Changes

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.  

====Clinical Signs====

====History====

 

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

====Clinical exam====

 

Typically normal, although focal muscle atrophy may be observed.  

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.

The protozoa can cause lesions sporadically in any part of the CNS which makes the clinical presentation highly variable. The three characteristic 'As' of EPM (ataxia, asymmetry, atrophy) suggest multifocal or diffuse disease, but are not pathognomonic.  It has been suggested that rapidly progressive presentations reflect brainstem lesions.  Spinal cord signs are most commonly seen and may include:

 

*asymmetric or symmetric paresis, spasticity and ataxia of one to four limbs

 

*focal or general muscle atrophy

 

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.

*upward fxation of the patella

*loss of condition

*cauda equina signs

*focal regions of inappropriate sweating, loss of reflexes or cutaneous anaesthesia

Lesions of the brainstem, cerebrum or cerebellum are less frequently recognized:

*depression

*head tilt

*laryngeal hemiplegia

*dorsal displacement of the soft palate (DDSP)

*seizures (may be the only clinical sign)

Without treatment, progression to recumbency and death is likely. This deterioration may occur smoothly or spasmodically over hours to years.

====Laboratory tests====

====Laboratory tests====