Diclazuril 8.3 % + Levamisole HCl 3% + Vitamin E Succinate 10,000 iu, Oral Suspension, 1000mL
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Equine protozoal myeloencephalitis (EPM) is a central nervous system (CNS) infection of horses with either of the apicomplexan protozoa Sarcocystis neurona or Neospora hughesi.1 EPM is a common neurologic disease of horses that occurs only in the Americas. EPM has been reported in most of the contiguous 48 states of the USA, southern Canada, Mexico, and several countries in Central and South America. In other countries, EPM is only seen occasionally in horses that have spent time in these environs.
Most cases of EPM are caused by the S. neurona protozoan. Horses become infected by ingesting the S. neurona sporocysts in contaminated feed, grass (while grazing) or water. The definitive host for S. neurona in North America is the opossum (Didelphis virginiana). These animals are notorious for eating or scavenging just about anything, and typically become infected by eating sarcocyst-containing muscle tissue from an infected intermediate host. Thereafter, infectious sporocysts are passed in the opossum’s feces.
EPM is an extremely serious disease that can cause devastating and lasting neurological damage in the horse and can ultimately prove fatal. It is also very common. In some areas of the U.S., over 90% of horses can be seropositive, meaning that they have been exposed to the S. neurona sporocysts. Horses with antibodies specific to N. hughesi have been found in 21 states and, in some locations, up to 20% of horses may be seropositive to this organism.2 The natural host(s) of N. hughesi have not yet been identified. Transplacental protozoal transmission with the birth of infected foals has been documented for N. hughesi but not for S. neurona.1 Fortunately, most horses are able to mount a sufficient immunological defense and only a very small percentage of horses seropositive to either parasite (around 1%) will develop clinical disease. EPM can also be difficult to diagnose because its signs often mimic other health problems in the horse and can range from mild to severe.
Common clinical signs of EPM can include:
- Ataxia (poor coordination)
- Spasticity (stiff movements)
- Abnormal gait
- Muscle weakness, particularly under exertion
- Muscle atrophy along the topline, or in muscles of the hindquarters
- Facial paralysis
- Difficulty swallowing
- Abnormal sweating.
- Head tilt
- Poor balance
- Leaning against stationary objects
Since the protozoawhich cause EPM can attack any part of the CNS, almost any neurologic indicator of EPM may present. EPM usually begins slowly and insidiously, but can also arise quickly and severely. Horses with EPM that involves the spinal cord often have asymmetric or symmetric weakness and ataxia of one to all limbs and muscle atrophy. In cases where the sacrocaudal spinal cord is involved, signs of cauda equina syndrome can present.1 EPM lesions in the spinal cord also may result in areas of spontaneous sweating, loss of reflexes and/or loss of cutaneous sensation. Signs of spinal cord involvement in EPM tend to be more common than signs of brain disease.
When brain disease as a result of EPM is present, the most common signs include depression, head tilt, and facial paralysis. Cranial nerve nuclei may be involved, and seizures, visual deficits or behavioral abnormalities can occur. Postmortem examinations of brain tissue of horses with EPM brain involvement evidence focal discoloration, hemorrhage, and/or malacia of CNS tissue.1,2 Protozoa may be found in association with a mixed inflammatory cellular response and neuronal destruction. Intravascular and tissue neutrophils and eosinophils, capillary endothelial cells and myelinated axons are also parasitized. In at least 75% of clinical cases, protozoa are not seen on H&E-stained sections.3
Any horse suspected of displaying clinical signs of EPM should be seen by an equine veterinarian immediately. EPM is treated with antiprotozoal drugs and immunomodulators.4 Many of these are currently available as compounded veterinary preparations.
Diclazuril exerts its anti-protozoan effect by inhibiting merozoite production. In horses, the oral absorption is 1.56% with a half-life of 43-65 hours. Other studies in horses have shown that at a dose of 1 mg/kg and 0.5 mg/kg the half-life is 55, and 87 hours, respectively, with peak concentration of 0.185 and 0.1 mcg/mL, respectively.4
Levamisole is effective against abomasal nematodes, small intestinal nematodes, large intestinal nematodes, and lungworms.4 Adult forms of species that are usually covered by levamisole include Haemonchus spp, Trichostrongylus spp, Teladorsagia spp, Ostertagia spp, Cooperia spp, Nematodirus spp, Bunostomum spp, Oesophagostomum spp, Chabertia spp, and Dictyocaulus vivipurus.
The Association of Racing Commissioners International Uniform Classification Guidelines for Foreign Substances has designated levamisole a CLASS 2 DRUG.
In addition to anti-protozoal medications, many veterinarians recommend supplementing these with between 5,000-10,000 IU per day of Vitamin E. In animals and humans, vitamin E has been shown to augment the function of the immune system. The literature holds that vitamin E may bolster the immune system to the point where the protozoa are unable to mount a defense against the medications being administered.
Where to buy Diclazuril + Levamisole + Vitamine E
Diclazuril + Levamisole + Vitamine E is available in the U.S. through veterinary custom compounding companies.
FOR RX ONLY: A valid prescription from a licensed veterinarian is required for dispensing this medication.
1Merck Veterinary Manual.
2Reed, S M et al. Equine Protozoal Myeloencephalitis: An Updated Consensus Statement with a Focus on Parasite Biology, Diagnosis, Treatment, and Prevention. Journal of veterinary internal medicine vol. 30,2 (2016): 491-502. doi:10.1111/jvim.13834.
3Dubey, J.P. et. al. (2001). A review of Sarcocystis neurona and equine protozoal myeloencephalitis (EPM). Veterinary parasitology. 95. 89-131. 10.1016/S0304-4017(00)00384-8.
4Mark G. Papich, M. Diclazuril: Pharmacology and mechanism of action. In: Saunders Handbook of Veterinary Drugs (Fourth Edition), 2016.