In horse therapy the horses take care of us, but afterwards it's time to take care of them! EPM has been around since the 70's and continues to frustrate horse owners all over America! Heres an article from TheHorse.com on the background, present, and treatment of EPM. In the mean time show some love by visiting our website, at Equine Courses.
"Equine protozoal myeloencephalitis (EPM) continues to frustrate North American horse owners and veterinarians as one of the most common neurologic diseases in horses--and one of the most challenging to diagnose and treat. At the 2011 Western Veterinary Conference, held Feb. 20-24 in Las Vegas, Nev., Steve Reed, DVM, Dipl. ACVIM, of Rood & Riddle Equine Hospital in Lexington, Ky., delivered an overview of the disorder and discussed diagnostic and treatment options.
Background
Reed explained that EPM was first noted in Kentucky and Pennsylvania in the 1970s, and the causative organism (a protozoon calledSarcocystis neurona) was first identified in the 1980s. Later, researchers determined that S. neurona has a two-host life cycle. To complete its life cycle, this organism requires a definitive host (the opossum), which feeds on the muscles of a dead intermediate host (such as a raccoon, skunk, cat, or armadillo) containing S. neurona sarcocysts. Once ingested by the opossum these sarcocysts mature to their infective stage (sporocysts), which the opossum passes in its feces.
Horses, which are generally considered "dead-end hosts" (meaning they typically can't pass the protozoa on to other animals), contract the disease by ingesting infected matter, often grass or hay contaminated with opossum feces containing S. neurona sporocysts.
Traditionally, the prognosis for EPM has been poor, with many cases ending in euthanasia of the affected horse. While there is no cure for EPM, some treatments can ease the effects of the disease and allow the horse a longer, healthier life with EPM.
Diagnosis
Once infected, horses generally begin to display clinical signs, many of which are consistent with other neurologic diseases, Reed said. These signs include:
- Asymmetric muscle atrophy (wasting);
- Cranial nerve dysfunction;
- Ataxia (incoordination); and
- Dysphagia (difficulty swallowing).
Although the disease was first recognized more than 30 years ago, veterinarians have not yet found one single test that presents 100% accurate results, Reed noted. Veterinarians generally begin their diagnosis process with a neurologic exam. A presumptive diagnosis can be made with the neurologic exam alone; however, most veterinarians continue the process by running a blood or cerebrospinal fluid (CSF) test.
These tests, Reed cautioned, will only determine whether the horse has been exposed to the causative agent. At this point, neither is able to render a 100% positive diagnosis of EPM.
Currently, the most common EPM test is a quantitative test using either an indirect fluorescent antibody test (IFAT) or a surface antigen-1 ELISA test (SAG-1 ELISA). The test Reed most commonly uses is a ratio test that measures antibody concentration in blood and CSF and compares the two. Older testing methodologies such as the Western blot are still used but lack the benefit of being a quantitative assay. Reed explained, "The (Western blot) gives a reading of positive or negative as to the presence of antibodies in the serum or CSF, but it does not quantify the extent. Nor does it determine if a horse is only showing antibodies from a previous exposure, which can lead to false positive results."
Another diagnostic tool Reed discussed was the IFAT, which identifies surface antibodies (protein trigger on the surface of a pathogenic bacterium or virus) to S. neuronain a blood sample and indicates whether the horse has been exposed. The IFAT produces a quantifying number, or titer, that expresses the concentration of antibodies circulating in the horse's blood. In theory, a high concentration of antibodies in the blood indicates the horse is, or has been recently, exposed. Comparative titers taken a few weeks apart indicate if a horse's antibody level is rising. If the horse has clinical signs of neurologic disease and that titer is rising, then the test confirms active infection.
The IFAT test has been shown to help establish a probability of whether a horse has EPM, but like all tests it is not 100% accurate in confirming EPM. However, the claim is based on a small number of necropsies in an area of the country that has a low frequency of positive EPM cases, Reed cautioned. Another ELISA measuring the surface antigen SnSAG1 has also been used, but some strains of the S. neurona organism do not contain this surface antigen.
Researchers at the University of Kentucky Gluck Equine Research Center in Lexington have recently developed an ELISA test to detect the surface antigens SnSAG2 and SnSAG 3/4 that appears to be very accurate when the blood and CSF values are compared. A normal concentration of surface antigens is expected in CSF based on the concentration found in the blood, and when the amount in CFS is greater than would be expected based on this ratio, it can be assumed the antibody production in the CSF is a result of primary infection in the nervous system.
Finally, Reed discussed a study that examined this new test in more than 300 blood and CSF samples from horses presented with clinical signs suggestive of EPM. After analyzing the samples and necropsy results, the team noted that the higher the CSF titer level, the more likely the horse is to have EPM.
Treatment
Only a handful of treatment options are available for horses with EPM, Reed noted, adding that several previously available choices have been removed from the market. Two FDA-approved products are currently available for use in treating EPM: ponazuril and diclazuril.
Reed explained that ponazuril (marketed under the trade name Marquis), a paste administered orally over a 28-day period, has been effective in treating EPM in horses. Additionally, few side effects have been noted in treated horses, he noted.
For treatment to be effective the medication must reach a certain detectable level in the blood; Reed noted that in his experience some horses do not reach that blood level until 11 days following the beginning of treatment, and in a typical 28-day course, this means the horse receives just over half the benefit of a full course of treatment. He suggested that a loading dose of the medication (which is not currently within the labeled instructions) might aid in boosting the blood level sooner, and he indicated that the medication's manufacturer is investigating this possibility.
Reed also discussed a newly released EPM treatment: diclazuril (marketed under the trade name Protazil). He said he believes that this recently FDA-approved pelleted form of an existing EPM treatment will prove very helpful to EPM horses. The recommended dosage for protazil is 1mg/kg body weight fed over a 28-day course, like ponzuril, and its alfalfa-based pellet used as a top-dressing on the horse's normal grain ration makes it more amenable to some horses than a paste or injection. He also added that it might one day be possible to use pelleted diclazuril as a preventive EPM treatment, but he stressed that no studies have been completed to test this hypothesis.
He also noted that some veterinarians use the injectable medications diclazuril and toltrazuril to treat EPM. Other medications used to aid EPM horses with their clinical signs, but not treat the root cause, are dexamethazone, flunixin meglumine (Banamine), and dimethyl sulfoxide (DMSO). Reed noted that adding natural vitamin E (not synthetic, as he noted it is not absorbed well) to an EPM horse's diet could help reduce neurologic signs."
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