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Horses with polyneuritis equi (PE) can have muscle wasting and an abnormal gait, sidewinder is a good description. Polyneuritis equi is associated with paresis of the tail, bladder, rectum, and anal and urethral sphincters. Paralysis of certain cranial nerves may be present, a drooping lip and ears, inability to blink and wasting of the facial cheek muscles. The characteristic pathology is inflammation of the peripheral nerves and nerve roots. Microscopy of diseased areas reveal demyelination and remyelination that indicats a remitting/relapsing disease. In 1987 Dr. Fordyce used a serum assay to identify horses with polyneuritis equi because afflicted horses often have antibodies against myelin protein (P2). Pathogenes uses similar assays (P2, MPP) to detect antibodies against myelin proteins to suggest immune mediated disease in horses with clinical EPM.

The field diagnosis of polyneuritis equi can be facilitated by transrectal ultrasound of the extradural sacral nerve roots (as they exit the ventral sacral foramina). It may be useful to perform a biopsy of the sacrocaudalis dorsalis lateralis muscle in horses that show hyperesthesia, followed by hypoesthesia, because histopathology can be highly suggestive of polyneuritis equi.

knuckling horse

Acquired equine polyneuropathy (AEP) is the most common equine polyneuropathy seen in Norway, Sweden, and Finland. Scandinavian knuckling syndrome describes the clinical presentation. Mortality is between 29 to 53%, however horses that survive can recover and return to athletic use. AEP is seasonal, appears in clusters, and has a strong association to diet. This disease results in paresis. Microscopic examination reveals large fiber demyelinating polyneuropathy (inflammation) with conspicuous Schwann cell-associated features.

Siv Hanche-olsen et al (Equine Veterinary Journal, 2017) discussed long-term follow-up of Norwegian horses affected with AEP and we wondered if these horses, like polyneuritis horses in the US and similar neuromuscular diseases in people, had circulating anti-myelin protein antibodies. After a few emails and bureaucratic appeasement, the serum arrived.

We expected to detect antibodies against P2 in symptomatic horses because demyelination is a component of the disease process although it is known that AEP and PE are different diseases. Circulating P2 and MPP antibodies in horses are not known to be exclusive to polyneuritis equi. EPM is not found in Norway. Sarcocystis is present, but not S. neurona. We found S. fayeri antitoxin in most of the samples and, as expected, none of the horses had antibodies against S. neurona. Only of the sera from the horses had a normal CRP value, the others were elevated (36-65µg/ml)! None of the horses had P2 antibodies. Although we tested a small number of serum from horses our results indicate that PE and AEP are demyelinating diseases with a different pathogenesis.

There are neurologic diseases in people that may help guide our understanding of these two diseases. Experimental allergic encephalomyelitis, experimental allergic neuritis, and acute disseminated encephalomyelitis are also helpful models to define the disease processes. These disease models demonstrate immune attack on neural tissue caused by viral infections or in some cases, vaccination.

In the experimental allergic encephalomyelitis-model, a peripheral neuropathy, P2 protein antibodies are a component of disease. The P2 protein makes up a small part of the peripheral nervous system, most likely localized to the cytoplasmic face of the Schwann cell membrane. The function of the P2 protein on the Schwann cell is undefined but may be like similar proteins that bind lipophiles, suggesting a role in lipid transport and storage in these cells.

Myelin proteins are largely conserved across species and that is why equine myelin served in many experiments conducted by those that study human Multiple Sclerosis. Generally, there are differences between peripheral nerve myelin when compared to myelin found in the central nervous system (CNS). However, horses have an unusually high amount of P2 protein in the CNS-myelin when compared with other species. It is expected that a peripheral immune-mediated neuropathy would affect the central nervous system in some equine disease conditions.

Guillian-Barre (GB) syndrome is an immune mediated attack on peripheral nerve myelin. Pathology is found at the level of the proximal nerve roots and is due to local cytokine production (inflammation) rather than the development of circulating antibodies. Patients with GB have circulating myelin protein antibodies. In horses with PE there is inflammation and antibody associated with the pathology that is like GB syndrome in people.

Heavily myelinated sensory fibers (muscle stretch fibers) and motor axons are direct parts of the reflex arc. Deep tendon reflexes are almost always lost very early in the course of human disease. Numbness and tingling (sensory) usually precede flaccid weakness and ascending paralysis due to affected peripheral nerves. Inflammation can be associated with nerves supplying cranial muscles, disease may look CNS-mediated but it is peripheral neuroinflammation. The cause of disease could be molecular mimicry because specific infections have been associated with Guillian-Barre syndrome. Often there are relapses with spontaneous waxing and waning of symptoms.

