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By Dr. Ali Forbes
Question: I purchased a mare with an unknown history about 3-4 years ago. We recently moved to a new barn, and she has been tripping and standing funny. She also has begun to lose weight. One of the other boarders mentioned that her horse had shown similar signs, and was diagnosed with EPM. What is EPM and how is it diagnosed? What treatments are available? Does it reoccur even after treatment? Thank you!
Answer:
Equine Protozoal Myeloencephalitis, or EPM, is a common neurologic disease found in our horse population. It is prevalent throughout the United Statesand Western hemisphere, and we see it frequently in the Mid-South. It is very non-discriminatory, and can affect all horses despite age, sex, and breed. The culprit? Parasites; specifically, Sarcocystis neurona and Neospora hughesi. The former is more common, while the latter was more recently discovered. Consequently, not much is known about N. hughesi. However, much has been researched and discovered about S. neurona.
How does your horse get infected? It’s a little complicated. The opossum is the definitive host (the animal that allows, inadvertently, the parasite to reach maturity). S. neurona completes its infective life cycle inside the gastrointestinal tract of the opossum, and then the horse, considered a “dead end host”, ingests fecal material that contains the parasite. This can be from water, grass, or anything else on the ground containing opossum poop that the horse finds tasty! Once in the stomach, the sporocysts (the infective stage of S. neurona’s life cycle) migrate from the gastrointestinal tract into the bloodstream, and then cross the blood brain barrier. Neurologic signs then can either occur rapidly, or be more progressive and subtle.
Once infected, one in about 50 horses will develop clinical signs. We are unsure of what makes some horses more predisposed than others. A horse’s immune system contributes, as well as the thought that horses who display clinical signs are infected by a more pathologic (virulent or severe) strain of the parasite. Parasite dose is also likely to be a factor. Horses that show clinical signs typically show the “three A’s” of EPM: asymmetry, atrophy, and ataxia. Ataxia is incoordination and not knowing where their legs are in space. Atrophy manifests in what comes across as weight loss, when really the horse is losing muscle mass. Both ataxia and atrophy can present as asymmetrical, or more apparent on one side of the horse than the other.
A definitive diagnosis of EPM can be difficult in the live horse. Typically, we try to meet three criteria: 1) the horse needs to have the clinical signs that make us suspicious of EPM, 2) confirm exposure by diagnostic tests, and 3) rule out other diseases that present similar to EPM. The first criterion is easy for veterinarians! The third criteria can consist of the following: x-rays of the skull and neck to help rule out diseases such as Cervical Vertebral Stenotic Myelopathy (Wobblers) or Temporohyoid Osteopathy (THO), and submitting tests to rule out Equine Herpes Virus, West Nile Virus, or other encephalopathies.
Once we have decided to test your horse for EPM, there are a few different options. In an ideal world, every horse would have both blood and cerebrospinal fluid (CSF) submitted for a SAG 2, 3, 4 ELISA test. Although this seems like a jumble of letters and numbers, what is analyzed is the ratio between CSF and blood titers (or exposure). If your ratio is less than 100, it is strongly suggestive of EPM. The CSF fluid can also be used to rule out other neurologic diseases. However, this does not test for the lesser known N. hughesi. Another test, which requires blood only and is thus less invasive, is called an IFAT, or immunofluorescent antibody test. Blood can be tested for both S. neurona and N. hughesi.
Once your horse is diagnosed, there are a few different drugs used to combat EPM that are approved by the FDA. The first is a combination of an antiprotozoal (Pyrimethamine) and antibiotics (sulfadiazine), known as Re-Balance. This combination is used for three to several months, and with the development of newer drugs, is not used much.
Ponazuril, or Marquis, inhibits the lifecycle of the parasite. This is given to your horse for 28 days, and can be repeated if necessary. Good success has been seen with Marquis. The last FDA approved drug is diclazuril, or Protazil, which is similar to Marquis, but is offered in impregnated alfalfa cubes for easy administration. As with all other aspects of equine health, treatment is multi-modal. Anti-inflammatories (Bute, Banamine, DMSO) can be used, especially during the first 1-2 weeks of treatment. Vitamin E and thiamine can also be used as neuroprotectants and are thought to aid in nervous tissue healing.
However you and your vet choose to treat EPM, there is always a possibility it will reoccur. Typically, because the horse initially responded well to the first treatment regime, we will use the same drug, just for a longer period of time. If necessary, we can change our treatment plan according to your horse’s response to therapy. Ways to either prevent your horse from contracting EPM, or minimize the possibility of recurrence, are: 1) watch for opossums and other pests, and “opossum proof” your barn, feed room, etc. 2) Monitor your horses closely during and after shows, transport, or any stressful event that may trigger the infection. 3) If you have any concerns at all, call your veterinarian! The sooner we get out there, the sooner we can begin making strides in diagnosing and treating your horse!
