AAEP's Dr. Sandi Farris answers questions on the debilitating disease, EPM.
Question: On October 23, 2012 I witnessed my 18-year-old paint gelding slip in the mud. He then began to side pass to meet me at the gate. Our veterinarian recommended a week of stall rest, but my gelding had little to no improvement. The veterinarian said came to evaluate my gelding, which included a lameness exam and radiographs of the left stifle. His diagnosis was severe sprain of the interior stifle, heat and apparent inflammation. Treatment consisted of bute and work him lightly building on strength and duration and a one to two week normal turnout routine. This didn't feel right to me, but I complied. On day 2, my horse became extremely lame on his right as well as original left . I contacted the veterinarian once again to discussed the current situation and response to treatment. His response to me was to keep him moving. Over the next week, my gelding tried to comply but lameness worsened. I had a second veterinarian reevaluate my gelding. He disagreed with treatment and told me to rest him and continue on bute. Over the next four weeks, my gelding's lameness worsened and seemed to loose control of his hindend. He almost seemed to have no clue where his feet were and had a pronounced right hind hip drop when moving. He looked one step away from falling.
Enter my farrier, who watched him move and suggested a lameness specialist and/or chiropractor. That said, a specialist came and did an evaluation, which included digital radiographs of both the head and stifle. She felt the horse definitely was neurologic in symptoms progressive of original injury. She felt there were three possibles, which included THO, EPM or West Nile. Radiographs showed moderate swelling of the right hyoid bone, and slight on the left. She started him on a high doses of Dexamethasone and would reevaluate him in one week, which did include some improvement. She then drew blood to hold for future EPM testing. I went online and watched several videos of EPM cases and felt this was what I was seeing in his movement. She then begain him on EPM medication along with Dexamethasone. Five weeks later he had significantly improved. I began walking him daily which we graduated to small hills backing and stepping over ground poles.
I now have two new problems. The first is that he has lost the hair over his left eye, and she thinks it is possible uveitis, which dex is used for. How do we know what drug is working on his ataxia, and dex is an immune supresser, could it be causing other problems? My specialist that took blood samples is currently out of the country as I would like her to run the bloods for EPM. But, what about the hyoid bones swelling? Is it possible this is and has been his normal all along and we are dealing with EPM? And the hair loss over his left eye; is this some kind of immune response to the drugs or the disease in question? My gelding has been good-natured and patient throughout all of this. However, I am confused and frustrated!
Oh my, you do have a number of issues in your horse right now. This case has a high number of variables between the early history of lameness and the response to EPM medications and finally a question about the hyoid bone and the hairloss. I can't comment on a diagnosis for your gelding but I can suggest either contacting your last veterinarian for guidance or if she is unable to re-examine him contacting a referral center that can take your gelding's symptoms one at a time. I don't know where you are located but most areas have fairly good access to a Veterinary Teaching Hospital or if you'd prefer, a local private referral clinic. Referral centers and Universities tend to see a number of unusual and/or complicated cases each year
and may have more diagnostic tests available to pinpoint a diagnosis for you.
Question: Is there a test available to see if my barn cats are carriers? If so, what is the name of it? Do most small animal vets perform the test or will I need ask my Equine veterinarian?
I own an 8-year-old Gypsy gelding that has been battling EPM since April of 2012. We first tried a course of the Sulfa suspension medication, and now he is running through a course of Marquis. I have been extra careful with keeping the wildlife carriers of EPM out of my barn, but would like to see if our barn cat is carrying it.
Cats have been tested experimentally to determine if they carry serum antibodies to Sarcocystis neurona. Researchers determined the domestic cat is one of the natural intermediate hosts for the causative agent of EPM. Some studies report that 5% of all farm cats have been exposed to S neurona in areas with opposum. Your question about testing your own cats is a good one. Although research labs have used the tests it is not a common test in the private clinic setting. A Polymerase Chain Reaction (PCR) test is required to differentiate exposure of the cat to the parasite from actual infection with S neurona. Zoologix Lab, among others, does offer a feline S neurona PCR. It can be run on blood or nervous system tissue. Talk to your veterinarian about the practicality and use of this PCR in your barn!
Question: My 13-year-old Appendix Quarter horse mare developed EPM at the age of 7. The disease was very severe and I nearly lost her, but she recovered well. She is sure footed, rides well and even jumps. The only setback she had was one paralyzed vocal cord (per bronxhoscopy). She is now in foal and due March 12. She is exhibiting symptoms of EPM again. I know foaling is stressful, but wondered if Marquis would be safe to give her before foaling? If so, for how long? If not, can it be given after foaling with a foal at her side?
EPM is unfortunately a disease in which stress of the horse plays a large part in recurrence of symptoms. Pregnancy and lactation are arguably the most physiologically taxing periods in a mare's life. Sarcocystis neurona has a tendency to recur during these times. The resulting neurologic deficits cause concern about the health and safety of mare and foal.