Multiple Sclerosis (MS) is an immune disease mediated in the central nervous system. Because the optic nerve is an extension of the CNS the optic nerve can often show lesions. There are geographic areas with a very high incidence of disease (1 in 300 people) yet in nearby areas the disease is unknown. It is strongly thought that an environmental factor is associated with disease. An etiology is presently unknown although neuroborreliosis (Lyme disease) is a risk factor. Interestingly, moving from a high-risk to a low-risk area after the age of 15 does not appear to reduce one's chances of developing MS. It appears that whatever triggers the immune reaction that is active during MS does not appear to be present at the time of diagnosis. It is likely that both infectious and immune mechanisms contribute to the pathogenesis of MS. Antimyelin antibodies are present in patients with MS and may have predictive value for disease. A viral infection may trigger an inappropriate immune response with antibodies to a common virus-myelin antigen.

Some similarities of polyneuritis equi to Guillian-Barre syndrome and Multiple Sclerosis are circulating P2 antibodies, cytokine mediated inflammation, and remitting/relapsing disease. Polyneuritis equi and GB are peripheral diseases while MS is a central nervous system disease. Horses express more P2 in the CNS myelin than other species and may indicate why some horses exhibit CNS signs during disease. It was suggested by Allman (2009) that controlling inflammation in horses with polyneuritis equi may enhance the regeneration of nerves in horses with PE. Diagnosis and treatment of inflammation associated with polyneuritis equi is the subject of one of our clinical trials.

We did not find P2 antibodies nor MPP antibodies in five horses with acquired equine polyneuropathy suggesting a difference between PE and AEP. Acquired equine polyneuropathy is a peripheral inflammatory demyelinating polyneuropathy targeting large fibers associated with Schwann cells. A possible mechanism of disease in AEP is suggested by the experimental allergic neuritis model in rats. In the rat model a leukocyte receptor gene mediating activation of natural killer cells and macrophages by immune complexes was induced in cauda equina and sciatic nerves during the period of increasing weakness. The accumulation of the leukocyte receptor was attributed to macrophages and other cells of the immune system in the neural tissues rather than induction of the expression of the receptor by the Schwann cells. Examining the immune response by inflammatory cells after the inciting trigger for the inflammatory response during clinical disease may be interesting in AEP.

It is suggested by our work that equine polyneuropathies, like human neuromuscular disease, can look similar but have different cellular targets that require different treatments.

sidewinder3 (2)Horses with neuromuscular disease that are unresponsive to the usual treatments can be frustrating for veterinarians and horse owners. This post encourages you to get in touch with us if you have a horse with "EPM" and is not responding to treatment. ELISA Submission Form


We are following 38 horses that have clinical signs consistent with polyneuritis equi or cauda equina neuritis, an often overlooked syndrome associated with EPM. Our goal is to develop a treatment protocol for veterinarians dealing with these cases. Sometimes these horses are weak on one side, they have hemiparesis, and that prevents them from tracking normally.  The weak rear end falls to the weak side.  A commonly used descriptive term is "sidewinder". Ellison 2015 MPP MP2 Assay

There are other clinical signs of this disease.  Dragging limbs, tripping, or even drooling and dropping feed (cranial nerve dysfunction) are observed. The tongue can be atonic.  Another sign in these horses can be dripping urine or an inability to empty the bladder.  The most common comment in the history is multiple EPM treatments. We developed tests that can lead to a diagnosis of polyneuritis equi. Pathogenes Testing Options

Historically, the distinction between polyneuritis equi and cauda equina neuritis was the presence of cranial nerve involvement.  Discerning the disease by cranial nerve signs may not be accurate because horses with cauda equina may also have cranial nerve deficits.  In terminal cauda equina, horses are unable to urinate and often colic.  We don’t distinguish the two diseases by cranial nerve function because the owners and veterinarians involved with the horses we track often report difficulties with chewing, droopy lips, or facial muscle atrophy. These signs are often responsive to specific treatment.

