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Infection with Sarcocystis seems inevitable.  Sarcocystis are niche organisms, they’ve adapted to infect the intestine of limited hosts and complete their destiny as a muscle cyst.  Generally, the host is unharmed.  Occasionally, things run amuck and the host becomes diseased.  It is estimated that 80% of horses in the US get infected with Sarcocystis .  Most of the time the horse-adapted fayeri infects muscles where it makes a sarcocyst, this disease is equine muscular sarcocystosis or EMS.  Less than 10% of horses with EMS show signs of disease, but some infected horses do get sick.

Most horses in the United States also encounter S. neurona and most infected horses are none the worse for it. Horses don’t get sick because the immune system eliminates the organism. Sarcocystis neurona-infected horses develop antibodies and bountiful cytokines that are effective in killing the protozoa. A most important cytokine is interferon-gamma. But occasionally, the most recent estimate is 14 of 10,000 horses, suffer the devastating disease EPM.

It is believed that the organism invades the central nervous system (CNS) and causes physical damage. In nearly all cases of experimental  (natural challenge) S. neurona infections in horses, no organisms were found in spite of producing clinical signs.  Histologists noted plenty of inflammation present in CNS tissues of the infected horses. Were the organisms there and removed quickly?  Could the organisms hide out in other tissues waiting for the right moment to manifest? Were the samples taken at an inopportune time? Was inflammation the culprit and no organisms ever got into the CNS?  Those are unanswered questions that are being investigated.

There is circumstantial evidence that some horses don’t develop the right kind of immune response to eliminate the parasite, maybe these are the horses that get organisms in CNS tissues. It was surprising when horses with deficient immune systems, Arabian foals that show severe combined immune deficiency syndrome (SCID), were infected with S. neurona and surprisingly, they got plenty of organisms in their blood stream, none in the CNS, and no clinical signs.  It looks like an inflammatory response (the SCID foal can’t produce) is responsible for transporting organisms to the CNS and producing clinical signs. When a population of normal horses were likewise challenged they got clinical signs, but no organisms were found.

Some expect that  horses will only improve by 1 grade (on a scale of 0-5) with treatment.  Also, 10-25% of those horses that do respond to treatment are expected to relapse after treatment begging the questions:  Are horses relapsing because they are re-exposed and have a new infection or is the initial infection latent-ready to manifest at any opportunity? How long can a protozoa hide before re-emerging? Can the horse make protective immunity?

As scientists ponder the best way to prove what is happening (and don’t forget it could be more than one mechanism!) you need to know some things to effectively evaluate new information.

It is important to understand how protozoal parasites mature.  I will use the term synchronous to mean they all mature at the same time.  Protozoa progress through their life-cycle stages on a one-way path to complete their destiny as a sarcocyst. Parasites (merozoites) go through a couple of replications, move to the next stage, and finally when they reach the muscle they encyst as slow metabolizing bradyzoites.  Bradyzoites aren’t expected to move from a muscle fiber to another muscle to make new cysts.  Cysts degenerate, unless they are passed to the definitive host where the parasite can complete the sexual part of the life-cycle and begin a new generation of infectious organisms.  After the initial gut infection (sporozoite) and a few rounds of replication the resulting merozoites can’t go back to an earlier stage.

In 2001 we showed that S. neurona could be released from some cells, but not others, using an ionophore. The optimum time of release was 10-20 days after infection and this could be repeated once in another 30 days.  When we examined the stages of the parasites by electron microscopy it was apparent that the parasites were not synchronized because there were multiple stages in the cells.  We didn’t find a method that satisfactorily synchronized the cultures. Even cloning a culture from one cell resulted in asynchronous maturation of the colony.

In one particular cell line parasites grew very slowly, it took 120 days for them to establish a colony.  The slow growing culture was infectious when transferred to a more traditionally used cell line and when transferred, they matured quickly.  The colony was still asynchronous. In horses we expect the gut infection is asynchronous.

Sarcocystis are generally restricted to the hosts they infect. For example, S. muris can infect mice but not horses. S. canis infects dogs but not horses. One point of interest is that opossums can be a definitive host for many sarcocystis-ones that infect skunks, cats, birds, mice, and horses. True hosts are ones that support the life-cycle. Aberrant hosts are hosts that don’t support the completion of the life-cycle.