Current medications available for treating EPM can have a variety of adverse effects on a pregnancy and should be used carefully and under the advisement of your veterinarian. Risks and benefits to treating your mare while she is in foal will need to be assessed. Most commonly these drugs are folate-synthesis inhibitors which, as we are aware in human pregnancies, when used long-term can lead to birth defects and bone marrow arrests in the fetus.
Medicating your mare with the foal-at-side may be safer than treating during the pregnancy, and again you will want to discuss the specific risks and benefits with your vet. The Marquis drug insert does contain the broad statement that risk of use in breeding horses is unclear.
Question: I live in north central Virginia and have an 11-year-old Irish Draft gelding. Can/should I vaccinate him against EPM? Can this vaccine be given with other vaccines or should it be done at a separate time?
In the past, EPM vaccines were available on the market for use in horses. Protection in those horses was, unfortunately, poor, and the vaccines were removed from manufacture. As of now, there is no USDA-approved vaccine against EPM. What a help it will be when there is one with a high level of protection! The best horse owners can do now to protect against the protozoal disease is to minimize the intermediate hosts (opposum, cats, raccoon, and skunk are most likely culprits) by keeping grain and water sources secured, decrease host access to horse pastures, and keep your horses as healthy and stress-free as possible. I am sure the ongoing research will one day lead to a useful vaccine.
Question: My 27-year-old mare presented the following symptoms on the evening of 11/8/12: barely able to walk; could not cross the threshold to stall without help, fell down in stall, which resulted in an emergency call to the veterinarian. They submitted blood drawn from my mare to MI State University for testing (S. neurona IFA Titer test), which was 320 suggesting + for antibodies against S.neurona. The clinical picture was consistent with EPM as well. She was then administered on a 28 day treatment with Marquis, which has shown improvement with her gait/balance, etc. I question that specific test as to what it is testing and have read that while the IFA test is believed to be an improvement over the Western blot relative to predictive ability; newer ELISAs are more quantitative. If the appropriate tests are used (whatever that would be) would a decreased antibody titer after treatment be useful? And, if symptoms re-appear, would it help to have this information and then re-test if I suspect a relapse?
Such a good question...this is one of the toughest pieces in the EPM puzzle right now. Serum (blood) tests for EPM have improved over the past decade but still are not altogether definitive in diagnosing clinical disease caused by the EPM agent Sarcocystis neurona. The first test used was known as a Western blot, a procedure which was revolutionary in the 1990's but had limitations with a high number of false positives. Since then, polymerase chain reaction (PCR) and immunofluorescent antibody (IFAT) testing has improved the value of the results. Each test has individual limitations; a negative PCR does not rule out the presence of S neurona, IFAT may be more subjective than quantitative.
Research is ongoing and new methods are being developed. It is possible that enzyme linked immunoabsorbent assay (ELISA) tests may currently be an ideal choice for accurate test results. That said, an elevated S. neurona serum titer is evidence of infection (exposure) than of actual disease. Titer levels can vary based on the number of organisms found in the horse, the immune system status, and the presence of concurrent or previous medical treatment.
Many cases of EPM are treated based on historical clinical signs in the presence of a strong serum titer. Presumptive treatment with an anti-protozoal with improvement in signs can be considered a diagnostic tool in itself. The most exciting new research Dr. Dan Howe, of the University of Kentucky Gluck Equine Research Center, has found proteins on the surface of the S. neurona parasite, which have the ability to create a strong immune response in the horse. The proteins, labeled snSAGs, elevate in ELISA titers on serum and cerebrospinal fluid (CSF). CSF is sampled via a spinal tap. Similar to previous testing methods serum snSAGs titers alone are not completely foolproof. CSF titers coupled with serum titers for snSAGs remain a more credible positive for EPM diagnosis. Check with your veterinarian for more information on using the newest snSAGs ELISA titers.
Question: My 13-year-old mare came up with a low positive on the EPM test when she returned to upstate NY from Va.as a 3 yr old. She was testy (wringing tail) about weight on her back and even tripped and fell once when being ridden but otherwise was perfectly fine. I treated her for one month with a medication that is now off the market. She never got wobbly but since I couldn't really make any progress with her dressage work, I stopped riding her. She is in foal now. Is there any way to know if the EPM was causing this behavior?
You don't specify which test was used in your mare; there are some differences in interpretation depending on the method used. Low positives on any serum (blood) test may indicate an early response of the horse to the Sarcocystis neurona protozoa, a low dose of S. neurona in the body, or may be a a cross-reaction to another type of sarcocystis and actually be a false positive. Because of the length of time that has elapsed it would be difficult to attribute your mares signs to EPM.
