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Recently JAVMA published a letter to the editor and we’d like to give the author kudos!  He was disappointed that after years of using a particular product, a clinical trial revealed the drug was not effective.  He placed his faith on recommendations from trusted and respected colleagues, board certified specialists and continuing education speakers. They didn’t base their opinions on clinical data and that led to years of using a drug for pain in dogs that was just shown to have a complete lack of effect.  We all recognize the importance of new scientific evidence, lack of funding for many projects, and the burden on the people that provide treatment recommendations to know and understand the supporting data- or lack thereof-before dissemination of their opinion.  We concur with the statement in response to the letter that  many clinicians, if they looked at the information used in the daily treatment of patients, would likely be shocked to find out just how little clinical data are truly available to support current recommendations, or how many opinions are not based on experience or understanding-just a conflict of opinion.

We have taken a different path with our work.   Rather than patenting the intellectual property (IP) and  then licensing the technology, on completing research we decided to make our work available to those who needed it, and open the discussion.  Has it cost us in many ways?  Yes.  But then, I grew up in the scientific community at a different time.  Once upon a time, that would be the 1970’s, we shared data and discovery.  I was a lab rat back then, spending many hours with the fluorescent microscope-looking at how Chinese hamster ovary cells responded to ATP stimulation.  OK, I get it.  But the experience was good.  We shared samples and “stuff” that moved knowledge forward.  I used that experience to look at Leptospira and Moon Blindness, another immune mediated condition, for my Masters thesis.  Then off to veterinary school.  While I was practicing veterinary medicine in the field over the next 20 years, things changed.  There was the biochemical revolution that spawned the field of molecular biology, and PCR, and proteomics.  Suddenly things like PCR, had monumental value.  Everything was DNA and  genes.  Heck, whole organisms are patented-Neospora comes to mind, (quick update, the patent office won’t do that anymore).  To use the IP, one has to have a license and pay royalties.  The revolution was in the 80”s to the 90’s, the patent for PCR was filed on June 17, 1987.

When I returned in 1999 to work on my PhD, in molecular biology of course, everything went through the University’s Office of Licensing and Technology (OLT).  Universities recognized the value of IP.  No more sharing.  No more shared discovery.  Heck, recently I wanted to use a video to help veterinarians get CSF taps using a standing procedure.  I was told there would be a largish up front fee followed by a royalty due for each use…one fee for every veterinarian that viewed the tape. It was explained to me the video is like a Beatle’s song-and they wanted to hold my hand.  I made my own video and freely gave it out hoping to get veterinarians to collect CSF and support our Orogin trial. Oh, we were criticized, one veterinarian wanted the video removed and not shared because all those horse owners would be getting CSF taps on their own horses.

We persevered, partially due to the words of one of my PhD professors, Ellis Greiner, “Science is self-correcting”.  If I continued to do work, collaborate with those with true curiosity and an open mind, we would eventually see the day when our ideas would receive acknowledgement and open discussion.  Because that is what science is, open discussion of ideas. To that end we publish our work, in peer reviewed journals, and submit our papers and abstracts for presentation at scientific meetings.  We collected and shared samples, (DNA, RNA, organisms), and imparted ideas, traveled to NIH and Washington and beyond; we teleconferenced, (with Germany, the Netherlands, Japan, and even Kentucky), with those who  were open to the burden of review.  There was plenty of criticism from those who didn’t take the time to understand, review and hold an open discussion.  We carefully persevered, leaving breadcrumbs.  Sure, we patented some IP.  And made some IP  public so that  others can’t patent it.  The IP is available to everyone.

I think the long awaited day is dawning.  The discussion at the upcoming EPM special information session will have a panel discussion on the evidence of the role of S. neurona in infection and disease.  Is it a disease of low parasite burden-host mediated pro-inflammatory response or is disease a reflection of high parasite burden resulting in direct injury to the CNS? they ask.  We are presenting two papers, the most important is our recent data on polyneuritis equi.  Our work is important because our evidence supports, and may identify, one inflammatory pathway for disease.  The story we tell is one of relapsing disease and hope of treatment.  Our story identifies a protagonist molecule and the hero horse heading off with all four legs moving in proper order.  We look forward to SIG participants that will critically review what we have done.  We welcome suggestions or guidance on our errant interpretations. Perhaps some will return to their laboratories and repeat our work. Or collaborate without IP on the mind.  They may claim no funding-we are used to that because we are self-funded.  No big grants, although we’d gladly accept one.*  We are optimistic that this may be the moment.  We’ll let you know Dr. Greiner, and if our time has not come, we will continue to drop those breadcrumbs.