Two serum tests, MPP and MP2,  measure anti-myelin protein antibodies.  Horses with polyneuritis equi often have circulating antibodies that are reactive against myelin protein and/or a reactive site on myelin.  The presence of antibodies are evidence that an autoimmune reaction is involved in the disease process.  A positive test can assist in diagnosis and potentially life-saving treatment.  2015 EPM and MPP

Eventually we think we will be able to stage to degree of damage using these tests. The C-reactive protein assay (CRP) may be the most useful test for case monitoring after a diagnosis is made.  The CRP assay is useful because response to treatment precedes a reduction in the pathologic inflammatory cycle. It may be that polyneuritis is the early stages of disease that ends in cauda equina syndrome.  That is to say, chronic idiopathic polyneuritis left untreated will eventually develop into clinical cauda equina.

If we understand the disease process correctly, it may be possible to prevent the progression of disease.  We are following the clinical course of 38 horses, their therapy, and the outcome of treatment.  We are assembling the data for a statistical analysis of the diagnostic and treatment options.  This data-based approach will be very useful to veterinarians trying to manage these horses.  The long game is devising a standard treatment protocol for afflicted horses to keep them healthy,  but we are not there yet.

Recently Dr. H. wrote a quick email asking if it was concerning that the CRP (C-reactive protein) level remained elevated in his patient, a 7 year old mare with a 3-year history of relapsing disease.  The good news is that she is currently clinically great while receiving treatment.  He wanted to know what is next.  What can be expected?  Unfortunately for Dr. H.,  we don’t have all the answers.  We sent back all the variables, the possibilities, and the literature he could review to make his clinical decisions.

Dr. Laura Benedetti is busy contacting veterinarians, asking for gait scores to update our records and requesting blood samples on the horses we’ve identified that could have this condition.  She answers emails about polyneuritis equi.  What is missing from the process is a forum for owners to discuss their horses with other owners similarly diagnosed horses.  While there are numerous forums and posts about individual horses with suspected EPM, these sites aren’t that useful for those facing a polyneuritis equi diagnosis for their horse.

We were pleased with the support offered to Taylor Lin (Blaze was posted on January 22 at Pathogenes Inc. Facebook), who initially felt alone before finding others who had been there before and kindly posted comments.

Horses with polyneuritis equi and cauda equina should receive a potential diagnosis and an individualized treatment protocol based on data that includes clinical examination by a veterinarian and laboratory testing.  Sub-clinical disease is an important aspect of chronic idiopathic polyneuritis. Dr. H’s mare  looks great and is performing well.  However, serum testing indicates she still has disease that needs to be treated.  Often the CRP can be used determine an endpoint to treatment.

We welcome you to post your questions and observations on Pathogenes Inc. Facebook page.  The information will be useful for others facing this disease in their horse.  Pictures and short videos are also welcome.  Individual treatment options are discussed privately with veterinarians because these need to be tailored to the specific cases.

It is an ill wind that bloweth no man goodJohn Haywood 1562

Autoimmune polyneuritis is a disease that causes weakness and ataxia in horses.  It is related to horses diagnosed and treated for EPM. It is not a new disease but hasn't been in the EPM-discussion.  This post explains polyneuritis equi and using CRP levels to monitor the disease process.

A Little History The possibility of contracting variant Cruetzfeld-Jakob disease (the human form of bovine spongiform encephalopathy) was recognized when Mad Cow disease blew into Europe.  Risk spurred scientists to replace the well-characterized bovine neural tissues that were used in MS (multiple sclerosis) research with equine tissues. The flurry of equine experiments led to some very useful information.  In 1981, scientists raised the possibility that circulating antibodies to myelin protein played a role in neuritis of the cauda equina in horses.  An ELISA test was reported in 1987 for the differential diagnosis of cauda equina neuritis and other neuropathies in horses. Polyneuritis equi (PE) is the more correct term for neuritis of the cauda equina. Ellison 2015 MPP MP2 Assay ELISA Submission Form Pathogenes Testing Options

Several diseases are encompassed by the term polyneuritis equi. That complicates the understanding of this syndrome.  Suffice to say, much research is needed to determine cause and effect as well as the pathogenesis of polyneuritis equi in horses.

The pathology of polyneuritis equi is characterized by inflammation of the nerve roots that form the cauda equina (typical) and any other peripheral nerves (atypical) that are involved.  Histological examination of the affected nerves can show areas of demyelination and remyelination. These lesions are similar to experimental allergic neuritis.  Horses with clinically and pathologically diagnosed polyneuritis equi  had circulating antibodies against myelin protein that were similar to lesions in the experimental model. When it becomes necessary there is a procedure that may be used to confirm the diagnosis. Aleman 2009 PNE

The cause of polyneuritis equi is elusive.  A viral or an immune-mediate etiology are each possible.  These two theories may not be incompatible because an infectious agent may initiate an immune-mediated condition that stimulates a common pathologic pathway.