Dr. David Lindsay is a master of growing Sarcocystis and published papers on chemicals that delay, but don’t kill specific protozoa. He published an interesting experiment that treated Toxoplasma-susceptible mice and then infected them with Toxoplasma.  The take-home-message from his work was that mice that were allowed to produce an immune response faired better with later challenge when they were compared to animals that were treated during the infection process. When mice were treated they didn’t produce a protective immune response and subsequently succumbed to toxoplasmosis. He also published work that showed diclazuril fails to eliminate S. neurona from laboratory cultures and showed the ability of decoquinate to render the cultures sterile.

In a recent experiment it was shown that the interferon gamma-defective mouse could be infected with a mouse-opossum strain of S. neurona.  Untreated mice were diseased and the organisms could be recovered from CNS tissues. The experiment further showed that diclazuril could inhibit S. neurona activity, but not eliminate the parasite, providing evidence that recurrent disease could be a result of persistent infection and treatment failure rather than simple reinfection in this mouse model. The take home message was that S. neurona can resume its activity after cessation of diclazuril in a live interferon-gamma deficient mouse.

One must be careful when interpreting study data from one animal to another.  In the mouse experiment, the mice were injected with cultured organisms that did not allow stimulation of a natural immune response in the gut.  A similar experiment in 2001 used mice that ingested sporocysts of the same Sarcocystis strain as the above experiment (a natural infection) and also administered diclazuril in the diet.  After discontinuing treatment the mice did not have organisms in the CNS.  The discordant results may be the method of administration of the protozoa or even when tissues were examined. after the discontinuation of therapy  Obviously, there is more work to be done.

All the above considered, we have an issue with diclazuril used for our non-inferiority study.  It isn’t a fear of persistent infection and relapse after treatment because that has not been shown in the horse. We did test several hundred horses with clinical EPM for a lack of interferon-gamma and didn’t find one.  Our insurmountable task is showing that in our study a comparison drug, diclazuril, is as effective as it was when licensed.  We have the daunting task of showing that diclazuril is 67% effective in treating EPM. If the statistics don’t support 67% of diclazuril-treated horses clinically improve when diagnosed with EPM (the horses must have CSF tap confirming disease before treatment) the study is not acceptable.  When diclazuril was licensed to treat EPM clinical improvement was seen 59% when based on clinical signs.  Because diclazuril was considered successful when antibody declined the CSF when there was no clinical change. the reported stats are 67% effectiveness. That didn’t fit our criteria of success and we won’t be asking for a post-treatment CSF sample.  Other factors that render the data unacceptable are concomitant drugs with diclazuril, like DMSO, levamisole, steroids, phenylbutazone, flunixin , or firocoxib.  If the attending clinician administers these treatments while waiting for CSF analysis, the case is not useable.

While we put on our thinking-cap, please fill out our survey if you treated your horse with diclazuril for 28 days (no other treatments within 6 months of treatment) and let us know the outcome of treatment.  We can use the data to know if 67% effectiveness is an attainable goal.


Toxoplasmosis is a disease caused by Toxoplasma gondii , Toxo infects most mammals and birds. Cats (the definitive host) shed the infective material making cat litter a risk factor for people and other animals! In horses, toxoplasmosis is usually asymptomatic, thus the disease is considered subclinical. Cysts form in horse tissues and antibodies are found in the serum from this chronic, subclinical infection.  The seroprevalence in horses in the United States varies widely and is reported to be between 0 and 90%!  Risk factors for horses include water contaminated with cat litter or feces.

The biology of Toxo makes the tests that are used in studies that detect antibodies against Toxo important.  Some strains of Toxo are more infectious than others (virulent strains), and some strains don't cause disease at all. Toxo is a protozoa that can be lethal in some animals (a mouse for example) but the same strain isn’t damaging to another species--that makes the selection of strains used in experiments and diagnostics important.

