Changes

====Description====

====Description====

Primary cause of multifocal, asymmetric, progressive CNS disease.  Can mimic any neurologic disease (Pasq)

Primary cause of multifocal, asymmetric, progressive CNS disease.  Can mimic any neurologic disease.  Infectious but not contagious disease (Pasq)

====Aetiology and Epidemiology====  

====Aetiology and Epidemiology====  

The average incidence of EPM according ot the United Sattes Department of Agroiculture is around 14 cases per 10,000 horses per year.  The true incidecne is porbbaly underestimated due to the complexity of the clincial dx and difficulty in finding conclusive CNS lesions.  Racing and showing animals have been shown to be at higher risk than beeding and pleasure horses.  EPM is a disease of the Western Hemisphere, with cases outside of the Americas havign spendt time in endemic regions.  The diseas ehas been reporetd in England among horses imported from the Eastern US an din an Arbaian horse in South Africa imported from the US.  The cases demonstarte the porbbaility of persitent, subcliicsal, latent infections.  But a few reports exist of neurological horses with consistent cx, positivew immunoblot test results and no hx of travel in the American continent.  This may be due to cross-reactign Ags.  TBs, SBs and Quarterhorses are most commonly affected across the US and Canada.  this may refelct managemetn, env or use of these breeds rather than an innate breed charcterisitic.

The average incidence of EPM according ot the United Sattes Department of Agroiculture is around 14 cases per 10,000 horses per year.  The true incidecne is porbbaly underestimated due to the complexity of the clincial dx and difficulty in finding conclusive CNS lesions.  Racing and showing animals have been shown to be at higher risk than beeding and pleasure horses.  EPM is a disease of the Western Hemisphere, with cases outside of the Americas havign spendt time in endemic regions.  The diseas ehas been reporetd in England among horses imported from the Eastern US an din an Arbaian horse in South Africa imported from the US.  The cases demonstarte the porbbaility of persitent, subcliicsal, latent infections.  But a few reports exist of neurological horses with consistent cx, positivew immunoblot test results and no hx of travel in the American continent.  This may be due to cross-reactign Ags.  TBs, SBs and Quarterhorses are most commonly affected across the US and Canada.  this may refelct managemetn, env or use of these breeds rather than an innate breed charcterisitic.

====Signalment====

====Signalment====

====Diagnosis====

====Diagnosis====

Diagnosis:  

 

Hx (age), Cx (asymmetric multifocal ataxia & weakness), CNS Cx plus positive Western blot of CSF highly suggestive.  Presumptive: treat and rul out others.  Western blot serological test for CSF and serum, 50% horses positive serum.  CSF taps: normal or maybe increased protien & monocytes (pleocytosis).  Post multiple sections of spinal cord: multifocal & asymmetrci, gross: grey-brown dicsoloration, with H+, swelling & liquefaction, histo: nonsuppurative inflammatory focal malacia & H+, perivasucalr cuffing, gliosis, astrocytosis, neuronal necrosis & gitter cell proliferation, multinucleated giant cells.  Parasite in CNS defintiive, schizonts & merozoites at perhoepry of lesions, but may not be demonstarted (Pasq)

 

Postmortem diagnosis is confirmed by demonstration of protozoa in CNS lesions. An immunoblot (Western blot) test for S neurona is used as an aid to antemortem diagnosis. In horses with neurologic signs, demonstration of specific antibody in CSF (by immunoblot) is highly suggestive of EPM. A positive immunoblot test in serum only indicates exposure to S neurona . Conversely, a negative immunoblot result, in either serum or CSF, tends to exclude the diagnosis of EPM. In a few horses with EPM, CSF analysis reveals abnormalities such as mononuclear pleocytosis and increased protein concentration.   

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.

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.

====Differential Diagnoses====

====Differential Diagnoses====

Includes virtually all diseases of the CNS

Includes virtually all diseases of the CNS

Cervical compression (usually symmetrcial gait deficits, worse in pelvic limbs with spasticity and hypermetria, with good retention of strensght and no muscle wasting)

Cervical compression (usually symmetrcial gait deficits, worse in pelvic limbs with spasticity and hypermetria, with good retention of strensght and no muscle wasting)