The distinction between chronic inflammatory demyelinating polyradiculoneuropathy and acute inflammatory demyelinating polyradiculoneuropathy and several disease-associated polyradiculoneuropathies (cancer, diabetes, liver disease) is important in human and equine medicine because the course of disease and prognosis are different.

Our approach to investigating polyneuritis in horses is by serum testing for MPP and MP2 antibodies followed by observing a response to treatment. We hypothesize that polyneuritis in horses is immune-mediated and it is not specific to cause.  For example, sarcocystosis due to S. neurona or S. fayeri can stimulate polyneuritis.  So can Borellia, the agent of Lyme disease. The pathway that results in clinical signs and pathology are the same, the stimuli are different.  Because the pathogenesis of disease is by a common pathway, the initial treatment of polyneuritis equi is the same, irrespective of the stimulus.  However, the identification of the etiology is important to treat the underlying cause of the proinflammatory-stimulating pathway.

The immune response is over reacting to an infection. Most of the time an immune response turns off once an infection resolves.  In some horses with polyneuritis, a chronic inflammatory condition results because the immune system is stuck in the “IL6 <-> CRP” cycle, each molecule stimulating the production of the other.  No “turn off” switch is initiated when the pathway is stuck.  Just the opposite happens.  The end result of molecular reactions turn on the reactions to stimulate the cycle again. Our approach is resetting this cycle using a protocol that prevents the short term production of IL6 receptors.

The proposed pathogenesis of polyneuritis equi. The immune response in polyneuritis equi is possibly via an IL6 (pro-inflammatory) pathway. Our reasoning is that:

  • innate immune responses stimulate IL6 production;
  • myelin protein displays IL6 receptors.

An experiment demonstrated horses with abnormal IL6 pathways do not get signs of polyneuritis equi, as opposed to horses with normal IL6 pathways, when given the same stimulus.

  • Horses treated for abnormal IL6 reactions resolve their clinical signs with treatment.
  • Untreated horses with chronic polyneuritis (atypical polyneuritis equi) get worse.
  • Untreated chronic polyneuritis progress to an immune mediated demyelinating neuropathy.

The waxing and waning of the immune mediated disease eventually results in microscopic calcium deposition on nerves. This terminal condition, classical polyneuritis equi, has no treatment in horses. The recommendation for classical cases of polyneuritis equi, once the diagnosis is confirmed, is euthanasia due to the poor prognosis and intensive nursing care required, even for symptomatic support. We do not recommend euthanasia until a response to treatment is investigated.

Many horses with neuropathy have increased CRP (stimulated by IL6).  That is why CRP is important to monitor the presence of disease.  Sub-clinical disease is diagnosed when CRP levels are elevated and there are no clinical signs.  The CRP levels are useful in monitoring these cases, treatment is needed until the CRP levels are normal.  Again, treatment to decrease inflammation is not useful in chronic cases unless the underlying condition is resolved.

You’re probably reading this because you have a horse that has relapsed multiple times or you are concerned about the CRP value.  Here is our quick reference:

CRP level is trending to a normal value (less than 16):  indicates the inflammatory process is resolved.  If clinical signs are still present they are probably due to a physical cause and more diagnostics are warranted.

CRP level is elevated or going up: indicates the inflammatory process is not resolved, subclinical disease is present.  If the horse is clinically normal, it may be useful to deworm with QUEST.  Quest is required to eliminate encysted small strongyles that may be associated with chronic inflammation.  It’s cheap, safe, and there is nothing to lose.  Have you considered hind gut ulcers?

CRP level is elevated or going up: if the horse is not clinically normal or relapses after treating the inflammatory pathway,  the underlying condition has not been resolved. A possibility is that S. neurona is causing continued exposure and disease; S. fayeri toxin is present and S. fayeri infection has not resolved or there is continued exposure in the environment.  Our ongoing study is designed to distinguish these conditions and is accepting cases.  The study is for 1 year.

CRP level is elevated and MP2/MPP antibodies are present: indicates that autoimmune polyneuritis is present.  This condition will not respond to antiprotozoal drugs.  This condition will require a different treatment protocol.  We are consulting with veterinarians/owners with sick horses about this disease and providing the most up to date protocols. Treatment may resolve clinical signs. CRP is used to detect subclinical disease that should be treated before clinical signs manifest.  If the CRP continues to go up, and clinical signs progress, further diagnostics are indicated.