It is generally accepted that horses are less sensitive to the pathological effects of Toxo infections. In the United States, the best guess for the number of horses in the general population that are subclinically infected with Toxo is between 12-14%. That number was much higher in a group of horses studied in California-- about 25% of the healthy horses in that study were seropositive. The California study examined neurologic horses, those with clinical disease, and showed that they were more likely to be seropositive to Toxo when the sick group was compared to non-neurologic, or healthy horses. These results beg the question, are co-infections a risk factor for EPM in horses?

Marine mammals infected with both S. neurona (the agent that causes EPM in horses) and Toxo were associated with an increased severity of infection.  Co-infections were bad for these marine animals. When horses in the Eastern United States were evaluated for subclinical infections of Toxo and protozoal myeloencephalitis over a six-year period, co-infections were not found. These data indicate that horses seropositive T. gondii antibodies didn’t have an increase in clinical EPM.  The study made these conclusions looking at the organisms S. neurona and N. hughesi, the protozoans associated with EPM. Subclinical S. neurona sarcocystosis (seropositive, healthy horses) is most common--antibodies against S. neurona are found in more than 80% of horses, yet less than 1% of the horse population is diagnosed with EPM. Neospora hughesi is less common, 34% of healthy horses have Neospora antibodies and of those perhaps 2% have EPM.

There could be a relationship between other protozoa that infect horses; the first on our list is S. fayeriSarcocystis fayeri was more common in horses with neuromuscular disease (when compared to normal horses) as shown in two studies.  These studies didn’t show that subclinical S. fayeri facilitates EPM (caused by S. neurona) but, EPM was more prevalent in horses that had equine muscular sarcocystosis. Another interesting finding was that statistically, horses with sarcocystosis were more likely to have an elevated C-reactive protein (CRP). Interestingly, it was reported that horses seropositive for Toxo have a higher incidence of pro-inflammatory cytokines and CRP values.

When you ask us what can sustain an elevated CRP in a healthy horse we will give you a list that includes encysted small strongyle larvae, gastric and hind-gut ulcer disease, equine muscular sarcocystosis, and subclinical Toxo. Protozoa can keep pro-inflammatory cytokines active and that makes subclinical inflammation chronic in horses and chronic inflammation can produce disease.

What will it take to develop a useful diagnostic test for Toxo in horses?  First, a model of disease.  Koch’s postulates must be completed.  Linking disease to the infection is important, not just detecting antibodies that were made in response to subclinical infections that didn't  progress to disease. Experimentally inducing toxoplasmosis hasn’t been accomplished in horses.  It is more complicated that it appears on the surface because Toxo shows strain-related virulence differences in hosts.

It would be easiest to find a horse with acute, clinical toxoplasmosis and isolate the organism—that has not been done yet.  As prevalent as Toxo is, one wonders why. An organism isolated from a clinically ill horse could be used to infect horses, validate the model, and answer questions about species susceptibility. The available virulent mice strains or strains isolated from humans may not be useful strains to infect horses or used for diagnostics.  We wonder if there is a need for detecting Toxo in horses because, as mentioned above, in a 6-year retrospective study no Toxo infections were related to disease in horses.

However, determining that chronic inflammation is due to Toxo may be important in polyneuritis equi.  There are breadcrumbs that lead us in that direction, but as yet no hard evidence.  We’ll get back to you after we develop a model for toxoplasmosis in horses, followed by investigation of the statistical significance in various equine populations, diseased and healthy.

cyst microscopic cropSarcocystosis is one of the most frequent infections of animals, the organisms are found in the muscles and the central nervous system! There are, perhaps, 196 species of Sarcocystis, yet the complete life cycle is only known for 26 of them. Sarcocystis require a prey-predator, 2 host, relationship to survive. Each host supports different stages of the life cycle. Hosts vary for each species of Sarcocystis.  Intermediate hosts support several species of Sarcocystis, each species use different definitive hosts.

People get sarcocystosis, two species use people as the definitive host.  Humans also serve as intermediate (or aberrant hosts) for several other species. Raw beef can infect you with S. hominis and raw pork can give you S. suihominis. Gastrointestinal symptoms are present when Sarcocystis cause disease in people  definitively hosting the parasite. Muscle pain is reported in people that serve Sarcocystis as an intermediate host. Most of the time people are asymptomatic with muscular sarcocystosis. People can get sick from an enterotoxin associated with Sarcocystis that infect horse muscles. if horse meat is uncooked.

