Difference between revisions of "Equine Protozoal Myeloencephalitis"
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====Signalment==== | ====Signalment==== | ||
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> | 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==== | ====Clinical Signs==== | ||
− | The disease onset may be acute, peracute | + | 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.(Furr)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. (EPM3)The three characteristic 'As' (ataxia, asymmetry, atrophy) suggest multifocal or diffuse disease, but are not pathognomonic for EPM (Furr). |
− | Spinal cord | + | {| cellpadding="10" cellspacing="0" border="1" |
− | *Ataxia, paresis or | + | | '''Lesion Location''' |
+ | | '''Clinical signs''' | ||
+ | |- | ||
+ | |Spinal cord | ||
+ | |*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 | ||
*Loss of reflexes or cutaneous anaesthesia | *Loss of reflexes or cutaneous anaesthesia | ||
− | *Apparent lameness, particularly atypical or slight gait asymmetry of hindlimbs (not alleviated by local | + | *Apparent lameness, particularly atypical or slight gait asymmetry of hindlimbs (not alleviated by local anaesthesia) |
*Abnormal placing reactions | *Abnormal placing reactions | ||
− | *Focal muscle atrophy of individual muscle | + | *Focal muscle atrophy of individual muscle groups(Pasq), especially gluteal muscles, often asymmetrical |
*Generalized muscle atrophy or loss of condition | *Generalized muscle atrophy or loss of condition | ||
*Localized sensory deficits and 'strip sweating' of dermatomes | *Localized sensory deficits and 'strip sweating' of dermatomes | ||
*Sacrococcygeal involvement will produce signs that mimic ''polyneuritis equi'' | *Sacrococcygeal involvement will produce signs that mimic ''polyneuritis equi'' | ||
− | Peripheral nerves | + | |- |
− | *Upward fixation of the patella | + | |Peripheral nerves(may lead to injuries to muscle tendons or ligaments) |
+ | |*Upward fixation of the patella | ||
*Exertional rhabdomyolysis | *Exertional rhabdomyolysis | ||
*Back pain | *Back pain | ||
*Gait abnormality | *Gait abnormality | ||
− | Brainstem (cranial nerve signs, <5% cases) | + | |- |
− | *Atrophy of temporalis and masseter muscles, loss of sensation | + | |Brainstem (cranial nerve signs, <5% cases) |
− | * | + | |*Atrophy of ''temporalis'' and ''masseter'' muscles, loss of facial sensation (V) |
− | **VIII - vestibular signs | + | *Facial (VII) and vestibulocochlear (VIII) nerve deficits often seen together: |
− | **VII - unilateral facial paralysis | + | **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) | *Loss of tongue tone (XII) | ||
− | *Dysphagia(V, VII, IX, X, XII) | + | *Dysphagia (V, VII, IX, X, XII) |
− | *Dorsal displacement of soft palate (IX, X) | + | *Dorsal displacement of the soft palate (IX, X) |
*Laryngeal hemiplegia (X) | *Laryngeal hemiplegia (X) | ||
*Abnormal menace response (II, VII) | *Abnormal menace response (II, VII) | ||
*Headshaking(EPM 7) | *Headshaking(EPM 7) | ||
*Blindness with or without abnormal pupillary reflexes (Pasq) | *Blindness with or without abnormal pupillary reflexes (Pasq) | ||
− | Cerebrum, basal nuclei, cerebellum: | + | |- |
− | *Abnormal menace response | + | |Cerebrum, basal nuclei, cerebellum: |
+ | |*Abnormal menace response | ||
*Circling | *Circling | ||
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*Seizures (may be the only clinical sign)(82 in Furr) | *Seizures (may be the only clinical sign)(82 in Furr) | ||
− | *Abnormal EEG | + | *Abnormal electroencephalogram (EEG) |
*Asymmetrical central blindness | *Asymmetrical central blindness | ||
*Facial hypoalgesia | *Facial hypoalgesia | ||
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*Narcolepsy-like syndrome | *Narcolepsy-like syndrome | ||
− | + | Lesions of the brainstem, cerebrum or cerebellum are less frequently recognized than those of the spinal cord. Horse with severe EPM may be unable to stand or swallow and, if left untreated, progress to recumbency within 14 days to 6 months. (Pasq) This deterioration may occur smoothly or spasmodically (Merck) but is likely to result in death. It has been suggested that rapidly progressive presentations reflect brainstem lesions.(Furr) | |
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====Diagnosis==== | ====Diagnosis==== |
Revision as of 22:09, 19 July 2010
This article is still under construction. |
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]
Epidemiology
