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Also known as: | EPM Equine protozoal myelitis |
Description
A progressive, infectious,[1]neurological disease of horses, endemic in the USA[2] and only encountered elsewhere in imported equids.[3] EPM is one of the most frequently diagnosed neurological conditions of the Western Hemisphere[4] and the principal differential for multifocal, asymmetric progressive central nervous system (CNS) disease.[1] As it can resemble any neurological disorder, EPM must be considered in any horse with neurological signs if it resides in the Americas or if it has been imported from that area[2][5] The disease is not contagious.[1]
Aetiology
EPM results from infection of the CNS by the apicomplexan parasite Sarcocystis neurona or, less frequently, its close relative Neospora hughesi.[6][7] These protozoans develop within neurons[4] 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.[1]
Signalment
Mostly Standardbreds and Thoroughbreds aged 1-6years.[1] Foal infection may be possible.[2]
Differential Diagnoses
The protozoan can migrate to any region of the CNS[2], thus the differential list comprises almost all diseases of this system.[4]
Differential | Differentiating signs | Tests to rule out |
Cervical vertebral malformation (CVM, cervical compressive myelopathy, cervical vertebral instability, cervical spondylomyelopathy, Wobbler's syndrome) | Symmetrical gait deficits, worse in pelvic limbs[8] with spasticity and dysmetria, good retention of strength, no muscle wasting[4] NB:can be concurrent with EPM.[9] | Plain lateral radiography of C1 to T1[9], myelography. [10] |
WNV encephalitis | Systemically ill, pyrexia. Difficult if horse afebrile and has no excessive muscle fasciculations[11] | Leukogram, CSF analysis, IgM capture ELISA, plaque reduction neutralization test (PRNT).[10] |
WEE | Systemically ill, pyrexia, abnormal motor function[11] | Leukogram, ELISA, titres, viral isolation.[10] |
EEE | Systemically ill, pyrexia, abnormal motor functionCite error: Closing </ref> missing for <ref> tag
|
Leukogram, CSF analysis, ELISA, titres, viral isolation |
VEE | Systemically ill, pyrexia. | Leukogram, IgM ELISA[12] |
Equine herpesvirus-1 myeloencephalopathy | Sudden onset and early stabilization of neuro signs, multiple horses affected, recent fever, abortion[13]dysuria not often seen in EPM. | CSF analysis, PCR[4], titres, virus isolation.[10] |
Rabies | Rapid progression[14], behavioural alterations, depression, seizure, coma.[11] | Post-mortem fluorescent antibody testing of brain required for definitive diagnosis.[14] |
Polyneuritis equi (previously cauda equina neuritis) | Cranial nerve deficits are peripheral with no change in attitude[15] | Western blot analysis of CSF[16] |
Equine degenerative myeloencephalopathy | Symmetrical signs[17] | May get increased CSF CK[18] and reduced serum Vitamin E concentrations but unreliable ante mortem diagnosis.[17] |
Verminous encephalomyelitis | Acute onset | CSF analysis[19] |
Bacterial meningoencephalitis | Stiff neck[1] | |
CNS abscessation[4] | ||
Spinal trauma[1] | Hx (usually acute onset neurologica signs), usually solitary lesion localised by neurological exam[20] | Radiography, myelography, CT, MRI, nuclear scintigraphy, ultrasound, CSF analysis, nerve conduction velocities, EMG, transcranial magnetic stimulation.[21] |
Occipito-atlanto-axial malformation (OAAM) | Deficits develop before 6mths in Arabian horse[22] | Radiography.[10] |
Spinal tumors | Signs can usually be localized to one region of the CNS | CT, MRI, definitive dx requires cytology, biopsy, histopathology, CSF analysis[23] |
Sorghum cystitis/ataxia[1] | Posterior ataxia or paresis, cystitis, hx of grazing Sorghum species[24] |
Pathology
Widespread lesions of the CNS are typically observed in horses.[4]
Gross exam
Lesions may be up to several centimetres across.[4] They range from mild discolouration to multifocal areas of haemorrhage and/or malacia (Merck) of the brain, spinal cord and less commonly, peripheral nerves.[4]
Histopathology
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.[4]
In around 25% of cases, schizonts or merozoites may be found in the neuronal cytoplasm (Merck). Less frequently, protozoa parasitize intravascular and tissue neutrophils and eosinophils, capillary endothelial cells and myelinated axons[4] (Merck). Free merozoites may be seen in necrotic regions. If organisms are absent, the diagnosis relies on recognition of the inflammatory changes described above. (Merck)
Prognosis
Depends on duration and severity of neurological signs[3] but clinical resolution is more likely if the condition is diagnosed and treated early.[2] With standard therapy, involving 6-8months of ponazuzril or pyrimethamine-sulfadiazine (V), there is a recovery rate of around 25% and an improvement in 60-75% of cases.[25] A good prognosis might be expected if there is an improvement in clinical signs within two weeks of commencing anti-protozoal and anti-inflammatory treatment (V). The prognosis will be guarded to poor[1] for a horse with severe irreversible neuronal damage or one that has not been diagnosed or treated appropriately (V).
References
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 1.8 Pasquini, C, Pasquini, S, Woods, P (2005) Guide to Equine Clinics Volume 1: Equine Medicine (Third edition), SUDZ Publishing, 245-250. Cite error: Invalid
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tag; name "Pasq" defined multiple times with different content - ↑ 2.0 2.1 2.2 2.3 2.4 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. Cite error: Invalid
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tag; name "EPM8" defined multiple times with different content - ↑ 3.0 3.1 Vatistas, N, Mayhew, J (1995) Differential diagnosis of polyneuritis equi. In Practice, Jan, 26-29.
- ↑ 4.00 4.01 4.02 4.03 4.04 4.05 4.06 4.07 4.08 4.09 4.10 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.
- ↑ DEFRA, The Animal Health Trust, The British Equine Veterinary Association (2009) Surveillance: Equine disease surveillance, April to June 2009, The Vet Rec, Oct 24:489-492.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 9.0 9.1 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.
- ↑ 10.0 10.1 10.2 10.3 10.4 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.
- ↑ 11.0 11.1 11.2 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.
- ↑ 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.
- ↑ 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.
- ↑ 14.0 14.1 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.
- ↑ 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.
- ↑ 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.
- ↑ 17.0 17.1 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.