In This Issue
Fun Fact!
Researchers estimate that approximately 30 to 80% of the U.S. horse opulation has come in contact with the parasite and produced antibodies that can be measured in their blood. However, not all horses exposed become infected or develop clinical signs. In fact, the incidence of EPM may be less than 1%.

 
October Newsletter
Equine Protozoal Myeloencephalitis

  

 

Happy October!  Hurricanes notwithstanding (and here's hoping everyone stays safe this coming week with whatever Joaquin has in store for us!) October is an awesome month to live in New England and work with horses. 

 

This month we're due for a newsletter, where we delve a little deeper into a topic which seems to be relevant for the time period or something we're getting a lot of questions on lately.  We decided to expound a bit on EPM since it's a confusing disease, and there is a lot of misinformation circulating the internet regarding diagnosis and treatment.  We hope this makes things clearer for everyone!

 

Please take a look at our announcements as well - we've listed them first for convenience. 

 

Sincerely,
Drs. Matt and Ashley Kornatowski
Twin Pines Equine Veterinary Services, LLP
  
(Have an idea for a newsletter topic or an event?  We'd love to hear from you!  Just send us an email at office@twinpinesequine.com)
Announcements

Out of town
We will be out of town on October 11th and 12th.  We are currently arranging for emergency coverage during that time.  Please watch our website www.twinpinesequine.com for further updates!


Equitarian Outreach
As most of you know, one thing that we have always been passionate about is the care for equids in third world countries.  This January, Twin Pines will be travelling to Costa Rica to do just that!  We'll be spending 10 days travelling around the country with other veterinarians not only treating the animals, but also teaching the local inhabitants about animal husbandry.  Emergency coverage for our patients back home will be arranged, as always.  We'll continue to update you as more details develop.  Check out http://equitarianinitiative.org/ to see what an equitarian is and does.
Equine Protozoal Myeloencephalitis:
An Overview

 

EPM is a commonly diagnosed (commonly over-diagnosed, as well, but we'll get into that!) neurologic disease of horses in the US.  Let's break the name down a bit.  "Equine" obviously means it affects horses.  A microscopic parasite (a protozoa) is responsible for the disease, thus the "protozoal" part of the name.  And "myeloencephalitis" describes what happens: the spinal cord ("myelo-") and brain ("-encepha-") become inflamed ("-itis").  There is no breed or gender predilection, as all horses are susceptible.  There's also no specific time of year that transmission is more likely.  

 

The Organism(s) Involved
Click image to link to full size
The main organism that causes EPM is known as Sarcocystis neurona.  (Note that recently another organism has been discovered, and we'll get to that in a moment.)  While often infected, the horse is considered an aberrant host.  This means that in the life cycle of the protozoa, the horse is a tangent (kind of an accident). 

It's known that the reservoir for S. neurona is the opossum.  The organism reproduces in the GI tract and then sporocysts (basically an infective stage) is passed in the feces.  These sporocysts are then ingested by another host, typically a skunk or raccoon (and this also the point in time that a horse would become infected).  Recent studies have shown that horses may play a role as an intermediate host (like the skunk), but this has yet to be proven.  In the normal cycle, the infection enters the tissues (blood, muscle) of the skunk or raccoon, leading to its death.  The opossum feeds on the carcass and the cycle begins again. 
 
In horses, it is unclear how the organism crosses the blood-brain barrier to enter the central nervous system, but it is thought to be associated with the immune system.  One possibility is that the Sarcocystis is taken up by white blood cells which are then transported into the cerebrospinal fluid (CSF) - we don't need to get into any more specifics!  It is then able to run amok as it pleases (see the next box for specifics). 
 
  A second organism that has recently been discovered is Neospora hughesi.  There is on-going research in regards to this protozoa, and not a lot is known at this time.  What we do know is that it can cause similar findings to S. neurona infections.  For the purpose of this writing, we'll focus on S. neurona, but be aware there may be other causes of EPM.  To read more about N. hughesi, check out this article
Clinical Signs                 

 

"Could this be EPM?" This is a question we frequently get asked.  To understand the answer, the first thing is to know how the signs are caused.  

 

Once S. neurona gains access to the central nervous system it begins to travel through the spinal cord and brain.  Clinical signs develop due to inflammation and necrosis (cell death) caused by the tunneling of the organism.  Lesions can be macroscopic (visible to the naked eye) as shown in the spinal cord picture above, or microscopic. Most often the spinal cord and brain stem are affected. 

 

Given that information, it's easy to understand why the clinical signs are always related to a neurologic deficit.  However, since there' s no single path that the organism takes, the damage in the spinal cord can be quite random, leading to a variety of signs.  Most commonly we see muscle atrophy coinciding with unilateral or bilateral gait abnormalities.  This can sometimes be mistaken for lameness, but is actually a slowly progressive ataxia. 

 

Occasionally, more severe signs can be seen such as cranial nerve deficits (facial paralysis, dysphagia, or facial muscle atrophy.  These tend to correlate more to lesions in the brain. 

 

Things we do not see are signs associated with typical illness, such as fever, inappetance, or a dull attitude.   Generally horses with EPM are fairly bright, but may be anxious because they are not sure where they are placing their feet. 

