Solving EPM

http://news.google.com/news?hl=en&ned=us&q=Equine+Protozoal+Myeloencephalitis+&btnG=Search+News
http://www.google.com/alerts?hl=en

Yahoo! Search:
http://search.yahoo.com/search?p=Equine+Protozoal+Myeloencephalitis&ei=UTF-8&fr=FP-tab-web-t&x=wrt

Ontario Resources
http://www.omafra.gov.on.ca/english/livestock/horses/facts/epm.htm
Dr. Bob Wright - Veterinary Scientist, Equine and Alternative Livestock/OMAF;Dr. Leslie Woodcock - Manager, Innovation and Risk Management Branch/OMAF; Dr. Dan Kenney - Staff Veterinarian, Ontario Veterinary College/ University of Guelph
Inquiries:
livestock@omaf.gov.on.ca

Mississippi State University

http://msucares.com/pubs/infosheets/is1586.htm
http://www.cvm.msstate.edu/staff/hopper_richard.html

Richard M. Hopper, D.V.M., A.C.T.
ProfessorDepartment of Pathobiology and Population Medicine
CONTACT INFORMATION:
College of Veterinary Medicine
Box 6100
Mississippi State, MS 39762-6100
Phone: 662-325-2194

IDEXX Laboratories

http://www.idexx.com/equine/pharmaceuticals/navigator/epm_faq.jsp

Google Search:
http://www.google.com/search?sourceid=navclient&ie=UTF-8&rls=GGLD,GGLD:2006-04,GGLD:en&q=Equine+Protozoal+Myeloencephalitis

http://www.dclahdvm.com/articles/epm.htm

You may want to call these guys although Clara seems to be the place to start:

James E. Meeker, D.V.M
Gail M. Waldman, D.V.M.
Lisa N. Baucom, D.V.M.
336-998-7131

http://www.equine-research-inc.com/x-lame2.htm

Equine Research

Please contact Equine Research, Inc. at
erisales@equine-research-inc.com
tele: 903 894-0131
fax: 903 894-9361

http://www.easterndrafthorse.com/Health/epm.htm

EQUINE PROTOZOAL MYELOENCEPHALITISUnderstanding This Debilitating Disease

For more information regarding EPM, contact your veterinarian or the
American Association of Equine Practitioners,
4070 Iron Works Pike,
Lexington, KY 40511,
(859) 233-0147.

http://www.xcodesign.com/aaep/displayArticles.cfm?ID=248
Equine Protozoal Myeloencephalitis

http://www.epmvaccine.com/consumer/default.html
Equine Protozoal Myeloencephalitis

http://www.yourhorseshealth.com/epm/index.html

http://www.yourhorseshealth.com/epm/treat.html

New Treatment For EPM

Equine Protozoal Myeloencephalitis (EPM) is a progressive, degenerative disease of the central nervous system of the horse. The disease is characterized by asymmetrical ataxia with or without muscle atrophy. There are several diseases of the central nervous system that can mimic EPM. It is important for the veterinarian to do a thorough neurological examination with appropriate laboratory diagnostic support such as a cerebrospinal (CSF) analysis. Early, accurate diagnosis and treatment offer the best chance for success.

Until recently there were no approved treatment products for EPM. Veterinarians, out of necessity, had to use products that had not been evaluated for efficacy or safety when used in treating horses with EPM. In July of 2001, the FDA approved Marquis (15% w/w ponazuril) Antiprotozoal Oral Paste, the first medication for the treatment of EPM in the United States. Marquis is manufactured by Bayer in Shawnee Mission, Kansas.

Marquis is a prescription medication. It is a unique paste formulation with a gel-like consistency. The active ingredient of Marquis is ponazuril, an anticoccidial compound with cidal activity against the protozoal parasite that causes EPM. The dosage regimen is 5 mg/kg (2.27 mg/lb) body weight given orally, once per day, for 28 consecutive days. This product is packaged with four syringe barrels of paste per box and a calibrated dosing ring for accuracy and ease of administration. Each syringe contains enough paste to treat one, 1200 pound horse for seven days. The four syringes comprise the entire 28 day treatment program. Marquis should be stored at controlled room temperature, between 59 and 86 F. This product has a 24 month shelf life.