Many other variables can play a part in the difficulty of bringing a sport horse up the levels.
Behavior, training, nutrition, and other musculoskeletal and orthopedic processes can lead to a wringing tail and gait deficits. Equine polysaccharide storage myopathy (EPSM or PSSM) and vitamin E deficiency are two specific disease syndromes that can cause some of the same signs as EPM. It sounds like she is no longer exhibiting these signs as she is currently in foal and hopefully healthy and well-fed. It is possible that EPM signs can return in horses that were previously infected, regardless of treatment history. Stress of pregnancy and lactation could provide an opportunity for pre-existing S. neurona to "take hold" and create damage to the central nervous system. Watch for neurologic or balance and weakness issues in your pregnant mare and advise your veterinarian of her past episode of tentative EPM.
A team approach would be ideal in determining if your mare should currently be assessed for EPM. A cerebrospinal fluid test exists that can be more definitive in making an EPM diagnosis, but it is not without risk to the horse and may not be a good idea in a pregnant horse. Pregnant mares must be treated for EPM with caution: sulfadiazine/pyrimethamine combinations (Rebalance is a brand) have been shown to have toxic effect on foals. Marquis and Protazil are safe and have been used in pregnancies, though none are specifically FDA-approved for use in pregnant mares.
Question: I have a 20-year-old Tennessee Walking horse mare that was observed as having hind-end ataxia in Fall 2009. I am located in Santa Fe, NM where we have a lower population of the carrier mammals. She came from Tennessee a couple of years prior. Could she have acquired the organism and not exhibited symptoms until 2-3 years later? Two blood titers performed in 2009 and 2010 resulted in nearly the same probability: 70-something percent chance that she has the organism. I administered one round of Marquis in 2009, which seemed to help with some strengthening of the hind-end and reduced stumbling. Since then, her symptoms have not changed significantly. Is this EPM or is something else going on? She has foaled 13-14 times in her past life prior to my ownership.
There are a few possibilities with your mare. Changes in muscular strength from age and multiple pregnancies and a history of living in an area (TN) with the carrier opposum species could all contribute to the hind-limb ataxia (unsteady, unbalanced) you describe. Nutrition, exercise, and regional disease could also be variables in a diagnosis in your girl.
The organism of EPM, Sarcocystis neurona, can lie dormant in the horses central nervous system for years before a bout of illness, stress, or time alone results in disease symptoms. Stumbling, neurologic deficits, hindlimb weakness, and muscle atrophy, especially if asymmetric, are symptoms of EPM. The blood tests she received in 2009 and 2010 indicate that she has been exposed to and developed antibodies against S. neurona in her lifetime. This test is a useful tool to focus our suspicion on EPM, however the blood test alone is not definitive for a diagnosis of EPM. In some cases, owners and veterinarians decide to further identify the protozoa by collecting cerebrospinal fluid (CSF) from the horse. The spinal fluid is used as an aid in diagnosis in horses with active clinical signs such as those you describe in your mare. The collection of CSF is not without risk to the horse and contaminated samples can cause inconclusive or false results.
The CSF testing is often reserved for horses in which the diagnosis would significantly change the treatment plan or affect the horses performance or quality of life. In many cases, diagnosis is achieved by administering a round of EPM treatments, such as the Marquis product that your mare received, and assessing changes in the patient. Subsequent improvement in EPM signs can lead to a presumptive diagnosis of EPM. Once successfully treated, EPM may remain in remission for months or years, but multiple reports of horses with recurring neurologic symptoms indicate that the protozoa is a difficult parasite to eradicate.
Question: My Thoroughbred gelding is 24-years-old and has Cushing's Disease and now we suspect EPM. He is being treated for both. What are the odds of a full recovery from EPM - I mean will I ever be able to ride him again?
According to current research information, around 70% of horses treated for EPM with appropriate medications and protocols will respond and return to their previous performance levels. Your horse is suffering from two separate diseases, however; so his return will depend on how readily each affected system (hormonal, or endocrine, and neurologic) is able to respond to treatments. There may be some overlap in symptoms from each disease. Hopefully the medications and management strategies will allow your guy to reach his full potential again. Your gelding is lucky to have you!
Question: My 11-year-old Appendix gelding was diagnosed/treated for EPM when he was 5 years old. He only showed very mild symptoms (easily pulled off balance with tail pull, stands "quirky" with legs crossed). I've ridden him moderately over the years, even doing some low hunter courses with him, but lately he seems to be getting weak. He slips and slides in our indoor arena, apparently not getting his hind feet firmly planted while cantering around. My question - can EPM return after a long "remission" and what can I do to strengthen my geldings' back and hindlegs so he doesn't slip so easily? Should we treat him again with medication?