 

Keep in mind, though, that just because neurologic deficits or signs may be present, does not immediately make a diagnosis of EPM.  There are many other neurologic diseases that we have to watch out for as well.   So that leads us to our next point...

Diagnosis

   

It's easy to suspect EPM but much harder to verify.  The difficulty comes in interpreting titers, and making decisions to treat based on a serum titer, or perform more invasive testing to try to confirm a diagnosis.  We'll try to keep this relatively simple.

 

ELISA Testing
ELISA Testing

We can test for the disease in a number of different ways.  There's Western Blot analysis, ELISA and even IFAT!  It would take an entire newsletter to describe all these so let's just suffice it to say that each of these tests looks for specific proteins or concentrations of proteins to confirm exposure.  We currently send our samples to a lab which performs ELISA and looks for SAG2,3,4.  These are outer surface proteins of S. neurona. 

 

Okay, so, we do a blood test, and it's positive.  Now what?  Unfortunately, the serum just confirms exposure to the protozoa, and doesn't necessarily confirm clinical disease.  To understand why that is, remember that S. neurona is SUPPOSED to be found in the muscle or blood.  Only in horses, it sometimes goes to the spinal cord.  But (perhaps) not always.  So, if there are protozoa burrowed in the muscle, or for some other reason the horse cleared the infection on its own, we'll often still get a positive titer on serum.  Bummer.  It's reported that nearly 50% of horses in our area will test positive for EPM on serum, while only about 1% will actually have clinical disease. 

No, not that Spinal Tap!

 

So how do we make our diagnosis more sure?  Ideally, we  would do a paired sample of blood and  cerebrospinal fluid.  This means that a spinal tap would be necessary.  Spinal taps can be done under standing sedation in horses, but can be a bit tricky to get a good sample. That's not to say it can't be done, but your vet should go over the specifics with you prior to the procedure.   With a high titer for EPM on a CSF sample, we can be much more sure about our diagnosis. 

 

Our general recommendation is to run a serum test first - if the serum test is negative, we know that the clinical signs are not due to EPM.  If we have a positive serum test, we have the option of pursuing a spinal tap for a CSF test to confirm, or we can try a course of treatment and monitor for response. 

Treatment                   

 

So, we have our positive serum and/or CSF test, and we're going to pursue treatment.  Given the makeup of  S. neurona, and the fact that treatment must be directed at the central nervous system, medication options are quite limited. 

 

Historically, the disease has been treated with a combination of antibiotics (sulfadiazine and pyremethamine).  While somewhat effective, treatment was of LONG duration (3 - 9 months) and had side effects including anemia and colitis.  Overall, the success rate with this combination is just over 60%.  Today the product is sold as Re-Balance. 

 

The gold standard for treatment at this point is ponazuril, the trade name of which is Marquis.  This product is extremely safe as it's mechanism of action is directed at a cellular organelle that is contained in protozoa but not in mammalian cells.  (Pretty cool, huh?)  Studies have been performed to confirm safety with this medication up to 7 times the dose (!) with no side effects seen.  The typical treatment regimen is 30 days but in some instances it is doubled to 60 days.  Marquis comes in a paste with seven doses (for a typically-size horse) per tube.  A similar drug which recently became available is diclazuril, which is marketed as Protazil - this is a related compound to Marquis, but is manufactured as a top-dress pellet which can be added to the feed.  The results with Protazil aren't quite as good as Marquis, but for horses which will absolutely not tolerate a paste medication, it's a good alternative.

 

Adjunct treatment with neuroprotectants (such as vitamin E) and anti-inflammatory drugs (such as Banamine) are also important, especially at the beginning of treatment with these EPM drugs.  When the medications are begun, there is a slight risk for worsening of symptoms as the drugs work to kill the protozoa within the central nervous system.  These adjunct treatments can help reduce the body's inflammatory reaction to the dying protozoa. 

 

Please keep in mind that there are several other compounds which are available from compounding pharmacies, which have made claims to be very effective at treating EPM.  Be skeptical.  Be especially skeptical if the same lab who is advertising a test for EPM is ALSO selling a unique treatment.  Remember that MANY horses test positive on serum without actually having clinical EPM, so many of the "positive results" are horses that just needed tincture of time.  Always check with your veterinarian before pursuing testing or treatment for EPM. 

  
Prevention

Prevention of this disease is nearly impossible.  There is no vaccine available and you can't watch your horse 24/7. 
Opossum feces
Any prevention is aimed at reducing exposure to opossum feces.
Prevent access of hay and feed to opossums, and be aware of how close the woodline is to your pastures.  

Additionally, reducing stress can limit the progression of disease.  One thing that has had a positive correlation with disease is trailering.  Infected horses that were stressed by trailering were much more likely to develop clinical signs of disease than horses that did not trailer after infection.  Does that mean you should never trailer your horse?  Of course not, but keep it in mind as part of the history in case your vet ever suspects EPM. 
 
A quick search online brought up products that claim to prevent EPM.  Flat out please do not waste your money on these items as there is no proof that they work other than the manufacturer's word. 
EPM can be a very debilitating neurologic disease.   The sooner it can be diagnosed, the less damage will occur to the central nervous system.  The problem is, for clinical signs to arise, damage has already occurred.  And unfortunately that damage is irreversible.  While we may be able improve their neurologic status by a grade or two, complete resolution may never be possible in more severe cases.