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| − | |Signs can usually be localized to one region of the CNS.
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| − | |CT, MRI. Definitive diagnosis requires cytology, biopsy, histopathology or CSF analysis.<ref>Sellon, D.C (2010) ''Miscellaneous Neurologic Disorders'' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12.</ref>
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| − | |''Sorghum'' cystitis/ataxia<ref name="Pasq">Pasquini, C, Pasquini, S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''' (Third edition), ''SUDZ Publishing'', 245-250.</ref>
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| − | |Posterior ataxia or paresis, cystitis, history of grazing ''Sorghum'' species<ref name="Talcott">Talcott, P (2010) ''Toxicoses causing signs relating to the urinary system'' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 22.</ref>
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| − | |Demonstration of cystitis or pyelonephritis by laboratory methods, but not specific.<ref name="Talcott">Talcott, P (2010) ''Toxicoses causing signs relating to the urinary system'' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 22.</ref>
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| − | NB: EPM has been seen concurrently with equine motor neuron disease in a mule<ref>Finno, C.J, Eaton, J.S, Aleman, M, Hollingsworth, S.R (2010) Equine protozoal myeloencephalitis due to ''Neospora hughesi'' and equine motor neuron disease in a mule. ''Vet Ophthalmol'', 13(4):259-65.</ref>
| + | [[Category:Tissue_Cyst_Forming_Coccidia]][[Category:Horse]] |
| − | | + | [[Category:To_Do_-_Nina]] |
| − | [[Image:Equine_Protozoal_Myeloencephalitis.jpg|600px|thumb|right|''' Sarcocystis neurona stages and lesions. | |
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| − | (A). Cross section of spinal cord of horse with focal areas of discoloration (arrows) indicative of necrosis. Unstained.
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| − | (B). Section of spinal cord of a horse with severe EPM. Necrosis, and a heavily infected neuron (arrows), all dots (arrows) are merozoites. H and E stain .
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| − | (C). Higher magnification of a dendrite with numerous merozoites (arrows). One extracellular merozoite (arrowhead) and a young schizont (double arrowhead).
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| − | (D). Section of brain of an experimentally-infected mouse stained with anti-S. neurona antibodies. Note numerous merozoites (arrows).
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| − | (E). Immature schizonts in cell culture. A schizont with multilobed nucleus (arrow) and a schizont with differentiating merozoites (arrowheads). Giemsa stain.
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| − | (F). Mature sarcocysts with hairlike villar protrusions (double arrowheads) on the sarcocyst wall. H and E stain.
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| − | (G). Mature live sarcocyst with numerous septa (arrows) and hairlike protrusions on the sarcocyst wall (double arrowheads). Unstained.
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| − | (H). An oocyst with two sporocysts each with banana-shaped sporozoites. Unstained.
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| − | Created by the ''Agricultural Research Service, the research agency of the United States Department of Agriculture'', July 2005. ''Sourced from the USDA Agricultural Research Service page on EPM/Sarcocystis neurona, located via WikiMedia Commons.'' ''']]
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| − | ===Pathology===
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| − | Widespread lesions of the CNS are typically observed in horses.<ref name="Furr">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.</ref>
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| − | ====Gross exam====
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| − | Lesions may be up to several centimetres across.<ref name="Furr">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.</ref> They range from mild discolouration to multifocal areas of haemorrhage and/or malacia<ref name="Merck">Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial</ref> of the brain, spinal cord and less commonly, peripheral nerves.<ref name="Furr">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.</ref>
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| − | ====Histopathology====