*Disclaimer: We are a for profit company.  We do not accept tax-exempt donations. Nor do we accept generously offered dowry’s from grateful horse-owning newly weds-although we gratefully appreciated the gesture.

crystal ballThe orbuculum, or crystal ball, was invented about 3000 BC according to Wikipedia.  Mystical orbs were used in numerous cultures to communicate with the gods or learn of future threats. Wouldn’t it be nice to identify horses that are genetically pre-disposed to get sarcocystosis?  A genetic EPM-crystal ball.

Thirteen years ago, we participated in studies that sought to identify cell markers unique to horses with equine protozoal myeloencephalitis, EPM. The idea was that cell markers or the “gene expression signature” unique to EPM would be found in immune cells circulating in the blood. The differences in gene expression between animals with and without clinical evidence of EPM would be analyzed using several statistical measures. Genes that showed statistically significant differences in clinically positive horses were compared to those that were clinically negative, and the genes that showed a significant difference (those significantly up-regulated) would constitute the EPM-gene signature.

Controlled laboratory studies testing the hypothesis that a gene signature could be found and  be useful in the diagnosis and treatment of EPM were undertaken. A controlled infection (induced stress) study was used to accurately know the day of exposure. Sarcocystis neurona oocysts were administered to 20 stressed horses to elicit disease. Blood samples were taken 10 times over 28 days to collect RNA, the measure of a turned on gene. The up-regulated genes (identified by the RNA analysis) were assayed on a custom microarray for determining gene expression (the specific array was patented, but not by us). In this blinded study (veterinarians didn’t know which horses were infected) clinical exams were performed,serum and CSF were tested, and post-mortem exams were conducted to ensure that clinically ill horses did get EPM.

This experiment was eventually published with the infection data, but the gene analysis data was not reported. Remarkably, the horses that showed signs didn’t have organisms that could be demonstrated in the brain tissues. Inflammation was considered diagnostic of successful infection. Scientists conducting this study identified a gene signature. Success! There were differences between the up-regulated genes in the clinically ill horses that were infected and those that were not infected, control horses.

Time to test the gene signature. Field cases of suspected EPM were used in a second study. The gene expression from horses with suspected EPM, those that had serum and CSF analysis to be as sure as possible the horses fit the diagnostic criteria at the time, came from clinical cases. It took 6 weeks to process the samples and get a result because the assay is technical. An obvious down side of the endeavor was cost. The hundreds of dollars that the eventual assay would cost, and the six-week turnaround time, made it a clinical non-starter. More importantly, the assay didn’t diagnose chronic disease (disease that was present after 28 days from the initial infection). The cases presented to veterinarians are chronic. The acute gene signature did not identify field cases that the veterinarians diagnosed.

In a third study, 13 animals were used in a merozoite challenge model that did not use stress. The horses were randomly assigned to a group, 8 were challenged while 5 were sham challenged. This study ran 90 days to detect an acute and chronic gene signature. Cells were assayed for gene expression at 28 days (acute) and 90 days (chronic). If the acute gene signature was the same in both models, an accurate marker between the two studies could be identified to identify acute, possibly current, disease. Likewise, the chronic markers, significant expression of genes at 90 days should match the field study and identify horses with long term disease even if the organisms were eliminated.

The cumulative results of the controlled studies identified 31 genes that were highly statistically different at day 28 between animals that developed clinical EPM and those that did not. An EPM index score calculated for the gene signature, identified in the first controlled study, was successfully used to identify some, but not all, of the horses with acute disease in the third, controlled study.

Horses with chronic EPM, day 90 of the third study, were not identified using the signature developed in the first study. Further, chronic EPM could not be identified in clinical field samples using the gene signature developed from acute disease, day 28, in either the stress model or the merozoite model. Because many horses present with suspect EPM after having had clinical signs for weeks or months, the value of a genetic signature was doubtful.

We identified drugs that selectively reduce the expression of some of the upregulated genes that were stimulated during acute and chronic disease. Some drugs returned horses to normal, removal of the drugs allowed the horse to again show signs of disease. Surprisingly, some drugs we tested made horses worse! We found that the innate immune response and the genetic signature of host cells are the key to disease associated with sarcocystosis.

The data was useful. The upregulated genes included MHC Class II receptors, chemokine receptors, IgG molecules, natural killer cells, several interferon-induced proteins and a handful of others.