Marquis has demonstrated activity against Sarcocystis neurona (the causative agent of EPM) in both the laboratory and field setting. Efficacy studies were conducted in five states by seven different investigators. These studies demonstrated the effectiveness of Marquis against naturally-occurring cases of EPM. Marquis has also been demonstrated to be safe when used according to label directions. Target animal safety studies* at up to six times (6X) the label dose for two times (2X) the label treatment duration, produced sporadic inappetence, occasional loose stools and, in three of four study mares, moderate uterine edema. The safe use of ponazuril in horses intended for breeding purposes, during pregnancy, or in lactating mares, has not been evaluated.

It is important to note that while Marquis may effectively clear the horse of S. neurona, it will have no effect on irreparable, central nervous system damage caused by the parasite prior to treatment. The prognosis for animals treated for EPM may be dependent upon the severity of the disease and the duration of infection before treatment. Early and accurate diagnosis followed by immediate treatment are critical for best clinical results.

http://www.ivis.org/proceedings/aaep/1997/Fenger.pdf

Equine Protozoal Myeloencephalitis
By Michel Levy, DVM
Issue No. 1, 1998

Prognosis:

Early detection and therapy increase the chance of successful treatment. Response to treatment is highly variable; many treated horses return to their original level of function, however, some may not respond completely. In these horses, too many nerve cells are often destroyed to allow a complete cure. It is also estimated that approximately 10% of the cases relapse after treatment is discontinued. Some horses are currently on medication indefinitely.
EPM can be a frustrating disease. If you have questions about the disease, consult with your veterinarian or give us a call at (765)494-8548.

Clara K. Fenger, DVM, PhD, DACVIM
74232.1063@compuserve.com

Also look @ the searches under her name in Google: Clara K. Fenger

Here is her home phone number, don't ask.

CLARA FENGER
42031 PURPLEBUSH AVE
LANCASTER, CA 93536
(661) 722-2942

It looks to me like she is the expert. Definitely check out the google searches.

Google map to her house? http://maps.google.com/maps?li=rwp&q=LANCASTER,+CA+93534

JBS

I am an equine veterinarian, originally from California. I received my DVM from the University of California at Davis in 1988, and went on to practice in a general large animal practice in 1988 and 1989. I joined The Ohio State University in order to get specialty training in a residency program in equine internal medicine, and received my board certification from the American College of Veterinary Internal Medicine in May 1992. While at OSU, I developed a special interest in neurologic disease of horses, particularly EPM. This led me to pursue a Ph.D. at the University of Kentucky, where an active research program in EPM under Dr. Dave Granstrom was ongoing. I completed the requirements for my PhD in December, 1995. Now, I have a private consulting firm and I consult for individual veterinarians and clients with EPM problems, as well as for corporations. I have developed a modified Western blot for EPM diagnosis at Neogen Corporation. If you have further questions about EPM, or have suggestions about this webpage, you can E-mail me. However, if you have questions regarding your own horse, your best resource is your own veterinarian. I answer all E- mail about general problems that I have omitted from this page, excluding individual horse questions (I will answer any individual horse questions from veterinarians). Occasionally, my server does not recognize an E-mail address and my E-mail response is sent back. If you try to send me a note and I don't respond, you may want to try again, and include your E-mail address in the text of your message.

If you would like to make a tax deductible contribution to the research effort directed at prevention and treatment of this disease, you can send me an E-mail me, and I will forward information to you about donating to the most promising and active programs studying this devastating disease.

