Skip to content


Our business is consulting.  That means we dispense advice.  We don’t look into a crystal ball or read tea leaves. We base our opinions on an analysis of your case and immunodiagnostic testing.  Analyzing a case involves looking at laboratory values, the case history, and physical examinations done by licensed veterinarians.  The underpinning of our opinion is immunodiagnostic testing associated with neurological diseases and understanding the parameters and limits of each diagnostic test we use.

We are not on the sidelines when it comes to the literature on sarcocystosis. Our works are published so other experts, and you, can critically review our approach.  We rely heavily on works of others to develop new theories that are tested by direct observations.  Our hypotheses’ are scrutinized by our Statistician, he has a PhD in statistics, years in the pharmaceutical industry, and is considered one of the best in the industry.  So when we are asked a question, we answer with our objective opinion with statistical significance.

Recently we were asked, “Can you clarify your comment that the “titer” is an indication of duration of infection (vs the degree of disease) and explain the difference between a negative IFAT test and the SAG titer of 8?” It seems to be a simple enough question.  To get to the answer, one has to A) know how the organism behaves in the horse, B) correlate antibody levels with clinical disease in horses, C) understand the critical differences in quantitating antibody between test formats.

How does a Sarcocystis behave in an animals that it infects?  The authority would be Dr. Edith Box.  Throughout the 1980’s Dr. Box infected budgies with S. falcatula.  It is historically important that budgies were lethally infected by S. falcatula. An aside to the question posed above is the 1995 hypothesis by researchers from the University of Florida.  They presented molecular evidence that S. falcatula and S. neurona were the same organism!  Their hypothesis was refuted by demonstrating that S. neurona does not infect budgies at all. Horses are infected by S. neurona, budgies not. Budgies, but not horses, are infected by S. falcatula. Until proven otherwise, another study conducted at UF is the law of the land.  Their horse-infection study indicates that horses are not susceptible to S. falcatula infections. 

How does a Sarcocystis behave in a natural host? S. falcatula in budgies is the model. Box showed that the organism is distributed throughout the organs from the gut (the end result is a muscle cyst).  New flushes of organisms are not lingering in organs outside the gut.  New infections didn’t spring up from muscle cysts either. Box showed that some birds did get infections that went to the brain. (We always suspected S. neurona wasn’t special in a proclivity for brain tissue).

Wait, you say. What about organisms that are not in the natural host? The horse is not a natural host for S. neurona.  Usually Sarcocystis are highly host specific. Host specificity is how UF used biological studies to correct and retract their claims that neurona and falcatula were the same. When based on molecular data they were pretty darn similar.  When tested in animals, not so. Other studies support that horses with an immune system quickly remove organisms just as the bird model shows for falcatula. Interestingly, horses with abnormal white blood cells do not clear the organisms at all…and paradoxically the immune-deficient horses do not show clinical signs.  Heads up!  The immune response to the organism caused the clinical signs, not the organism.

And now back to the basis for answering the original question.  We did it by animal experiment, first developing an infection model in the horse. We infected 75 horses with S. neurona using white blood cells to mimic a “natural” infection. We didn’t evaluate the horses ourselves, we brought in EPM-experts from across the country (at least 2 for each study) to examine the horses as the disease progressed.  They were unaware of which horses were infected and which ones were not so we “blinded” the experiment.  Experts saw the horses before infection and then every month until the experiment was terminated four months later. They scored the disease using a meticulous neurological exam.  Yes, they documented the horses got worse over time.

The horses’ blood and CSF fluid was taken every month at the same time the exams were conducted.  We used a SAG 1 ELISA  test and also sent duplicate samples to a Kentucky laboratory. Both laboratories tested the samples for the presence of antibodies.  That way there was no bias in testing.  We used only one test because a SAG 1 strain of S. neurona was used for the infections.  In natural infections, there are three serotypes of S. neurona, SAG 1, SAG 5, and SAG 6.  Each SAG is mutually exclusive-only one SAG is present in an organism. Multiple serotype infections are possible in the field because an opossum can be infected by all three serotypes.  Three different infections. Our experiments were limited to a single serotype. We sent the KY lab a sample of SAG 1 to run in their test making sure they had the same marker that we had on our test. Thus, any difference between the tests would be a consequence of ability to detect and interpret a single protein.

Our Statistician crunched the numbers.  He concluded that as time progressed, the clinical signs got worse and that was statistically significant.  Also, as time progressed, antibodies increased, but the antibody level did not statistically correlate with the degree of clinical signs observed by the clinicians. 

And there was individual variation in the antibody response.  Some really sick horses had lower antibodies when compared to not-so-affected horses that had high antibodies. The Kentucky test was less likely to identify infected horses.  Twenty-five percent of the test results differed. That means that had we conducted the experiments only using the KY lab, the interpretation of the study would be different. That is why different scientists have different views of immunodiagnostics.  We base our opinion on study results.

Subsequent experiments showed that horses that had never experienced an infection produced less antibody and dropped the antibodies quickly when compared to “experienced” horses.  Experienced horses got a measurable antibody response quickly (the scientific word is amnestic response) and retain those antibodies for up to 10 months.