More studies are undoubtedly in the pipeline. As those studies are completed and in a few years published, they may be compared to the work done in 2005. Or perhaps the EPM-gene signature is already relegated to the cutting room floor, the genes frozen in time, yielding space in the freezer for newer endeavors and lost to analysis. Our experience showed us there are disease-signatures present in the blood samples and these are markers that can effectively direct treatment for horses with disease and identify horses that are resistant to disease. We don’t think there will be a crystal ball that predicts which healthy horse will be come sick when exposed to Sarcocystis, sadly it isn’t that simple.

An encephalitogen is an agent that is capable of producing encephalitis. Encephalitis is caused by infections or allergic reactions. Cytokines, released by the host to fight pathologic agents, act as encephalitogens. The clinical presentation can be similar in central and peripheral events because cytokines act outside the brain on peripheral nerves using common mechanisms. The purpose of this discussion is to review some human research that can be applied to encephalitogens that we investigate and suggest how you can participate in our research.

Inflammation, when treated, can resolve or it can become chronic.  Chronic inflammation destroys tissue and can eventually remove insulating myelin protein from nerves.  Tissue damage isn’t necessarily permanent.  The body repairs the damaged protein along with or after the inflammatory cycle.  However, left long enough, the body will permanently bandage the area by laying down calcium.  Once calcium is deposited, the damage is permanent.

An antemortem biopsy sample from horses with disease can help us in several ways.  Skeletal muscle innervated by nerves arising from the cauda equina can show abnormalities that may help us further define polyneuritis equi. The types of cells present in disease can be characterized by special stains and molecular analysis. The long term goal of these types of analysis is to provide veterinarians with effective treatment protocols. Veterinarians can send a biopsy sample to us for a free analysis. We will analyze the tissues, archive the tissue samples, and publish the results. Please find the biopsy submission form on the testing page or follow this link:

New research shows the beneficial effects of non-toxic, non-steroidal treatments that could potentially improve neuroinflammation, protect from demyelination and axonal loss in people with multiple sclerosis (MS). We wonder if that is also true for horses with polyneuritis.  The advantage MS-researchers have in studying this complicated disease is a good animal model.  MS is hard to understand because small parts of protein molecules can trigger a cascade of common reactions and that makes it difficult to parse out cause and effect.

A disease that looks just like MS can be induced in laboratory animals: guinea pigs, mice and rats.  In some guinea pig and rat models, steroids make the signs worse.  Yet other studies report a decrease in pro-inflammatory cytokines suggesting a beneficial effect.

Once disease is induced in the mouse model, steroids reversed the pathology associated with the MS-like condition. Following oral steroid administration, mice lost the disease-associated clinical signs and regained normal motility.  In the mouse model, mice become ataxic with induced disease.  The mice relapsed following withdrawal of steroids, usually in less than two weeks. Polyneuritis equi is similar in pathology to MS in people (or another neurologic disease, Guillian Barre syndrome).

Horses with polyneuritis equi can show spontaneous remission early in the disease process.  [The MS mouse model is one in which spontaneous remission is not seen, leading to the conclusion remission in the signs was due to the steroid treatment.]  While steroids resolve disease signs, it is not long-term and the autoimmune process associated with the model disease is re-initiated with steroid withdrawal. An interesting finding is that the efficacy of the dose used in the studies was similar over a range of doses, although occasionally a mouse treated with the lowest dose did not respond to steroids.  The outcome of treatment of polyneuritis equi is generally poor and there are no published treatment protocols.

Scientists looked at the type of cells that responded to steroid treatment in the animals with induced MS.  A specific type of inflammation (infiltrate) was noted and it was accompanied by demyelination.  Following withdrawal of the steroid, there was a sharp rebound in the infiltrate that was initially observed. The researchers were left questioning the types of cells that were suppressed and what type of cells rebounded to cause the relapse. They focused on developing strategies for treating autoimmune disease by eliminating inflammatory cells produced in the initial response.  Their impression is that there are  pathogenic clones of cells responding from the host’s immune system and possibly target organs.  They also focus on inducing life-long antigen-specific immunological tolerance to prevent development or activation of new pathogenic clones, in other words, a vaccination. They concluded that steroids may provide a beneficial immunosuppressive effect.

So why are steroids not effective in horses with polyneuritis equi? In MS ,steroids are not curative because withdrawing steroids initiate clinical and pathological disease relapses that are accompanied by a return of the infiltrate reactive to the initial encephalitogen.  When they looked at all the data, they felt new autoantigen-specific clones (of cells) were prominent in the relapse, the term for this is epitope spread. The body was making new responses to the tissues.