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| − | Microscopically, both grey and white matter may be affected with focal to diffuse areas of nonsuppurative inflammation, necrosis and neuronal destruction. Perivascular infiltrates comprise lymphocytes, macrophages, plasma cells, giant cells, eosinophils and gitter cells.<ref name="Furr">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.</ref> In around 25% of cases, schizonts or merozoites may be found in the neuronal cytoplasm.<ref name="Merck">Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial</ref> Less frequently, protozoa parasitize intravascular and tissue neutrophils and eosinophils, capillary endothelial cells and myelinated axons<ref name="Furr">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.</ref><ref name="Merck">Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial</ref>. Free merozoites may be seen in necrotic regions. If organisms are absent, the diagnosis relies on recognition of the inflammatory changes described above.<ref name="Merck">Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial</ref>
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| − | ==Treatment==
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| − | ===Antiprotozoals===
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| − | The Food and Drug Administration (FDA) has approved four treatments for use in horses with EPM, but not all of these are commercially available:<ref name="Johnson">Johnson, A.L (2009) Evidence-based review of diagnosis and treatment of ''Sarcocystis neurona'' infection (Equine Protozoal Myeloencephalitis). ''Proceedings of the Annual Convention of the AAEP'' - Las Vegas, NV, USA, 55:172-176.</ref>
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| − | *'''Sulfadiazine and pyrimethamine combination, ('Rebalance™', Antiprotozoal Oral Suspension, IVX Animal Health)''': administered PO daily for a minimum of 90 days. Due to availability and ease of administration, some use an off-label regimen of trimethoprimsulfa tablets with pyrimethamine tablets. Pyrimethamine must be given at least 1 hr before or after hay is fed.<ref name="Merck">Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial</ref> ''Mode of action'': trimethoprim, sulfadiazine, and pyrimethamine all inhibit enzymes of folic acid synthesis. ''Efficacy'': 61.5% improvement by one clinical grade.<ref name="MacKay">MacKay, R.J (2006) Equine protozoa myeloencephalitis: treatment, prognosis and prevention. ''Clin Tech Equine Pract'', 5:9-16. In: 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.</ref>''Potential adverse effects'': bone marrow suppression (mild anaemia, leucopenia, neutropenia, thrombocytopenia), fever, anorexia, depression, acute worsening of ataxia and altered reproductive performance in stallions<ref>Bedford, S.J, McDonnell, S.M (1999) Measurements of reproductive function in stallions treated with trimethoprim-sulfamethoxazole and pyrimethamine. ''J Am Vet Med Assoc'', 215:1317–1319. In: Johnson, A.L (2009) Evidence-based review of diagnosis and treatment of ''Sarcocystis neurona'' infection (Equine Protozoal Myeloencephalitis). ''Proceedings of the Annual Convention of the AAEP'' - Las Vegas, NV, USA, 55:172-176.</ref>, congenital defects<ref>Toribio, R.E, Bain, F.T, Mrad, D.R, Messer, N.T, Sellers, R.S, Hinchcliff, K.W (1998) Congenital defects in newborn foals of mares treated for equine protozoal myeloencephalitis during pregnancy. ''J Am Vet Med Assoc'', 212:697–701. In: Johnson, A.L (2009) Evidence-based review of diagnosis and treatment of ''Sarcocystis neurona'' infection (Equine Protozoal Myeloencephalitis). ''Proceedings of the Annual Convention of the AAEP'' - Las Vegas, NV, USA, 55:172-176.</ref>and abortion. Folic acid deficiency may also cause gastrointestinal disturbances such as glossitis.<ref>Piercy, R.J, Hinchcliff, K.W, Reed, S.M (2002) Folate deficiency during treatment with orally administered folic acid, sulphadiazine and pyrimethamine in a horse with suspected equine protozoal myeloencephalitis (EPM). ''Equine Vet J'', 34:311–316. In: Johnson, A.L (2009) Evidence-based review of diagnosis and treatment of ''Sarcocystis neurona'' infection (Equine Protozoal Myeloencephalitis). ''Proceedings of the Annual Convention of the AAEP'' - Las Vegas, NV, USA, 55:172-176.</ref>Blood dyscrazias are typically self-limiting and resolve on withdrawal of treatment.<ref name="Furr">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.</ref> Feeding high quantities of green forage should reduce the risk of anaemia after prolonged treatment. <ref name="Merck">Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial</ref>
