Skip to content


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.

Equine protozoal myeloencephalitis (EPM) is a syndrome that includes neuroinflammation. Recognizing the inflammatory component of the syndrome may make EPM a treatable disease, of course supporting a presumptive diagnosis requires a clinical examination and ruling out other causes of disease. Ruling out other diseases begins with a physical and neurological exam. Diagnostic tests can include radiographs and immunodiagnostics. Primary complaints that are related to an abnormal gait indicate a standard lameness exam (that includes nerve and joint blocks) should be performed. After routine diagnostic procedures, some veterinarians use a response to treatment to support a diagnosis.

When ataxia is apparent, ruling in/out the location of the problem is useful. Localizing the lesion is an achievable art. In early S. neurona infections vestibular disease is recognizable and can involve the peripheral or central vestibular system, brainstem, or cervical vertebrae. When localizing a lesion to the clinical signs an important consideration-- is it one lesion or a multifocal issue? The onset of signs can be sudden and indicate trauma, infections, inflammation, toxicity, or idiopathic causes. Chronic and non-progressive disease make trauma or infections more likely. A thorough examination and diagnostic testing can rule out or point to an etiology.

Induced EPM infections cause ataxia in horses. Prior to ataxia, central vestibular disease is apparent. Since publication of Early Signs of Equine Protozoal myeloencephalitis (Ellison, Kennedy, Brown, 2003. Journal of Applied Research in Veterinary Medicine p.272-278) the observations in 44 ataxic horses were documented. The determination of disease in horses in these blinded, placebo controlled studies was by a grade 2 ataxia. Observing the signs indicated in the chart below suggested central lesions quickly after S. neurona challenge.

The focus of EPM research is on the pathogenesis of protozoal encephalomyelitis. Vestibular disease is part of the disease process, as shown by documenting signs in challenged horses. In field cases, the most common causes of vestibular disease are trauma or infection. The clinical signs in horses are often acute. Management and treatment of these cases can be difficult. Central and peripheral lesions are treated differently with different prognosis and that makes differentiation between these two conditions important. Central vestibular disease (affecting the brainstem or ventral portion of the cerebellum) often results in severe signs including trouble eating, ataxia, and paresis in multiple limbs, or even recumbence. Central vestibular disease is often observed in cases of EPM. Early recognition of central vestibular disease associated with EPM combined with effective treatment can resolve clinical signs returning a horse to use.

The location of the protozoa in active EPM cases is currently under debate. Some practitioners argue that protozoa must be in the CNS to cause the observed inflammatory signs of disease. We argue that protozoa can occupy the CNS, breaching the blood brain barrier inside white blood cells (Trojan Horse model), but assert that this scenario is rare. Undoubtedly there are cases in which protozoa are found post mortem in horse with a diagnosis of EPM. The far more common condition is that protozoa are not found in histological samples. Histological specimens are rife with inflammatory lesions, considered evidence of protozoal infection. However, these lesions are not described as pathopneumonic. The term is idiopathic if a definitive diagnosis is not made.

The basis for our opinion is that protozoa are not found in the majority cases of suspect EPM that undergo post mortem examination. Even in the stress model used to induce EPM (Saville et al 2001. Veterinary Parasitology 211-222) the researchers were unable to demonstrate protozoa in the CNS of the challenged horses. Alleviation of signs can occur rapidly with treatment. Should necrotic lesions (due to parasites) be present in the CNS one would expect a long period for recovery including an aftermath of signs that could not be resolved.  A rapid response to treatment and return to use in suspect EPM cases is our goal.  Our goal is facilitated by an early recognition of central vestibular signs. No doubt EPM is a difficult disease to identify, treat, and manage. Our view is based on available literature, experiment, and clinical observations made by veterinarians. The optimistic view is that EPM is treatable because a large part of the disease syndrome is inflammation. Until scientific evidence shows us an alternative, defensible view, we will continue suggesting treating neuroinflammation as a practical approach to treating EPM.