If polyneuritis equi is stimulated by an organism, say Sarcocystis, then it becomes important to know if there is chronic exposure or if a one time infection caused disease.  These horses would react differently to treatment than for the antigen-associated autoimmunity.

Mouse-modelers also asked, What causes the clinical signs associated with the model? Is it the inflammation or the resultant pathology to the axons and myelin? Their data supported the concept that inflammatory cells, and the products they secrete, may be responsible for initiating and promoting the signs induced by the model. It is the immune response that caused disease. The mice completely recovered in the presence of existing lesions if that pathologic clone was absent. They suggest this is a direct influence of the lymphocytes, or their products, on the clinical signs of the disease.

Mice treated with steroids had less severe demyelination than untreated mice that already had disease or in mice with a relapse. There was less demyelination during remission suggesting that remyelination may have occurred in treated mice. The phenomenon of nerve regeneration or remyelination in a horse with polyneuritis equi was detected by histopathology and at the time, it was posed that enhanced regeneration could be possible if the inflammatory response was controlled early in the disease.

What does this mean to you and your horse?  Proteins that make up myelin are targets for immune responses in some diseases. The one we work with is MP2, myelin protein 2.  The pathogenicity of myelin proteins in human disease is envisioned because, in mice and rats and guinea pigs and horses, these proteins elicit an autoimmune response that leads to a disease that includes some degree of paralysis and motor impairment. The initial episode may become debilitating but most animals recover and are free of disease.  With time animals develop relapsing disease.

The widely held belief is that the basis for relapsing disease is a response to encephalitogens that are different that those there triggered the initial response, epitope spread, and was not detected in all studies. Researchers used mice to show that relapse was related only to the cells with the same specificity as the initial encephalitogen. They concluded with some encephalitogens epitopes don’t spread. Said another way, relapsing disease is due to the encephalitogen used to initiate the primary disease. Moreover, they could vaccinate and prevent relapses in mice. Because other researchers did demonstrate pathogenic epitope spread following encephalitogen-induced disease it is possible that outcome is dependent on the encephalitogen used to induce the primary disease episode.

The study to show this in horses is prohibitively expensive and there is no model to reliably create relapsing polyneuritis equi. Horses have different relapse rates, some months and some years. We can get meaningful data from natural cases.  If we analyzed biopsy samples from horses diagnosed with polyneuritis equi on a molecular level we could gather information on the types of lymphocytes present, the healing process, and document treatment protocols.  The biopsy can be done standing under local block by a field veterinarian.  Samples can be placed in the same fixative that is used for uterine biopsies.  Call to find out how you can help and if your horse would benefit from this study.

It is a common thought that infection by more than one disease-causing protozoa is linked to increased severity of disease.  This was shown in marine mammals with protozoan encephalitis, is it similar in horses?

One study sought to understand if horses with presumptive EPM had antibody evidence of infection with other protozoal infections. Documenting more than one protozoal infection is possible because horses get infections with Neospora and/or Toxoplasma.  The criteria for EPM in dead animals rested on the presence of lesions (not parasites) in central nervous tissues.  They included cases from live horses that had a presumptive diagnosis of EPM.  EPM was presumed when clinical signs were present, excluding other disease based on ancillary testing, and SAG ELISA positive serum and CSF for Sarcocystis neurona (in this study the ratio was less than or equal to 50).  The scientists compared the presence of Neospora or Toxoplasma antibodies in their selected cases to a group that were not expected to have protozoal infections.  The expected-negative group was comprised of horses with a diagnosis of cervical vertebral malformation (CVM) and negative for SAG ELISA of serum and CSF (in this study the ratio was less than or equal to 50).

Overall, they found 12.9% of horses were antibody positive for Neospora.  The proportion of EPM cases that tested positive did not differ from the proportion of CVM cases that tested positive.  A similar finding with  Toxoplasma, antibodies were found in 14.9% of suspect EPM cases and CVM horses.  A qualifier in the study was that these horses were from the eastern US.  It is possible that Neospora is more common in the west, however one study does not support that.

They found no horses with co-infections! Another interesting finding was that they didn’t find sub-clinical infection’s either. A sub-clinical infection was a case in which antibody was detected in the serum but not enough antibody in the CSF to be considered EPM.  They concluded that their data did not support protozoal co-infection as a common finding in horses with neurologic disease from the eastern US, and further co-infection with a protozoal species is unlikely to play an important role in development of clinical disease caused by S. neurona infection.