In endemic areas of the United States, around a quarter of referrals for equine neurological disease are attributed to EPM.[8] According to the United States Department of Agriculture, the average incidence of the disease is 14 cases per 10,000 horses per year. However, the challenges of obtaining a definitive diagnosis may mean this figure is an underestimate.[4] The disease has been identified in parts of Central and South America, southern Canada and across most of the USA..[4] EPM is noted occasionally in other countries, in horses that have been imported from the Americas.[9][10] It is likely that these animals underwent transportation carrying a silent but persistent infection. There have been reports of EPM in horses that have not travelled to or from endemic regions,[4] although cross-reacting antigens on the immunoblot test may explain this discrepancy. [4]
The route of infection remains unconfirmed,[1] but there is an increased risk associated with a young age (1-4 years)[11]and autumn months.[12] The reported age range for EPM cases is currently 2 months[2] to 24 years.[13] Thoroughbreds, Standardbreds and Quarterhorses are most frequently affected across the US and Canada.[14] This may relate to a breed predispostion or alternatively, managemental factors associated with these breeds.[15] Showing, racing and stress[16] have been linked to a greater risk of clinical disease.[17]
Increasing age and environmental temperature have been associated with an increased seroprevalence of S. neurona.[18] Seroprevalence for this species is typically higher than for N. hughesi.[4]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.[4]Case clustering may operate where all the risk factors occur, but the majority of cases appear in isolation.[4]
Life Cycle
The causative pathogen(s) have been isolated form species other than the horse including zebra, domestic cat, Canadian lynx, sea otter, straw-necked ibis, mink, raccoon and sunk. (Furr)
Signalment
Mostly Standardbreds and Thoroughbreds aged 1-6years.[1] Foal infection may be possible.[2]
Clinical Signs
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.(Furr)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. (EPM3)The three characteristic 'As' (ataxia, asymmetry, atrophy) suggest multifocal or diffuse disease, but are not pathognomonic for EPM (Furr).
Lesion Location | Clinical signs | |||||||||||||||||||||||||||||||||||||||||||||||||||
Spinal cord | *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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Peripheral nerves(may lead to injuries to muscle tendons or ligaments) | *Upward fixation of the patella
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Brainstem (cranial nerve signs, <5% cases) | *Atrophy of temporalis and masseter muscles, loss of facial sensation (V)
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Cerebrum, basal nuclei, cerebellum: | *Abnormal menace response
Lesions of the brainstem, cerebrum or cerebellum are less frequently recognized than those of the spinal cord. Horse with severe EPM may be unable to stand or swallow and, if left untreated, progress to recumbency within 14 days to 6 months. (Pasq) This deterioration may occur smoothly or spasmodically (Merck) but is likely to result in death. It has been suggested that rapidly progressive presentations reflect brainstem lesions.(Furr) DiagnosisDifferential DiagnosesThe protozoan can migrate to any region of the CNS[2], thus the differential list comprises almost all diseases of this system.
PathologyWidespread lesions of the CNS are typically observed in horses.[4] Gross examLesions may be up to several centimetres across.[4] They range from mild discolouration to multifocal areas of haemorrhage and/or malacia[38] of the brain, spinal cord and less commonly, peripheral nerves.[4] HistopathologyMicroscopically, 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.[38] Less frequently, protozoa parasitize intravascular and tissue neutrophils and eosinophils, capillary endothelial cells and myelinated axons[4][38]. Free merozoites may be seen in necrotic regions. If organisms are absent, the diagnosis relies on recognition of the inflammatory changes described above.[38] TreatmentPrognosisDepends 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.[39] 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). PreventionProphylaxisA killed vaccine, developed using S.neurona merozoites, was conditionally licensed for use in horses.[40] The vaccine proved to be ineffective in the prevention of EPM and has since been removed from the market.[4] There is evidence to suggest that the antiprotozoal, ponazuril, may be useful prophylactically to reduce the incidence and severity of clinical signs.[41] Implementing such a regime prior to and during stressful events may be beneficial, although the cost is likely to be prohibitive.[4] References
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