Horses get sarcocystosis from dogs, the organism causing infections is S. equicanis (bertrami). In the US the horse-infecting organism is named S. fayeri. Donkeys harbor S. asinus, but experiments may show that this is actually S. fayeri. The visible difference in equicanis (bertrami) and fayeri is the thickness of cyst walls in muscles observed under the microscope. Our picture above is fayeri,  a thick-walled sarcocyst.  S. bertrami forms a thin-walled cyst. Dogs shed infective betrami organisms 8-10 days after eating infected muscle tissue. Horses eat the organisms from dog feces-contaminated feed.  It takes two to three weeks before signs appear in horses.  Signs include fever, neurological signs, apathy, and inappetence  a couple of months after infection. Muscle enzymes can be elevated in infected horses and increased enzymes can be measured in blood samples.

Sarcocystis fayeri cysts are found in skeletal muscles and the heart.  Ten and 25 days after infection (two waves of organisms are released from the gut) the developing parasites are found in arteries of the heart, brain, and kidney.  Muscle cysts (sarcocysts) are first seen at 55 days .  And by 77 days the muscle tissue can infect dogs to start the cycle again. We are taught that S. fayeri is only mildly pathogenic, horses develop anemia and fever after infections and some horses may have a stiff gait. More virulent isolates can cause inflammation of muscles and, in one case, the horse developed autoimmune anemia.  People that eat raw horse meat can get food poisoning, this is due to a toxin associated with the cysts.  A fetus can be infected by S. fayeri by crossing the placenta, so foals can be born with mature cysts in their muscles.

Malnourished horses show clinical muscle inflammation (myositis) and muscle atrophy that can be associated with S. fayeri. Muscle cysts are usually unassociated with clinical signs or muscle inflammation, leading to conclusions that fayeri infections are benign. Most clinicians agree S. fayeri isn’t an issue in horses.  However, there are some researchers that think S. fayeri should be considered in horses with neuromuscular disease. Scientists at UC Davis examined muscle tissues from horses with and without a history of neuromuscular disease.  They found an association, but not statistical significance, between disease and cysts.  More horses with neuromuscular disease had S. fayeri cysts when compared to the number of cysts found in horses that died from other causes.

We decided to look at the problem a different way.  While UC Davis looked at cysts, we chose to look for S. fayeri antitoxin in the serum of horses. An advantage to antitoxin analysis is that the test is performed in the live horse.  We found that 24% of normal horses had antitoxin in their serum. We also found that S. neurona antibodies were more often associated with neuromuscular disease in horses  than S. fayeri antitoxin (antibodies against the toxin released from cysts). That said, horses were more often infected with both species of Sarcocystis, not just one strain.

Horses infected with S. neurona and S. fayeri were more likely to show disease. We looked at inflammation using CRP (C-reactive protein) and found that CRP was detected in horses with and without apparent disease. We did find that significantly more horses with neuromuscular disease had an elevated CRP when compared to normal horses (p= .0135).  However, the data we needed to link the UC Davis study and ours was missing.  We needed to show  the relationship of antitoxin found in horses (our test) with sarcocysts found on histopathological slides (the gold-standard test for fayeri-sarcocystosis).

We examined three tissues (muscle tissue from the heart, esophagus, and skeletal muscle) from thirty-two horses (that’s a big number in horse studies) and measured the presence of antitoxin.  Our results confirmed that our serum test was almost the same as the results you would get if a full post-mortem exam was conducted. Also, in our study the infected horses were asymptomatic.

The conclusions thus far are that S. fayeri can be detected pre-mortem and should be considered in horses with signs of sarcocystosis or neuromuscular disease that has no other cause.  Also, horses with neuromuscular disease are more likely to have an elevated CRP.  In our S. fayeri study horses did have elevated CRP values but the inflammation was associated with other gastrointestinal parasites, not EMS (equine muscular sarcocystosis).