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| − | *'''Ponazuril (Marquis®, Bayer Animal Health)''': PO daily for 28 days, use in pregnant animals is off-label. ''Mode of action'': ponazuril is a triazinetrione that targets the “apicoplast” organelle and inhibits the respiratory chain. ''Efficacy'': well absorbed PO, achieves steady state therapeutic concentration in CSF within 3 days<ref>Furr, M, Kennedy, T (2001) Cerebrospinal fluid and serum concentrations of ponazuril in horses. ''Vet Ther'', 2:232-237. In: 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.</ref>clinical response within 10 days, 60% improvement by at least one clinical grade, 8% relapse within 90 days of stopping treatment.<ref>Furr, M, Kennedy, T, MacKay, R, Reed, S, Andrews, F, Bernard, B, Bain, F, Byars, D (2001) Efficacy of ponazuril 15% oral paste as a treatment for equine protozoal myeloencephalitis. ''J Vet Ther'', 2:215-222. In: 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.</ref> ''Potential adverse effects'': none in a multi-centre field study<ref name="Johnson">Johnson, A.L (2009) Evidence-based review of diagnosis and treatment of ''Sarcocystis neurona'' infection (Equine Protozoal Myeloencephalitis). ''Proceedings of the Annual Convention of the AAEP'' - Las Vegas, NV, USA, 55:172-176.</ref>, no systemic toxicity even at high doses.<ref>Kennedy, T, Campbell, J, Selzer, V (2001) Safety of ponazuril 15% oral paste in horses. ''Vet Ther'', 2:223-231. In: 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.</ref>However, the manufacturer reports signs that may have been related to treatment including blisters on the nose and mouth, skin rash or hives, loose stools, mild colic, and a seizure.<ref name="Johnson">Johnson, A.L (2009) Evidence-based review of diagnosis and treatment of ''Sarcocystis neurona'' infection (Equine Protozoal Myeloencephalitis). ''Proceedings of the Annual Convention of the AAEP'' - Las Vegas, NV, USA, 55:172-176.</ref>
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| − | *'''Diclazuril''': PO, daily for 28 days, approved by FDA for use as top-dress tablet but not commercially available. ''Mode of action'': chemically similar to ponazuril but mechanism of action unknown. ''Efficacy'': one study reported clinical improvement in 58% of cases.<ref name="MacKay">MacKay, R.J (2006) Equine protozoa myeloencephalitis: treatment, prognosis and prevention. ''Clin Tech Equine Pract'', 5:9-16. In: 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.</ref> ''Potential adverse effects'': none found in one efficacy study.<ref name="Furr">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.</ref> Reported problems in a multi-centre field study included worsening neurologic status and laminitis but these were not proven to be related to treatment.<ref name="Johnson">Johnson, A.L (2009) Evidence-based review of diagnosis and treatment of ''Sarcocystis neurona'' infection (Equine Protozoal Myeloencephalitis). ''Proceedings of the Annual Convention of the AAEP'' - Las Vegas, NV, USA, 55:172-176.</ref>
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| − | *'''Nitazoxanide, NTZ ('Navigator®', Idexx Pharmaceuticals)''': no longer commercially available in the US. ''Mode of action'': a member of the 5-nitrothiazole class of antiparasitics that inhibits the pyruvate:ferredoxin oxidoreductase (PFOR) enzyme dependent electron transfer reaction essential for anaerobic energy metabolism.<ref name="Johnson">Johnson, A.L (2009) Evidence-based review of diagnosis and treatment of ''Sarcocystis neurona'' infection (Equine Protozoal Myeloencephalitis). ''Proceedings of the Annual Convention of the AAEP'' - Las Vegas, NV, USA, 55:172-176.</ref> ''Efficacy'': 60% success rate in an FDA-regulated study.<ref name="MacKay">MacKay, R.J (2006) Equine protozoa myeloencephalitis: treatment, prognosis and prevention. ''Clin Tech Equine Pract'', 5:9-16. In: 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.</ref> ''Potential adverse effects'': adverse effects and death at high doses<ref name="MacKay">MacKay, R.J (2006) Equine protozoa myeloencephalitis: treatment, prognosis and prevention. ''Clin Tech Equine Pract'', 5:9-16. In: 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.</ref>, fever, anorexia, diarrhoea, lethargy, depression and laminitis recorded at lower doses. Toxic signs usally resolve upon cessation of treatment.<ref name="Furr">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.</ref> '''''Caution: 'administration of nitazoxanide can disrupt the normal microbial flora of the gastrointestinal tract leading to enterocolitis. Deaths due to enterocolitis have been observed while administering the recommended dose in field studies.'''''<ref name="Johnson">Johnson, A.L (2009) Evidence-based review of diagnosis and treatment of ''Sarcocystis neurona'' infection (Equine Protozoal Myeloencephalitis). ''Proceedings of the Annual Convention of the AAEP'' - Las Vegas, NV, USA, 55:172-176.</ref>