You had us nodding our heads in agreement until they said “protozoal species”.  We assumed that an implied qualifier might be “the data did not support protozoal co-infection with Toxoplasma or Neospora”…yes.

We disagree that co-infections aren’t present in horses with S. neurona! We presented evidence to the attendees at the 2nd EPM Society Workshop in Tahoe City, CA on October 26, 2017 to show that Sarcocystis fayeri and Sarcocystis neurona antibodies were present in horses with clinical neuromuscular disease.  And in some horses with sub-clinical disease, antibodies present and not ataxic. And in normal horses!  We showed that 87% of normal horses have co-infections with Sarcocystis and is in direct opposition to the findings in the above experiment. Two protozoal infections in one animal.  We might speculate that S.fayeri is protective against developing EPM in S. neurona exposed horses.  We can find some data to support this speculation because the protein we use to measure S. fayeri is a protein that protects animals against Toxoplasma infections. Our data would not argue against their findings, we just disagree that horses can’t harbor two species of protozoa.

Some of the diseased horses we examined had two Sarcocystis infections and met the bar of serum/CSF ratio (<100), confirming EPM.  In diseased horses, we found 74% were Sarcocystis positive!  In diseased horses dual infections were more common than single species infections. When we only looked at single species infections we found that neurona was more common in diseased horses. These data still support the finding that a single infection is more pathogenic or sometimes S. fayeri is present but not protective. We found that some S. fayeri strains may not produce the protective protein under some as yet undefined conditions. The EPM-Neospora-Toxo study discussed above may have been stronger if they considered S. fayeri as a factor or stated that there are other protozoa that co-exist in normal and diseased horses. The relationship between Sarcocystis that infect horses remains undefined.

We, and UC Davis, have reported finding S. fayeri in horses with neuromuscular disease, although we look for the disease in different ways. We ran a study to compare our way (serum ELISA) with the UC Davis method (post-mortem tissue exam) finding a pretty good correlation between the methods.  Good enough to suggest pre-mortem serum testing is more palatable to the owner. The point is that multiple protozoa infect horses, multiple protozoa are in diseased horses and it takes a good (diagnostic eye) to discern the cause of clinical signs.


Horses with clinical signs of equine motor neuronprzewalski-1972728__340 disease (EMD) or vitamin E deficient myopathy require supplementation with vitamin E.  Horses that graze green grass should be fine without supplementation.  Supplements are expensive, here is a primer to guide you.

The critical factors associated with vitamin E are: determining that your horse is deficient (solution: test the serum levels); deciding what supplement is most appropriate (solution: determine what are you treating); delivering the dose efficiently to the horse (formulation and dose); and when to discontinue treatment (test the serum levels!)

Supplementing with the intention to increase vitamin E in the central nervous system (CNS) of a horse with neurologic disease requires a different protocol than supplementing for diet deficiency in a normal horse (a horse that has no access to green grass).  Studies show that some supplements do not increase the levels of vitamin E in brain tissue.  Studies show that vitamin E supplements do not increase the levels of the vitamin in muscle tissue.  And some supplements are active at five to six times other formulations!

There are no studies describing toxicity in horses from too much supplementation.  Vitamin E can be toxic because it is stored in fat (lipid) and is not excreted like water soluble vitamins are. It is possible that vitamin E inhibits vitamin A, another fat soluble vitamin although there are no published studies. In other animals, including humans, neurologic complications result from overdosing vitamin E!  There is no reason to suggest toxicity won’t occur in horses.

Horses showing no clinical signs of vitamin E deficiency

Supplementing with vitamin E can be expensive and can put a horse at risk for toxicity. If you suspect a deficiency you can easily test the serum concentration.  Pathogenes offers a discounted program for testing vitamin E in association with our clinical trials.  Call us for more information and be sure to send the sample with our Test submission form.

Is it time to stop supplementing?  A simple test will tell you.  Because there is a rapid decline of serum levels after discontinuing some forms of vitamin E, it is best to wait a week after stopping vitamin E dosing before sending a serum sample for testing a long time supplemented horse.

Clinically ill horses

Horses showing clinical signs of equine motor neuron (EMD) disease or vitamin E-deficient myopathy can benefit from treatment.  Often suggested, but not proven, vitamin E is supplemented in  cases of active equine protozoal myeloencephalitis (EPM), with or without measured low levels.