Why are we still interested in S. fayeri? Certainly our results support the strain of S. fayeri  infecting our 32 horses was non-virulent and support the view of most clinicians that S. fayeri may not be an issue in most horses, just some of them.

For us, it’s about the toxin.  The toxin is an actin-depolymerizing factor (ADF).  Another Apicomplexan, Toxoplasma gondii, has a very similar ADF. The TG-ADF can protect lab animals against T. gondii infections. Interestingly, some animals with lethal S. neurona infections also were infected with T. gondii. The difference between protection (mice) versus no-ADF protection (sea otters) could be stage of infection (with TG), ,strain-virulence, or something we didn't think of yet.

Can S. fayeri-ADF protect against S. neurona infections in horses? Is ADF species specific? Is ADF a virulence factor or even a survival factor for the organism? Are there cyst-producing S. fayeri organisms that don't produce ADF? Does S. neurona produce an ADF? And, can a S. neurona be incorporated into a fayeri sarcocyst? These are all questions to be answered by experiment.

Here is our opinion. It is worth monitoring S. fayeri infection in horses. It is worth considering S. fayeri infection as a cause of neuromuscular disease in horses showing weakness, muscle atrophy, and inflammation for which there is no other explanation. The disease EMS should be considered in old and debilitated horses.  Sarcocystis fayeri should be considered in horses with chronic inflammation. When  horses showing weakness do not have antibodies against S. neurona, EMS should be considered. Horses that provide meat that is fed to dogs should be monitored for S. fayeri.

If you have questions about S. fayeri, give us a call.

Come mothers and fathers throughout the land
And don't criticize what you can't understand
Your sons and your daughters are beyond your command
Your old road is rapidly agin'
Please get out of the new one If you can't lend your hand
For the times they are a-changin'

(Bob Dylan, recipient of a Nobel prize literature)

We find Bob Dylan’s words particularly inspiring. No doubt the diagnosis and treatment of neurological disease is in flux.  A new road to understanding! We welcome questions about our work and opinions from those that have experience with our work. Published studies support that inflammation is a significant cause of clinical signs related to neurological disease in humans and animals. Equine protozoal myeloencephalitis (EPM) is not the only cause of neurological signs in horses! A horse with an abnormal neurological exam may be difficult to diagnose.  Often as not an exam may be abnormal after EPM treatment. We are trying to do something about that by putting our research into practice.

Our FDA concurred studies have open enrollment.  Each protocol is designed to treat clinical signs of inflammation associated with neurological disease in a specific target population.  The differences between the studies may be subtle and the purpose of this blog is to help you parse the difference in the study protocols to select the most appropriate course of action.


One study is intended to treat horses with lingering or recurring syndrome after EPM treatment.  We call the syndrome PTEDSpost-treatment EPM disease syndrome.  The name is similar to that given by CDC (Center of Disease Control and Prevention) for post-treatment Lyme disease syndrome (PTLDS).  The short explanation is that after treating Lyme disease, or in our case EPM, there can be residual inflammation.  The inflammatory syndrome may look like the original disease, but clinical signs are unresponsive to antimicrobials. After years of frustration with “chronic Lyme disease” it is generally recognized that PTLDS is the culprit.  The term “chronic Lyme disease” is no longer supported by the experts.  Also, CDC reports that studies have not shown that people who received prolonged courses of antibiotics do better in the long run than people treated with placebo for PTLDS (formerly “chronic Lyme disease”). Furthermore, long-term antibiotic or alternative treatments for Lyme disease have been associated with serious complications.

To enroll in study 219-FE-1.1 the horse must have been properly diagnosed and then treated with a full course (per label instructions) of a licensed anti-protozoal drug.  The treatment must be within 90 days of enrollment into the study.  If the horse was treated with compounded medication the horse may not enroll.  If the horse received additional medication with the anti-protozoal, the horse may not enroll. Some additional medications that negate eligibility are DMSO or steroids. Horses that got double-dosed, extra doses, or longer duration over the label instructions would also be excluded.