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| − | Prolonged, off-license treatment is often instigated after 1 month, based on repeated clinical examination. Even successfully treated cases may remain immunoblot positive for long periods, thus aiming for seronegativity is unrealistic.<ref name="Furr">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.</ref> A lack of response to treatment suggests that the diagnosis should be re-assessed. Another month's worth of the same treatment is recommended for partial responders, with switching to a different chemical class if this fails. The efficacy of currently approved antiprotozoals against ''N.hughesi'' is unknown.<ref name="Furr">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.</ref>
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| − | ===Ancillary medication===
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| − | *'''NSAIDs''': DMSO IV as 10% solution, thought to reduce CSF pressure and improve clinical status. Recommended for severe cases of EPM or to avoid worsening inflammation that may be induced by parasite kill.<ref name="Furr">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.</ref> Caution: DMSO may cause intravascular haemolysis.<ref name="Pasq">Pasquini, C, Pasquini, S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''' (Third edition), ''SUDZ Publishing'', 245-250.</ref>
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| − | *'''Corticosteroids''': a short course of dexamethasone may be beneficial whilst waiting for antiprotozoals to take effect. However, use is controversial because cell-mediated immunity is required to control parasites<ref name="Pasq">Pasquini, C, Pasquini, S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''' (Third edition), ''SUDZ Publishing'', 245-250.</ref> and stress is a proposed risk factor for EPM.<ref name="Furr">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.</ref>
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| − | *'''Immunomodulators''': '''Levamisole''' influences T-cell mediated immunity and enhances phagocytosis. '''Parapox ovis virus (PPOV)''' immunomodulator (Zylexis, Pfizer Animal Health, Kalamazoo, Mich). This vaccine has been shown to upregulate the secretion of cytokines including IFN-γ in several species.<ref>Frieb, A, Siegling, A, Friederichs, S, Volk, H-D, Weber, O (2004) Effects of inactivated parapoxvirus ovis (orf virus) on human peripheral immune cells: induction of cytokine secretion in monocytes and Th1-like cells. ''J Virol'', 78:9400-9411. In: 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.</ref>IFN-γ is thought to be essential for the clearance of ''S.neurona'', thus PPOV may be useful in EPM.<ref name="Furr">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.</ref>
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| − | *'''Multiple vitamin B supplement'''.<ref name="Pasq">Pasquini, C, Pasquini, S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''' (Third edition), ''SUDZ Publishing'', 245-250.</ref>
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| − | ===Supportive management===
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| − | Box rest with deep bedding and good footing or turn out in a flat, grassy field. Ensure all obstacles are removed and avoid turning out ataxic animals with dominant herd mates. Recumbent horses will require dedicated support and a sling if available.<ref name="Furr">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.</ref>
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| − | ==Prognosis==
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| − | Depends on duration and severity of neurological signs<ref name="EPM3">Vatistas, N, Mayhew, J (1995) Differential diagnosis of polyneuritis equi. ''In Practice'', Jan, 26-29.</ref> but clinical resolution is more likely if the condition is diagnosed and treated early.<ref name="EPM8">Gray, L.C, Magdesian, K.G, Sturges, B.K, Madigan, J.E (2001) Suspected protozoal myeloencephalitis in a two-month-old colt. ''Vet Record'', 149:269-273.</ref> With standard therapy, there is a recovery rate of around 25% and an improvement in 60-75% of cases.<ref name="MacKay">MacKay, R.J (2006) Equine protozoa myeloencephalitis: treatment, prognosis and prevention. ''Clin Tech Equine Pract'', 5:9-16. In: 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.</ref> A good prognosis might be expected if there is a response to treatment within two weeks. The prognosis will be guarded to poor<ref name="Pasq">Pasquini, C, Pasquini, S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''' (Third edition), ''SUDZ Publishing'', 245-250.</ref> for a horse with severe, irreversible neuronal damage.