By Dr. Ali Forbes
Question: I purchased a mare with an unknown history about 3-4 years ago. We recently moved to a new barn, and she has been tripping and standing funny. She also has begun to lose weight. One of the other boarders mentioned that her horse had shown similar signs, and was diagnosed with EPM. What is EPM and how is it diagnosed? What treatments are available? Does it reoccur even after treatment? Thank you!
Answer:
Equine Protozoal Myeloencephalitis, or EPM, is a common neurologic disease found in our horse population. It is prevalent throughout the United Statesand Western hemisphere, and we see it frequently in the Mid-South. It is very non-discriminatory, and can affect all horses despite age, sex, and breed. The culprit? Parasites; specifically, Sarcocystis neurona and Neospora hughesi. The former is more common, while the latter was more recently discovered. Consequently, not much is known about N. hughesi. However, much has been researched and discovered about S. neurona.
How does your horse get infected? It’s a little complicated. The opossum is the definitive host (the animal that allows, inadvertently, the parasite to reach maturity). S. neurona completes its infective life cycle inside the gastrointestinal tract of the opossum, and then the horse, considered a “dead end host”, ingests fecal material that contains the parasite. This can be from water, grass, or anything else on the ground containing opossum poop that the horse finds tasty! Once in the stomach, the sporocysts (the infective stage of S. neurona’s life cycle) migrate from the gastrointestinal tract into the bloodstream, and then cross the blood brain barrier. Neurologic signs then can either occur rapidly, or be more progressive and subtle.
Once infected, one in about 50 horses will develop clinical signs. We are unsure of what makes some horses more predisposed than others. A horse’s immune system contributes, as well as the thought that horses who display clinical signs are infected by a more pathologic (virulent or severe) strain of the parasite. Parasite dose is also likely to be a factor. Horses that show clinical signs typically show the “three A’s” of EPM: asymmetry, atrophy, and ataxia. Ataxia is incoordination and not knowing where their legs are in space. Atrophy manifests in what comes across as weight loss, when really the horse is losing muscle mass. Both ataxia and atrophy can present as asymmetrical, or more apparent on one side of the horse than the other.
A definitive diagnosis of EPM can be difficult in the live horse. Typically, we try to meet three criteria: 1) the horse needs to have the clinical signs that make us suspicious of EPM, 2) confirm exposure by diagnostic tests, and 3) rule out other diseases that present similar to EPM. The first criterion is easy for veterinarians! The third criteria can consist of the following: x-rays of the skull and neck to help rule out diseases such as Cervical Vertebral Stenotic Myelopathy (Wobblers) or Temporohyoid Osteopathy (THO), and submitting tests to rule out Equine Herpes Virus, West Nile Virus, or other encephalopathies.
Once we have decided to test your horse for EPM, there are a few different options. In an ideal world, every horse would have both blood and cerebrospinal fluid (CSF) submitted for a SAG 2, 3, 4 ELISA test. Although this seems like a jumble of letters and numbers, what is analyzed is the ratio between CSF and blood titers (or exposure). If your ratio is less than 100, it is strongly suggestive of EPM. The CSF fluid can also be used to rule out other neurologic diseases. However, this does not test for the lesser known N. hughesi. Another test, which requires blood only and is thus less invasive, is called an IFAT, or immunofluorescent antibody test. Blood can be tested for both S. neurona and N. hughesi.
Once your horse is diagnosed, there are a few different drugs used to combat EPM that are approved by the FDA. The first is a combination of an antiprotozoal (Pyrimethamine) and antibiotics (sulfadiazine), known as Re-Balance. This combination is used for three to several months, and with the development of newer drugs, is not used much.
Ponazuril, or Marquis, inhibits the lifecycle of the parasite. This is given to your horse for 28 days, and can be repeated if necessary. Good success has been seen with Marquis. The last FDA approved drug is diclazuril, or Protazil, which is similar to Marquis, but is offered in impregnated alfalfa cubes for easy administration. As with all other aspects of equine health, treatment is multi-modal. Anti-inflammatories (Bute, Banamine, DMSO) can be used, especially during the first 1-2 weeks of treatment. Vitamin E and thiamine can also be used as neuroprotectants and are thought to aid in nervous tissue healing.
However you and your vet choose to treat EPM, there is always a possibility it will reoccur. Typically, because the horse initially responded well to the first treatment regime, we will use the same drug, just for a longer period of time. If necessary, we can change our treatment plan according to your horse’s response to therapy. Ways to either prevent your horse from contracting EPM, or minimize the possibility of recurrence, are: 1) watch for opossums and other pests, and “opossum proof” your barn, feed room, etc. 2) Monitor your horses closely during and after shows, transport, or any stressful event that may trigger the infection. 3) If you have any concerns at all, call your veterinarian! The sooner we get out there, the sooner we can begin making strides in diagnosing and treating your horse!