Determine the base line levels of serum vitamin E before supplementing.  In diseased horses requiring supplementation, 5000 IU/day of a soluble, natural form is useful.  Not all horses respond the same way to supplements- there is individual variation!  After two weeks of supplementing the serum level should be assessed and adjust the dose accordingly.  A tapered regime with a gradual transition to a natural powder form of vitamin E is  appropriate.  The natural power form of vitamin E will return a horse to a normal serum value in 7 weeks but  normal CSF levels are not achieved with this supplement-form.

Levels of vitamin E

Normal serum levels of vitamin E in horses are greater than 2.5 µg/ml.  A level that is considered adequate is a range between 1.5-2.4 µg/ml.  Horses with serum levels less than 1.5 µg/ml are deficient.

Normal levels decline significantly in just 18 days in horses that are not allowed access to grass and are fed a pelleted ration that is not supplemented.  Considerations here are horses stalled due to colic surgery, metabolic syndrome, or other similar conditions.  Horses don’t have green grass in northern climates during the winter, something to consider.

Vitamin E levels in serum
Normal 2.5 µg/ml
Adequate 1.5-2.4 µg/ml
Deficient less than 1.5 µg/ml

It is interesting to note that in a controlled study there were no differences in the mean concentration of CSF vitamin E in un-supplemented (normal levels were present) or supplemented horses (all supplements).  Or in deficient horses, before and after supplementation!  There was a significant (linear) correlation between serum and CSF concentrations, the higher the serum level the higher the vitamin E in the CSF of most horses.  It is possible there is a limit to the amount of vitamin E that can be measured in the CSF (does it all go to the cell membranes) or it is a fault in the testing protocol (little correlation of values with test results).

Types of supplements

Vitamin E is available as an injection, usually in conjunction with selenium, and is a form that is by prescription for use by a licensed veterinarian.  Some serious and life threatening reactions can occur with intravenous or intramuscular injections of vitamin E-selenium.  The injectable form bypasses the inhibition seen in some oral formulations. Oral synthetic and natural vitamin E preparations are available.  The synthetic has eight stereoisomers (the molecular shape of the molecule and its rotation).  Animals have a preference for only one.  Natural vitamin E comes in only one isomer, the one preferred by the liver.  There are two synthetic forms of acetate, the powder is twice as available to the animal as the pelleted form, the powder increasing serum concentrations in about two months.  The water soluble, liquid form, is five to six times as available for uptake by the horse and increased concentrations are accomplished in 12 hours.  Thus the acetate forms elicit a gradual increase when supplemented.

What?  Who said sulfur inhibits vitamin E?

Vitamin E and selenium are intertwined with sulfur metabolism.  There is a relationship between selenium and vitamin E overcoming sulfur-induced depletion in the body.

What the vitamin E Guru’s suggest

Horses that have no clinical signs of deficiency can be supplemented with the less expensive acetate forms at 10 IU/kg body weight per day over months to achieve normal serum vitamin E levels.

The acetate form isn’t a good choice in horses with clinical signs of EMD or vitamin E deficient myopathy.  These horses require an immediate increase in serum and CSF vitamin E concentrations.  The veterinarian can use an injection to rapidly increase levels and the treatment can be repeated at 5-10 day intervals.  This form is labeled for selenium-tocopherol deficiency syndrome that presents clinically as rapid respiration, profuse sweating, muscle spasms and stiffness accompanied by an increased SGOT (liver enzyme).

Levels can be restored to normal by giving 5000 IU/day of the soluble vitamin E and then tapering the regime to transition to 5000 IU/day of the oral acetate. This protocol resulted in horses with a prolonged increase in CSF concentrations 8 weeks after beginning supplementation.

Sulfur in the digestive track can inhibit vitamin E uptake, in sulfur-inhibition resulting in deficiency, an injectable form is preferable.

What we suggest

Test the serum  vitamin E levels before supplementing this essential nutrient and again after 7 weeks of supplementation. After 7 or more weeks, discontinue the supplement for 7 days and then test.  It may be wise to re-evaluate serum vitamin E levels after several weeks on the acetate form to ensure concentrations remain within a normal range. It may be of value to determine vitamin E levels in horses suspected of EPM.  A diagnosis of the neurologic disease EMD can be supported by measuring a low serum vitamin E concentration.  Test these horses when they are tested for suspected EPM and once on therapy, 7 weeks later.  Horses with equine degenerative myeloencephalopathy (EDM) will not respond to vitamin E.  EDM is an inherited condition that prevents uptake of vitamin E early in life.  Once neurological signs are present they usually don’t get worse…or better in these EDM horses.