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| − | ==Prevention==
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| − | ===Prophylaxis===
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| − | A killed vaccine, developed using ''S.neurona'' merozoites, was conditionally licensed for use in horses.<ref name="Saville1">Saville, W.J.A, Reed, S.M, Dubey, J.P (2002) Prevention of equine protozoal myeloencephalitis(EPM). ''Proceedings of the Annual Convention of the AAEP'', 48:181-185.</ref> The vaccine proved to be ineffective in the prevention of EPM and has since been removed from the market.<ref name="Furr">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.</ref> There is evidence to suggest that the antiprotozoal, ponazuril, may be useful prophylactically to reduce the incidence and severity of clinical signs.<ref>Furr, M, MacKenzie, H, Dubey, J.P (2006) Pretreatment of horses with ponazuril limits infection and neurologic signs resulting from S.neurona. ''J Parasitol'', 92:637-643. In: 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.</ref> Implementing such a regime prior to and during stressful events may be beneficial, although the cost is likely to be prohibitive.<ref name="Furr">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.</ref>Protocols involving intermittent administration of ponazuril may also show promise in the prevention of EPM.<ref>Mackay, R.J, Tanhauser, S.T, Gillis, K.D, Mayhew, I.G, Kennedy, T.J (2008) Effect of intermittent oral administration of ponazuril on experimental ''Sarcocystis neurona'' infection of horses. ''Am J Vet Res'', 69(3):396-402.</ref>
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| − | ===Control===
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| − | Control of EPM is challenging because there are a variety of intermediate hosts for ''S.neurona'' and this parasite is very widely distributed.<ref name="Furr">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.</ref> The definitive host, the opossum, is also a scavenger and will consume road-kill, including species that are putative intermediate hosts for ''S.neurona''.<ref name="Saville1">Saville, W.J.A, Reed, S.M, Dubey, J.P (2002) Prevention of equine protozoal myeloencephalitis(EPM). ''Proceedings of the Annual Convention of the AAEP'', 48:181-185.</ref> A number of control measures are recommended:
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| − | *Deny wildlife access to feed (use rodent-proof containers, protect forages in enclosed facilities,<ref name="Furr">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.</ref> remove fallen fruit and bird feeders)<ref name="Merck">Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial</ref>
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| − | *Prevent access of opossums to horse-feeding areas
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| − | *Remove carcasses from roads and property (especially those of skunks, raccoons, armadillos and cats which may act as intermediate hosts)<ref name="Saville1">Saville, W.J.A, Reed, S.M, Dubey, J.P (2002) Prevention of equine protozoal myeloencephalitis(EPM). ''Proceedings of the Annual Convention of the AAEP'', 48:181-185.</ref>
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| − | *Opossums can be trapped and relocated<ref name="Merck">Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial</ref>
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| − | *Monitor high-risk horses closely to help detect EPM early<ref name="Furr">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.</ref>
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| − | {{Learning
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| − | |literature search = [http://www.cabdirect.org/search.html?q=title%3A%28%22Equine+Protozoal+Myeloencephalitis%22%29+OR+title%3A%28EPM%29+OR+title%3A%28%22Equine+protozoal+encephalomyelitis%22%29+OR+title%3A%28%22Equine+protozoal+myelitis%22%29 Equine protozoal myeloencephalitis]
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| − | |full text = [http://www.cabi.org/cabdirect/FullTextPDF/2010/20103149572.pdf ''' Evidence-based review of diagnosis and treatment of Sarcocystis neurona infection (equine protozoal myeloencephalitis).''' Johnson, A. L.; White, N., II; American Association of Equine Practitioners (AAEP), Lexington, USA, Proceedings of the 55th Annual Convention of the American Association of Equine Practitioners, Las Vegas, Nevada, USA, 5-9 December 2009, 2009, pp 172-176, 27 ref.]
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| − | [http://www.cabi.org/cabdirect/FullTextPDF/2006/20063226204.pdf '''Equine protozoal myeloencephalitis - a review.''' Waghmare, S. P.; Shafiqur Rahman; Intas Pharmaceuticals Ltd, Ahmedabad, India, Intas Polivet, 2006, 7, 1, pp 59-63, 18 ref.]
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| − | [[Category:Expert_Review]] | |
| − | [[Category:Neurological Diseases - Horse]] | |
