DICLAZURIL 8.3% / LEVAMISOLE 3% / VITAMINE E 10,000 iu Suspension For Treatment of EPM in Horses
Equine protozoal myeloencephalitis (EPM) is a disease that affects the central nervous system of horses and which is caused by the protozoal organism. The name given to the protozoan organism shown to be the primary causative agent for EPM is Sarcocystis neurona.
Background
Equine protozoal myeloencephalitis was first described in the 1960s as "segmental myelitis." By 1974, it was determined that this disease was caused by a protozoan organism. In the late 1990s, an organism called Neospora hughesi was shown to also cause EPM in horses,1 but in rare instances only.
EPM is a disease primarily of the Western Hemisphere and is not commonly seen in other parts of the world. According to the literature, many horses are exposed to the S. neurona parasite, evidenced by specific testing that has been on blood samples taken from horses around the country. These animals become seropositive for the S. neurona organism, but this does not reveal whether or not the horse has or will ever develop EPM. Fortunately, only a very small percentage of horses seropositive to either parasite (S. neurona or N. hughesi) ever develop EPM.
The Life Cycle and Transmission of EPM
Although much has been learned in recent years with respect to the life cycle of S. neurona, there remains much that is unknown. Sarcocystis neurona has a complex, two-host life cycle. This life cycle includes both a definitive host and several possible intermediate hosts. For clarification, the definitive host is that animal which sheds in its feces an infective form of the parasite, S. neurona.1 The intermediate host is that animal which does not shed an infective form but is a host where the parasite resides and is necessary for the parasite to complete its life cycle.
In 1995, the opossum was determined to be the definitive host of this parasite (there may possibly be other definitive hosts for this organism and we have just not yet identified them). The opossum sheds the infective form of the parasite in the feces; we call this infective form a “sporocyst.” The sporocyst is then ingested (eaten) by the horse. Once inside the horse, there is much that we do not know regarding what occurs next. The parasite does go through a maturation or reproductive phase and eventually produces a form of the parasite we call “merozoites.” Eventually (in only a very small percentage of horses) the merozoites reach the central nervous system, damage this vital area and create the disease condition we call EPM.1
Several animals fall into the category of intermediate hosts for S. neurona. Among these are skunks, armadillos, raccoons, cats and sea otters. Since it is not believed that the horse is a natural host for this parasite, the horse is often referenced as an "aberrant intermediate host."2
Symptoms of EPM in the Horse
Since EPM is a disease of the central nervous system (brain and spinal cord) and can affect multiple locations within the brain and spinal cord, the signs and severity of this disease can vary dramatically.
In recognizing and referencing symptoms of EPM, veterinarians usually cite "The 3 A's” of this disease: Asymmetry, Ataxia and Atrophy.
1. Asymmetry is a term we use to describe a symptom that is worse on one side of the body than on the opposite side. In other words, with EPM, the signs are generally worse on the left side than on the right or visa versa.
2. Ataxia is a term we use to describe incoordination or the inability of the horse to know exactly where its legs are, resulting in inability to move its legs and trunk normally.
3. Atrophy describes a condition where the muscles shrink from their normal size. With EPM, this results from damage to the nerves that normally control or “innervate” these muscles. Muscle atrophy is not seen in all cases of EPM, so it is not as consistent a sign of disease as is the asymmetrical ataxia.1
Thus, when EPM is present, "we will see horses that are uncoordinated and this uncoordination is usually worse on one side of the body as compared to the other side. These horses may or may not develop muscle atrophy. It is also common to see muscle weakness in these horses."1 Some horses may display abnormal gaits, lameness and loss of sensation along the face, neck or body.
EPM may progress rapidly or very slowly. Horses generally deteriorate over time, but some plateau for a period of time, only to worsen days, weeks or even months later. Strangely, it is reported that most horses afflicted with this debilitating disease continue to have a bright, alert temperament.
Diagnosis
Unfortunately, there is no single test for EPM that can be done which is 100% accurate in the live horse, although there are tests that can be utilized by the veterinarian to support their diagnosis of EPM, as well as to rule out other diseases which may present like EPM.
The most important evaluation done by the veterinarian in cases of suspected EPM is a neurologic examination.2 This is a specialized exam that is done to evaluate the function of the central nervous system of the horse. It may also be necessary that radiographs be taken of the neck region of the horse to determine if there is compression on the spinal cord, since clinical signs from pressure on the spinal cord can look very much like EPM.
The veterinarian may also draw blood during the examination process. In some cases, he or she may decide to collect spinal fluid from the horse by doing a spinal tap. The most accurate of the currently available EPM tests require submission of both blood and spinal fluid to the diagnostic lab. Analyses of blood and spinal fluid samples both support the diagnosis of EPM and also help rule out other diseases of the central nervous system.1
Prevention and Treatment of EPM in Horses
Treatment of EPM is challenging because S. neurona is an intracellular parasite and an expert in avoiding immune system attack. The three different anti-protozoal treatment modalities that have been typically used work on entirely different pharmacological principles. Traditionally, EPM was treated with combinations of pyrimethamine and a sulfonamide.2 This combination was, for many years, the only known treatment for EPM, although the duration of treatment was often prolonged.
In recent years however, medications to treat EPM have been refined significantly by custom compounding pharmacies. As indicated above, veterinarians did use the combination of sulfadiazine and pyrimethamine in the early days of EPM treatment, and it previously could be obtained as a compounded drug.
More recently, formulations containing diclazuril have been approved by the FDA. The function of diclazuril is in attacking the chloroplast function of the protozoa. These novel formulations often include antiparasitics such as levamisole, and Vitamin E to provide support for muscles that have atrophied.
For the prevention and treatment of EPM, the formulations mentioned above are available through custom compounding pharmacies in paste or suspension form. They are both given orally, but the type chosen will usually be contingent upon the owner or veterinarian's personal preference, the animal's temperament, the number of animals that need to be treated, travel considerations, and the like.
Suspension Preparations - Pros & Cons:
Pros
- One bottle treatment (30ml per day for 30 days)
- Not too thick to draw in a syringe
- Cost effective
- Easy travel bottle - Saves space
Cons
- Messy administration
- Potential for loss of medication if horse spits it out
- Bottle must be shaken to mix, with uneven distribution possible
- Spills and loss if bottle is dropped or tipped over
Both the paste and suspension versions are given orally, but the type chosen will usually be contingent upon the owner or veterinarian's personal preference, the animal's temperament, the number of animals that need to be treated, travel considerations, and the like.
1MacKay,
R., Morgan, K. DVM. Equine Protozoal
Myeloencephalitis. aaep.org.
2Equine Disease Quarterly, Jan. 2007.
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