The FDA standard for a proper EPM diagnosis starts with a neurologic exam.  Additional testing includes cervical radiographs that are normal (for the age and breed of the animal) and the IFAT serum:CSF ratio value (that is published) and  supports protozoal infection as the etiology.  The CSF cytology must fall within parameters that support protozoal infection.  The vitamin E level had to be normal, the serum EHV-1 and West Nile Virus test needed to be negative (or consistent with a vaccine titer). The 219-FE-1.1 selects a study population that is  “properly diagnosed and treated” followed by treatment failure or relapse within 90 days of treatment.

If a horse continues to show clinical signs of EPM or the signs resolved, and then reappeared (relapsed), then the horse is eligible for enrollment. The clinical signs need to be demonstrative (that means scored by the veterinarian with a gait analysis between 2-4).  We have a gait analysis score sheet that can help determine the level of clinical signs.  For this study, the neurological deficit must be obvious at normal gaits or postures and the signs are exacerbated with manipulation (this would be a GAS of 2).  Horses that have very prominent deficits and give the impression they may fall (GAS 3), or profound deficits with frequent stumbling or tripping and may fall with manipulation (GAS 4) are eligible.  Horses that fall are a GAS 4. Horses that are down and unable to get up are not eligible. This is a placebo controlled study. The animal has 2 out of 3 chances of receiving the study medication and not the placebo. Although horses can be removed from the study at any time, a minimum of 5 days may be needed to see an effect from the study medication.

If the horse did not have a diagnosis of EPM the study 219-FE-3.7 is more appropriate.  When is EPM not likely to be the cause of clinical signs? If there are no antibodies to S. neurona in the serum.  This study does not have a requirement for CSF fluid analysis or a previous history of testing CSF to enroll.  Study 219-Fe-3.7 includes a study population that is likely to have PNE. If the horse is seronegative for Sarcocystis neurona confirmed using IFAT or ELISA tests, it is generally accepted by the experts that EPM isn’t the cause of clinical signs. Other causes of neurological disease are ruled out by history (no trauma), negative osteoarthropathy (this can be ruled out by endoscopic exam).  There are other factors that are supportive that PNE is a likely diagnosis—no history of recent respiratory illness or history of a recent fever. The acceptable Clinical Score is between 2-4 for the study.

You may wonder why a gait assessment isn’t used to enter 219-FE-3.7.  It is because the six published cases of PNE were diagnosed by observing signs that were not related to gait.  Horses with PNE show skin hypersensitivity and then lose sensation. Horses show some other signs, familiar to veterinarians, that differentiate a PNE horse from an EPM horse.  The gait shown by a PNE horse becomes weak later in the disease process.  Unfortunately, the six published cases were all untreatable and most had gait deficits.  It is our goal to identify and treat these horses before they become untreatable.

The scoring system for a horse with PNE is a little different than the system used for EPM.  If the signs are mild and do not interfere with the intended use of the horse, the Clinical Score is 1.  These signs are too minimal for a veterinarian to fully evaluate a treatment response; even if an owner is locked in on the aberrant signs, this case would not qualify for the study.  A horse that has moderate signs of PNE are found by a neurological examination and interfere with the intended use, or are the signs are so severe that they compromise the intended use and euthanasia may be considered.  These are horses that should consider entering this study. All study animals will receive study medication.  As in all field studies, horses can be removed from the study at any time.  A minimum of 5 days may be needed to see an effect from the medication.

We believe that inflammation is associated with parasitic protozoa and inflammation is most likely responsible for the clinical signs of disease—this concept is probably widely accepted by equine veterinarians.  However, we diverge from the old road and address the inflammatory response in an EPM treatment. We don’t understand why this is a controversial issue or why it has been overlooked by pharmaceutical development companies.