Chronic relapsing disease with an elevated CRP that is unresponsive to treatment requires additional diagnostic workup. There are some diagnostics to assist in the ante-mortem diagnosis of classical polyneuritis equi. Aleman 2009 PNE The field procedure is a transrectal ultrasound of the extradural sacral nerves.  Also, biopsy of the sacrocaudorsalis dorsalis lateralis (the base of the tail) is useful.  There are  case reports describing the procedures and the results in two cases that may be useful.

We provide new and novel ideas for the treatment of conditions that are previously diagnosed as “EPM”.  Our work also makes sense of some of the most perplexing issues surrounding S. neurona sarcocystosis. Our papers are published and available to everyone.  You may give us a call for guidance with these cases, however to support our work and our time, we ask that you please submit samples for testing.  Our test results and responses to our protocols provides us with information that can lead to new treatments for these very complicated diseases.  There are few veterinarians working and publishing in this area. Supporting our work guarantees there will be more options in the pipeline.

Occasionally horses that have been treated for EPM will relapse days or weeks later. Recurrence of signs of EPM can be due to S. neurona, S. fayeri, or polyneuritis equi. This blog introduces the experiment to investigate disease conditions in relapsing horses.

Clinical disease is associated with Sarcocystis fayeri and Sarcocystis neurona infections in horses. Both of these infections will produce inflammation that can produce a disease called polyneuritis equi.  Equine protozoal myeloencephalitis is a  tough disease to understand and the following question was posed by the EPM society as an area of high interest: a) can S. neurona establish a persistent but unapparent infection in the horse? We are investigating the seroprevalence of antibodies to S. neurona, S. fayeri, and polyneuritis equi in these relapsing horses in an effort to answer that question.

The Trojan horse model taught us that any horse can get disease, at least those we challenged showed signs. But some horses were more susceptible than others. We observed that organisms could more easily enter the cells of some horses.  Does that mean that genetics plays a part? We’re not sure yet.  The model taught us that antibodies horsegroupwere produced by day 17 of the infection, clinical signs could be as early as day 10, and in every case the signs were sequential.  That means each horse showed the same signs in a very predictable way.

In field cases of suspected EPM we start by measuring antibodies. In most of these cases, the disease is not acute, but has progressed to a chronic state.  A statistically significant finding in acute cases was that antibodies against S. neurona increased as the infection progressed, yet the clinical signs varied with the horse.  That means some horses which had experience with the organism would have more pronounced signs than those which were infected for the first time.  We learned about the immune response and protection against S. neurona by using our challenge model.  The immune responses were similar in the experimentally challenged horses and horses that were naturally infected.

What we couldn’t do with the model was create a chronic condition that mimicked what we see in field cases. Field cases offer various disease manifestations however we don’t know when the horse was infected or the immune background (experience) of the animal.  Sorting this out takes many observations over a long period.  Observations and measurements require objective tests, run many times, with the data evaluated statistically.

Our long term objective was to gather data from a lot of horses, over a year, and produce meaningful analysis.  We analyzed over 17,000 blood samples and saw a pattern in a hundred or so horses.  These horses were chronic and their signs reoccurred after treatment.  It could take a few weeks. or happen after years of being healthy.  Some horses responded to treatments we suggested but they would eventually show signs again.

After manikins-puzzle-four-orange-cartoon-characters-colored-pieces-white-background-34676756developing tools and identifying horses, we designed an experiment that could answer  the question posed by the EPM society.  The experiment is finishing up after 1 year.  Enrollment was staggered and new horses are enrolling, some horses are still completing 3, 6, 9 and 12 month evaluations.  The exciting, novel, and interesting findings are that we were able to define 3 disease conditions associated with EPM.  The data from the experiment is available from the International Journal of Applied Research in Veterinary Medicine, Vol 15, No 1, 2017.  The paper will show up on their web page. The next 3 blogs will define the three diseases and explain what it means to the horse and potential treatment.


We believe new treatments are transformational when talking about protozoal disease. What inspires transformational thoughts and ideas?  Some think it is a mysterious process, right out of the blue, a light comes on.  More likely, innovation springs from many years of questioning, hard work, vigorous testing, and careful analysis.

We have reached the proverbial 10,000 hours (ref: Malcolm Gladwell, Outliers) studying EPM, creating models, and we are ready for a final analysis.  Our research started using models that defined the disease process and indicated that we could develop a beneficial treatment.  Years later, it’s time to put the models aside and statistically test our model.  Our first placebo controlled study for NeuroQuel is available, limited to 60 horse owners.  This is a study that will be part of our Freedom of Information Summary and because it is an FDA study it has a few strings attached.

