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Equine Protozoal Myeloencephalitis is a very rare brain disease that is associated with protozoa that causes neurological disease.  Historically, horses with this disease had a poor prognosis.  It was unexpected that horses could resolve the clinical signs of EPM because it was thought that parasites caused physical damage in the brain or spinal cord. It turns out that there are three diseases masquerading as EPM, the good news is that these diseases are common and can be identified and treated.

Our view is different because we identify the cause and consequences of infection.  Infection causes inflammation of the nerves in the body and central nervous system.   Protozoal-induced inflammation can be effectively managed and treated. In some cases protozoal disease can be prevented.

Causes and risk factors of EPM   Sarcocystis neurona is a parasitic protozoa that was isolated from horses with EPM. Another organism, Neospora hughesii  is a very rare cause of EPM. Studies using postmortem data show most EPM horses were young Thoroughbreds, Standardbreds, and Quarter Horses.

Causes and risk factors of Sarcocystosis  If you look at seroprevalence data (a measure of antibodies in horses) almost all horses are positive for S. neurona because they had exposure to the organism and quickly resolved this very common infection.  Most horses do not get EPM and most horses resolved sarcocystosis.  Horses can get clinical signs associated with inflammation from diseases that look like EPM.

Causes and risk factors of polyneuritis  Polyneuritis is a generalized neuromuscular disease that can be caused by S neurona, S fayeri, or other factors (vaccination reaction, bacterial infections, viral infections, Lyme disease). Almost 1/3 of horses in this country have muscle cysts that are the end stage infection of Sarcocystis fayeri.  Usually this infection is benign, unless the horse is debilitated.  However, as the cysts breakdown they can release substances that induces an inflammatory response.  These horses have “sub-clinical” disease and become clinically ill as the inflammatory cycle isn't turned off. The cycle of inflammation produces signals that keep the inflammation going, in turn producing more pro-inflammatory signals.

Diagnostic testing There are no EPM tests!  There are antibody tests to detect S neurona and other organisms associated with EPM, such as S. fayeri.  All  “EPM” tests in the live animal are different methods of detecting antibody against S. neurona.   Antibody tests based on S. neurona have been used to predict how likely it is that a horse may have EPM.  The problem is that antibody lingers after S. neurona is gone.  And the level of antibody reached during and after infection is not statistically related to infection. S neurona tests are useful to rule in or rule out S. neurona as the cause of disease, but is not useful to detect current infection. Tests for S. neurona are specific (SAG 1, 5, 6) or non-specific (SAG 2, 4/3). Non-specific tests use carefully diluted serum to remove cross-reactive antibodies such as those that detect S. fayeriSarcocystis fayeri  tests detect antibodies directed against disease causing proteins and are associated with disease.

Inflammation causes clinical signs during infection.  The inflammatory component of disease causes inflammation of the nerves, called neuritis.  Inflammation can become the issue (polyneuritis equi) and the inflammatory cycles causes chronic disease.  Uncontrolled chronic inflammation can be life-threatening and is recognized as cauda equina syndrome.

A panel of tests that include the likely causes of  neuromuscular diseases are SAG 1, 5, 6, S fayeri, MP2/MPP, Lyme, and CRP levels.

Treatment  There are several approaches to treatment. Each animal is different and responds differently to treatment, however if clinical signs aren’t improving after initiation of treatment a review of the test results, further testing, and a change in treatment are indicated.  Double dosing an ineffective treatment is not a good treatment plan. If the disease process is inflammation, it is important to monitor the inflammation using CRP testing, treat until the inflammatory process has resolved (often weeks after the resolution of clinical signs), and then prevent relapses by monitoring the level of inflammation.

Prevention  If it is determined that a horse is continually exposed to S neurona or S fayeri  preventing infection is possible.  Preventing the production of antibody to S neurona with some drugs has been proven ineffective for preventing disease.  It is important to test and determine if there is continued exposure to the parasite because overuse of antimicrobials is unwise. Preventing pathologic inflammation is best accomplished by monitoring the CRP levels.blogger-image-702499765

Reference paper: Ultrasound-guided cervical centesis to obtain cerebrospinal fluid in the standing horse  Anthony Pease, Ashley Behan, George Bohart Vet Radiol Ultrasound 2012 53(1) 92-5

In some cases a cerebrospinal fluid analysis is used to support a presumptive diagnosis of equine protozoal myeloencephalitis.  The presence of antibodies against S. neurona is considered, by some, as evidence that parasites are in the central nervous system.  Research done so far on on oocyst challenge infections fails to support this view.  We believe that the inflammatory component of the EPM syndrome should not be ignored.

There is a need to define cases that are associated with S. neurona and those that are unassociated with protozoa; for some clinicians a CSF tap may be the defining test.  Testing CSF fluid will help us obtain the data to make an assessment of the utility of CSF analysis in field selection of treatable cases of EPM in a statistically meaningful study.  We don’t charge for antibody determination on CSF fluid when it is submitted with a serum sample for SAG 1, 5, 6 testing.  The veterinarian-signed paperwork must accompany the submissions for the no charge CSF testing.

Resistance to field collection of CSF are justified.  The lumbosacral space is used for CSF collection in the standing horse.  The limits of this procedure are technical expertise, blood contamination, and the distance from the cranium, the proposed site of the lesion.  In the field the risk of trauma to the veterinarian is great due to the close proximity of the clinician to the rear limbs.

Alternatively, a sample can be obtained from the atlanto-occipital space under general anesthesia.  Experience with obtaining an AO tap is a plus with this technique.  The risk of injury during recovery from general anesthesia in an ataxic horse is high.  And transporting an ataxic animal is not advised.

 

The ultrasound-guided cervical centesis was used in normal horses in the above referenced paper and may be a viable alternative for field veterinarians that want a sample from an ataxic horse.  A brief survey of veterinarians indicates that this was not a procedure that is in common use for acquiring a CSF sample from an ataxic horse, therefore we are reviewing the procedure here. The hypothesis is  that obtaining a tap at C1-2, with assistance from ultrasound, may provide an alternative to collection of CSF in a standing horse.  The horses used in the Pease study were in stocks.  The horses were sedated with detomidine hydrochloride followed by morphine.  The area is aseptically prepared prior to the sample collection.  A nose twitch is used when the needle is placed.

A 10-4 MHz, microconvex curvilinear transducer (oriented dorsoventrally) is placed at the level of C1-2.  An 18g, 3.5 inch needle with stylet is advanced to the dura mater, in a dorsomedial direction approximately 4 cm through the dura mater (with the stylet) and into the subarachnoid space.  The CSF sample is then collected with gentle suction (changing syringes after the initial 5 ml decreases blood contamination).  Post collection observations are conducted for 48 hours.  We have a demonstration video of this procedure available on line. Call for information.