It is not kosher to just add anti-inflammatory agents to anti-protozoal drugs because there are unintended consequences from mixing drugs.  That is why FDA requires studies, review processes and a path for licensing treatments.  That is our goal: giving the equine community a licensed EPM medication.  To that end, the Study 092-SE-1 is a placebo controlled study—the placebo is Protazil.  This type of study is called a non-inferiority study because the animal is treated and the response to the treatment is compared between groups of treated animals.  The proper diagnosis of EPM is required for entry into this study, starting with a neurologic exam. Additional testing includes cervical radiographs that are normal (for the age and breed of the animal) and the IFAT serum:CSF ratio consistent with a diagnosis of EPM.  The CSF cytology analysis must show that the analysis is consistent with a diagnosis of EPM.  The serum vitamin E level had to be normal and the serum EHV-1 and West Nile Virus tests need to be negative (or consistent with a vaccine titer).

If you have a horse that may qualify for a study we are running give us a call.  We promise not to sing.


20150924_1503271531-e1493401997820-169x300This horse has muscle atrophy.  The cause can be one of any number of three letter acronyms.  Acronyms for equine neurological diseases can be very confusing.  You probably understand EPM and PNE--equine protozoal myeloencephalitis and polyneuritis equi. Have you heard of EDM and EMD--equine degenerative myeloencephalopathy and equine motor neuron disease?  What are their causes and what are the signs your horse may have when afflicted with one of these mysterious conditions?  And of paramount importance-can they be treated?

We  provided exhaustive reviews of EPM and our guide to understanding polyneuritis equi.  If you missed them you can catch up at  Just search for Siobhan Ellison and the available books pop up.

The cause of equine degenerative myeloencephalopathy remains a mystery.  EDM damages multiple areas of the spinal cord resulting in muscle and locomotion disorders. Quite some time ago, EDM was the second most common diagnosis of spinal cord disease at Cornell University. There are a few folks that believe EDM has a genetic basis. In young horses EDM and EMD can occur together. The signs occur early on and will stabilize (not continue to get worse) when the horse is 4 or so, but signs won’t improve either. Another disease that is recognized in young horses is Wobblers, or cervical vertebral malformation, CVM.  The neuromuscular disease and an uncoordinated gait in CVM is due to physical restriction of the spinal cord in the spinal canal. CVM is recognized when young horses are started under saddle, although the condition was  present before that. As the horse grows and matures CVM gets worse. The important point is that these conditions are recognized in young horses.

Equine motor neuron disease is also a degenerative disease of the spinal cord.  EMD affects multiple areas of the nervous system.  Most signs in the horse are based on muscle weakness and loss of innervation to the muscles used in locomotion. Perhaps the stiff gait and low head carriage help differentiate EMD from EPM, EDM, CVM, and PNE. Remember Lyme disease (Borreliosis) also produces a stiff-gaited horse. The vector for Lyme disease is a tick and the disease is found more commonly in the Eastern US. EMD is induced experimentally by feeding a diet deficient in Vitamin E for a little over 3 years. Treating EMD with natural Vitamin E in the early stages can improve the outcome of the disease.  Grazing on good quality pasture is the best natural source of vitamin E for horses.

Based on what is known, Vitamin E supplementation can help with early onset EMD, but don’t expect vitamin E to help with EDM. Perhaps you can remember which one is treatable…EMD is “E to Medicate” and EDM is “E doesn’t Medicate”.  These are mnemonics that work for me. Sadly, some horses can develop more than one of these conditions at the same time. When horses have multiple diseases it will take a planned approach to rule in or rule out the cause of the signs. The first step is listing the clinical signs. Testing is an important part of ferreting out a diagnosis. Testing can include serum analysis for Vitamin E, muscle biopsy, and additional serum tests for infectious disease like protozoa or Borrelia.  Medicating and watching for a change in signs often leads to an expensive misdiagnosis.  Here is a comparative list of signs that can be observed in horses with EPM, EMD, and EDM. Your veterinarian can help you determine the proper approach to obtain a diagnosis and select an appropriate therapy.

Shifts weight on rear legs X
Difficulty standing X X X
Lays down a lot X
Muscle fasciculations/trembling X X X
Stiff gait X X X
Low head carriage X
Muscle atrophy X X X X
Weight loss X X X
Ataxia-symmetric X X X
Wide based stance X X X
Proprioceptive deficits X X X X
Diagnosed by post-mortem exam X X X
Weakness X X X X
Abnormal behavior X X X
Lameness X
Difficulty swallowing X X
Seizures X