NeuroQuel is a drug that is designed to control the residual or recurrent clinical signs due to inflammation associated with Equine Protozoal Myeloencephalitis (EPM) following antiprotozoal therapy in horses.  The field study will enroll horses that have failed to improve, or have relapsed after licensed EPM treatment (Marquis, Protazil, or Rebalance). The horses will receive NeuroQuel and we will evaluate the response to the treatment.

This is a placebo controlled study.  The first form, the Owner Consent form, is required.  The owner consent form informs the horse owner that there is a chance (a statistically calculated chance, 1 out of 3) that the horse will receive a placebo treatment.  Your horse will not be considered for entry into the placebo controlled study without this form in place.  If you haven’t signed this form, you are not in this study.

Does the horse qualify for enrollment?  Not surprising, the documentation for qualification is called the Qualification Record. There are three conditions that must be met to qualify 1) the horse was previously diagnosed and treated for EPM.  2) The animal exhibits recurrent or residual clinical signs with a minimum of a Grade 2 deficit, and the easy one 3) the animal is 6 months or older weighing 600 pounds or more.  A Grade 2 deficit is defined as “a defect that is easily detected and exaggerated by backing, turning or neck extension.  The horse may sway at a walk.  There may be a wide based stance after tight circling.  The horse is weak on the tail pull-easily pulled off track and does not return to a normal walk for 3 steps.”

There is a second part for the qualification into the study.  There are situations that will un-qualify a horse.  The horse can’t be in another study or unsuitable for this study.  The horse can’t enroll if it has another disease.  If the horse can’t get up, or the owner can’t get medication into the horse (or multiple folks will treat the horse) it won’t meet the qualification criteria.

There are some other forms to fill out, the Physical Exam form, the Data Collection form at day 0 and day 14, and a Supplemental History form (these document the criteria used to support the original diagnosis of EPM).  There is a blood draw before and after treatment, the blood is collected in a couple of red top and lavender top tubes, accompanied by a Sample Collection form.  Owners participate in the observations by completing check boxes on the Client Observation form for behavior, appetite, respiration, and occurrence of diarrhea.  Additional space is provided for owner comments.

So far, so good.  But the first inclusion criteria is the most difficult requirement for this study.  The original diagnosis of EPM must be supported by testing and other diagnostic testing as needed. The FDA set the standard as CSF analysis to support the original diagnosis.  After bioassay for antibodies in the CSF the horse must have received a full course of an FDA approved treatment, per label instructions: dose, duration, and frequency, no loading doses or multiple treatments.  Treatment must be what the sponsor intended when they licensed their treatment.  Treatment must be within 90 days of enrollment.  At the end of the FDA approved treatment, if signs (minimum Grade 2) are present, then the horse will qualify for this study.  Also, if within 90 days the horse “relapses” with a Grade 2 deficit, then the horse will qualify for the study.

We recognize that CSF taps are not generally obtained in the field and most veterinarians  test serum, or don’t test at all.  We strongly hold that testing allows the selection of the correct treatment and can be accomplished by serum testing.  Hopefully data from this study will support that rationale, CSF taps aren’t the best criteria to determine a horse that will respond to treatment.

However, until there is a paradigm shift at FDA, we provide a CE course (3 credits) and teach a technique to obtain a CSF tap, in the field, in a standing horse.  Field sedation techniques, using drugs most veterinarians have on hand, allow a veterinarian to get a CSF sample from the neck.  With a bit of practice, the tap can be obtained in a couple of minutes. You can email us for the link or go to the Learn More tab and copy the link from the slide presentation that describes Pathogenes CE program.

We will continue to use models that advance our ideas because idea-modeling will result in more treatment options for horses and their caretakers.  For example we learned about the effect Sarcocystis fayeri, a common protozoal infection in horses, can have on neuromuscular disease.  Another example is the presence of autoimmune disease in horses, when treated early the horse can have several more years of useful life. A  limited enrollment, placebo controlled study gathers statistical data.  After the “reasonable expectation” of clinical benefit study a conditional license is issued and a larger field effectiveness study is conducted.

We are far from finished and need your to help in these studies if new equine treatments are desired in the pipeline.  From idea to models to field use, it’s expensive and time consuming.  It’s highly rewarding.  This is our commitment to the horse community and any part you can play is appreciated.