The experiments in 75 experimental infections allow us to say that in horses the antibody response to SAG 1 will increase over time and linger longer in an “experienced” horse and antibodies are more a reflection of duration of infection, not degree of disease.

A couple of things help explain part C of the question quantitating the difference between two tests.  It is important to recognize that testing formats are different.  That is to say what is measured (antibody against a protein) and how the protein is prepared for testing are different.  It has been known for a long time that reducing conditions change how antibodies recognize a protein.  Without going into the fascinating field of protein chemistry, suffice it to say, a protein is a string of amino acids.  The amino acid sequence is the primary structure of the protein and that is determined by the DNA that codes for the protein. 

The secondary structure of a protein is determined by folds in the backbone of the protein.  This means side groups don’t interact in determining the secondary structure.  The overall tertiary structure of the protein, its 3D structure, is determined by the reactions and bonding between side groups.  The charge of individual amino acids, the affinity or aversion to water, and special bonds are important in tertiary folding of a protein. The amino acid cystine has very strong disulfide bonds to contribute to 3D structure. I digress to point out that Sarcocystis surface proteins characteristically have a lot of cystines and it can be expected these amino acids give important tertiary structure to the SAG’s. One would speculate, without any other knowledge about the protein, that the cystines give the protein its functionality.

A horses’ immune response is to the tertiary structure of the SAG proteins making antibodies to the 3D molecule, not the primary structure.

Think of a protein as a rope, twisted it up upon itself into its 3D structure.  Now mentally dip that twisted up protein into a vat of dye-lets imagine red.  You have tie-dyed your protein!  When it is unfolded into its primary (linear) structure you will see where areas of the protein, that were far apart, touched when folded.  Red marks are distributed seemingly randomly along the molecule and there are long areas between the marks that have no dye.  The scientific term for the areas that touched are “conformational epitopes” and the areas that are side by side are called  “linear epitopes”. An “epitope” is a section of  amino acids that induce an antibody reaction in a host.  You can correctly guess the amino acids do not have to be side by side to make the host react, in fact you expect the 3D structure to be more important in inducing a response.  Conformational epitopes are important in immunodiagnostics.

Some testing formats use chemicals to stretch out the proteins into linear molecules.  Other formats retain the 3D conformation of the protein.  You can correctly guess that each test would measure antibodies that recognize the same protein, but by different markers.  We have always favored conformational epitopes and run our tests without protein-straightening chemicals. Our thoughts are not original. It is long known that Sarcocystis infections are more recognizable when diagnostic tests that use conformational epitopes are selected.

We evaluated SAG 1 and recognized a relationship between breaking tertiary bonds and the concentration of chemicals used to break those bonds. It was dose dependent. That means that the KY lab that tested samples from the experimentally infected animals looked for linear epitopes. and depleted the reactions to SAG 1. We keep the SAG 1 for detection folded in its happy state. 

You correctly point out that an IFAT test uses the whole organism.  Are the surface proteins altered in the IFAT test?  It depends.  It matters how the organisms are prepared for the test. More important to the argument is that commercial IFAT tests are run on SAG 1 strains.  Great for experiments using SAG 1 organisms to cause infections, but not so great in field infections that are caused by SAG 5 and SAG 6 strains, as well as the more common SAG 1 strain.

There are other complicating issues: Sarcocystis are known to selectively stop displaying some proteins during infection, different testing labs use different dilutions of the serum, some tests are measured by machine and some are subjectively evaluated by lab technicians. All things considered, an IFAT reported as negative at a 1:40 dilution tested on a SAG 1 strain is not comparable to a 1:8 dilution (titer) on a SAG 5 surface protein.

We take these things into consideration for you as we consult on your case.


funny rat We predict that in the year 2050 there will be no animal experimentation.  That includes animal testing for drug licensing.  Today, 100 million animals are used in experiments, about 13% of those are involved in studies that are required to license drugs.

Happily, a large step toward the goal of providing alternatives to terminal animal studies was published recently.  The FDA commissioner Scott Gottlieb, MD, stated that the FDA is trying to reduce, replace, or refine the use of animals in research. This is heartening news. We hate the current standards for new drug development that require euthanizing animals in studies. Even if a drug is commonly used in other species—if a new indication is under investigation, terminal studies are required. We’ve repeatedly argued against this position.  We lost the debates. But FDA is not insensitive to the issue.

On the horizon are simulation models that include in vitro (non-animal) dissolution tests and computer modeling that will replace animals in some studies.   A first step to animal-alternative testing is the validation of simulation methods designed to show the equivalence of a proposed generic formulation to an approved drug. We can predict a future that allows these same models for new drug development.  Currently, FDA requires data to understand how a drug performs in a live animal.  In our case, mountains of data obtained from goats and dogs and cats won’t substitute for horses.

A part of the generic licensing process involves an animal drug developer to perform “bioequivalence studies”.  These live animal studies compare the originally approved product and a proposed generic version to see if they are similar enough to link them in terms of safety and effectiveness. These are expensive studies and these studies are ignored by compounders.  Another subject for another day.