Unfortunately, EPM is a disease process that can relapse after an apparently successful treatment regimine. The protozoal agent, Sarcocystis neurona, can lie dormant for many years before causing a horse to have any signs of neurologic instability. Weakness, balance deficits, lameness, and lack of coordination can all be symptoms of EPM. The same signs are found as well in a multitude of disease processes, including equine motor neuron disease, equine polysaccharide storage myopathy, and west nile virus syndrome. That said, I would strongly suggest having your veterinarian perform a full physical examination of your gelding to determine if an EPM relapse is happening. It is possible your vet will want to treat with another, longer-term course of medications. Traditionally sulfa drugs coupled with pyrimethamine were used to "paralyze" the protozoa. Newer drugs have come into use including ponazuril (Marquis) and nitazoxanide, or NTZ, (Navigator). Ponazuril is a form of a coccidiostat, a drug class that inhibits the replication of coccidia protozoa but may not effectively kill every organism in the central nervous system. Nitazoxanide was originally developed for human AIDS patients and has also been found to kill the sarcocystis protozoa. In the meantime, use caution working your gelding in order to prevent him from stumbling or falling and causing injury to himself or a rider/handler. Once he has been examined and a diagnosis made, exercises for restrengthening his topline and his hind limbs can include lots of walking, stretching his head, neck, and back long and low to activate his lumbar and gluteal muscles and lift his belly. Ensure that your arena footing is firm, not too deep, and not slippery. Walking up hills is an excellent strengthening routine once he is deemed safe to work.
Question: We seem to have a revolving door of opossums in our barn, despite trapping and relocating them. My concern is obviously EPM. Do we know what percentage of opossums carry the disease and how easily they can transfer it to horses?
Opossums are a tricky business in some barns! Like rodents, they are drawn to horse and cat feed, low-lying water sources and human garbage. Opossum prefer densely forested environments and riparian areas alongside rivers and streams along the West Coast and the southeastern coastal states. Horses become infected with S. neurona after ingesting the protozoa from the feces of opposum on pasture or in grain or hay, even in feeds shipped across country. EPM has been reported in nearly every region of the United States. It is difficult to say precisely what percentage of opossum carry the protozoa, but it has been found that an intermediate host is necessary to complete the sarcocystis life cycle and cause infection in the horse.
At this time, the natural intermediate host is not known definitively but is suspected to be raccoons, armadillo, birds, skunks, and/or cats. A study by Dr. Steven Reed et al found that 59% of tested raccoons were positive for S. neurona. Another study reported in the Canadian Journal of Research that 7% of domestic cats carry the parasite. The good news for your barn is that although many horses are exposed to S. neurona by opossum, the majority are able to mount an immune response and prevent infection. Studies show that only 1% of horses will suffer neurologic disease after being exposed to sarcocystis. Unfortunately, young, old, ill, or stressed horses are much more at risk for clinical EPM disease. Because the horse is an aberrant, or dead-end host of S. neurona, positive horses can't infect other horses.
Management at your barn should include sealing feed containers and keeping cat food out of reach, using high-sided tubs for feeding, keeping your horses healthy and current on vaccinations and deworming, and feeding heat-treated pelleted feeds to minimize the infective sporocysts in the ingredients. Wire-mesh fencing may deter the opossum from entering the barnyard. Minimizing the presence of intermediate hosts will decrease the infected opossum population.
Question: I have a 23-year-old gelding that was diagnosed and treated for EPM, but not sure when....at least a couple of years ago. He has been having the hind leg spasms since I've had him (one year now), but over the last month or so, he's occasionally been suffering from narcolepsy. He catches himself before he falls. He has also been stretching out his stance when just standing around. Are these signs of progression and will it become worse? I have given him ABC's holistic supplement without folic acid, but will this help him? He is in good weight, has a good appetite but doesn't lay down to sleep very often. Anything I can do for him? ANY info you can give me about EPM and what to do for him will be greatly appreciated.
A horse with Equine Protozoal Myeloencephalitis (EPM) may exhibit a variety of neurologic symptoms, including poor balance, spastic leg movements, or the signs you describe with the appearance of narcolepsy. Sarcocystis neurona, the parasitic protozoal agent of the disease, is found most commonly in geographical areas inhabited by the opposum. Horses that graze pastures where opposum have defecated are most at risk for acquiring S neurona. Amazingly, a number of these exposed horses never show EPM symptoms though some horses will harbor the dormant parasite for years before becoming ill.
Given the history you mention, I suspect your horse is one of the 10-20% of patients that suffer a relapse of EPM after previous successful treatment. A veterinary examination of your horses neurologic system and physical condition would be ideal at this time. Your veterinarian can help rule out other causes of 'narcolepsy' such as sleep deprivation leading to the buckling you describe as well as determine if another round of EPM antiprotozoal treatment would be useful.