Back to the good news. There are studies afoot at FDA that will create a physical model to simulate properties of a specific drug when tested in live animals. The proposed studies use dogs. The live animal data will validate the simulations for anti-parasite formulations that are currently used in dogs.  If the studies are successful, animal drug sponsors may use these data to aid in designing in vitro studies.  And that will save the lives of animals.  The initial studies used to equate the simulation to the live animal are designed to use a small number of anima.  The animals are subjected to minimally invasive procedures, perhaps as simple as a blood draw. And more good news, the lab-dogs will be adopted as pets.

The FDA is encouraging drug companies to develop and validate alternatives to animal testing, including in vitro dissolution tests and computer modeling. For now some drugs may still require live animal studies, and these studies may require euthanizing the test subjects to support a new animal drug. We’d like to get back to the future.  We developed a simulation method that is designed to test the equivalence of a proposed generic anti-protozoal medication against approved drugs.  As licensed EPM drugs age out of patents there will be an opportunity for licensed generics. We are refining an animal model that can prevent excessive horse use and will design and test the validation parameters.  I suspect that it will take a year or so to get the rubber stamp on a validated model.  We would like to be instrumental in the movement to decrease animal experimentation.

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.


In January of 2017 CBS Evening News (Lee Cowan) reviewed a book by Doug Preston…The Lost City of the Monkey God.  I won’t spoil the story for you--it’s a must read if you are obsessed with parasitic protozoa as we are.

The Lost City is a captivating true story and reveals a curse bestowed on man.  Legend has it that this ancient and magnificent Lost City, located in the rain-forested mountains of Mosquita was cursed.  Mosquita is a 20,000 square mile section of Honduras and Nicaragua.  The inhabitants lived in the area between 2600 B.C. and 1800 B.C and somehow incurred the ire of the Gods.  The angry Gods brought on a series of catastrophes.  Diseased and devastated, defeated inhabitants melted into the jungle, leaving everything behind, perhaps to appease the Gods.  The Lost City was not Mayan, yet it existed at the same time as the Mayans. These prosperous civilizations vanished at the apex of their existence.

Since the Lost City was first reported by Cortés in 1526, explorers and charlatans searched for them in vain.  That is, until the invention of LIDR in 2010.  The modern three-dimensional radar technology enabled mapping of the ruins beneath the dense canopy. It wasn’t the ruins that revealed the curse--the explorers may be cursed.

If you ask bestselling author Doug Preston, he’ll say he doesn’t believe in curses. And yet, here he is, being treated for leishmaniasis that he contracted while on expedition to The City. Half of the expedition party have contracted leishmaniasis--I believe at least one member died and some are not able to get treatment. The parasite is transmitted by a sand fly, the bite releases the protozoa into the skin and causes lesions that may take years to heal--cutaneous leishmania. Effective treatment at this stage may be life-saving but there are no current satisfactory treatments for cutaneous leishmaniasis.

As disease progresses, the parasite migrates to the mucous membranes of the mouth and the nose, and eats them away; this is mucosal leishmaniasis. The nose falls off, the lips fall off, and eventually the face becomes a gigantic open sore.  Organisms move on to the the organs, and visceral leishmaniasis is often fatal. Visceral leishmania is the second leading cause of parasitic death worldwide. The treatment is rough because it poisons the patients organs.  Patients die from treatment complications of renal or liver failure. Dogs get leishmania and are often euthanized when the diagnosis is made. Horses get leishmania, two cases were reported in Florida. When you read the book, you will realize why the curse reached Western Civilizations. We lead lives that prevent us developing immunity to this developing 20th century threat.

We are invigorated because there are some novel studies to report, and they parallel our investigations.  A promising combination therapy showed a complete clinical cure in 75% of the patients (human) with cutaneous leishmaniasis! The study also reported that 10% of the patients had a partial improvement and alas, the remaining 15% had an underlying chronic diseases and they had no response to the treatment. There were no cytotoxic effects associated with the drugs in the range of the experiments.  The mechanism of action of the drugs predicted promotion of some cytokine gene expression levels and reduced others.  The experiments supported the anticipated changes in cytokines. This is great news because researchers are understanding how to target parasitic protozoal diseases by modulating the response to infection. This has been our mantra for years.

What gives us satisfaction is revealing that the patients were unresponsive to the anti-leishmania drug, Glucantime, but responded when when Glucantime was combined with the immune modulating drug levamisole. Here is some evidence that end-stage unresponsive parasitic protozoal disease in patients is treatable when combined with levamisole.  The absence of cytotoxicity in the treated patients when given the combination of drug/levamisole is also highly noteworthy.

In the last 100 pages of The Lost City, Doug Preston suggests the Curse may be the downfall of Western Civilization--a result of invading parties driving civilizations to extinction by not so unintended consequences and bringing back malady-in-kind.  While we doubt the impact of our studies with levamisole (in horses with EPM and polyneuritis equi) will save the world, we think our efforts are worthy. Support us in our research.  You never know where it will lead.

leishmanialeishmania 2

Leishmania parasites are shown in a host cell and in tissues.

Photos were taken from

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