Copies of my dissertation are available from University Microfilms, Inc. Keeping watching this space for specific ordering information.

http://ourworld.compuserve.com/homepages/drfenger/

The most exciting new development in the area of EPM research is the advent of new and different alternatives for treating EPM. There are no FDA approved drugs for the treatment of this disease, but a number of drugs have been used off-label, or imported from other countries for treating EPM. The most common treatment is still a combination therapy of pyrimethamine (1.0 mg/kg daily), in combination with sulfadiazine (20 mg/kg daily), most commonly available from compounding pharmacies . This combination is protected by a patent, and current legally licensed pharmacies include Vet's Choice (888-809-3710). Horses should remain on both drugs for the duration of treatment, because protozoa have been shown to become resistant to pyrimethamine in the absence of sulfas. Trimethoprim is not recommended, and probably should be avoided, if possible, because it is likely to add to the toxicity of the pyrimethamine, without adding to the efficacy (Fenger et al., 1997, b). Beware of compounding pharmacies that compound a combination product with trimethoprim, pyrimethamine and sulfadiazine, because the trimethoprim is contraindicated. Ideally, CSF should be obtained and determined to test negative by immunoblot before the treatment is discontinued (Fenger et al., 1997, b), although this approach is likely to be extremely conservative, and many horses may actually continue to test positive for several months after the protozoa is killed.

Antiinflammatory therapy is indicated in acute EPM cases. This may include treatment with phenylbutazone or banamine (1.1 mg/kg 1-2 times daily for 3-7 days), as well as the addition of DMSO (1 g/kg in a 10% solution) administered either intravenously or by nasogastric tube. Corticosteroids may be used if necessary. Antiinflammatory drugs are occasionally necessary at other times during the first six weeks of treatment. Some horses actually get worse during treatment, presumably because of a reaction to the dying parasites (Fenger et al., 1997, b). Supplementation with vitamin E, folic acid and thiamine may be helpful adjunct treatment (Fenger et al., 1997, b). Some recent evidence has put the use of folic acid supplementation into question. However, it is probably safe and recommended for most performance horses, but not recommended for use in pregnant animals.

Thank you for visiting the EPM home page. Look for regular updates as more research becomes available. This website is under construction and should undergo many changes as my HTML literacy increases. Look for photos of cases and parasites in the future. The author is a veterinarian and a primary researcher studying EPM, not a professional computer whiz. If you have specific questions about EPM, or ideas that would improve my site, please let me know. The data maintained in this website is intended to educate horsepeople and veterinarians, and not intended to diagnose or prescribe treatment for any specific horse. The information kept here has been carefully researched, but inaccuracies may exist due to lack of information at this time, or typographical errors. Because of this, I cannot be responsible for any problems that arise as a result of the information on this website. If you have questions about a specific case, your best resource is your own veterinarian.

Pepper's current daily treatment and preventative regime

In Water Daily:
Put all water supplements in one bucket during the day, add second bucket for overnight
1 tbsp Epsom salts
2 tablets Nuxvomica (do not let pellets touch hands – put in cap and directly in water)
4 tablets Apis Mellifica (do not let pellets touch hands – put in cap and directly in water)
capful of imprint water
1 litre of colloidal silver water (big jug)

Sublingual (under Pepper’s tongue):
1000 mcg B12 twice daily (1 tablet)

In Feed:
3 tablets selenium twice daily (200 mg each)
1 capsule Vit E twice daily (400 IU)
2 capsules Moducare twice daily
1 Ginseng capsule twice daily
2 tbsp blackstrap molasses twice daily
2 tbsp sulphur twice daily
1 scoop Biotic 8 twice daily

2 Tbsp Tetracycline twice daily

1 tsp limestone ONCE daily
1 scoop Synovicare ONCE daily

10 cc Lubrisyn TWICE daily (Hyluronic Acid liquid) with syringe into side of mouth

Pepper’s grain feed is oats and cracked corn – no pelleted or extruded feed

Carrots at each meal

About 8 flakes of hay per day spread over 6 feedings

What Is EPM?: The History

Equine protozoa myeloencephalitis (EPM) is a progressive neurologic disease of horses found in both North and South America. The disease was first identified by in 1964 by J.R. Rooney, who recognized the protozoa in spinal cord lesions in Standardbreds (Rooney as cited in MacKay, 1997). Similar lesions were also identified by R.Macruz in Brazil around the same time (Macruz as cited in MacKay, 1997). Since this time, EPM has appeared in most of the lower 48 states as well as Panama and Canada with some "unofficial" reports from Venezuela, Argentina, and Mexico.
When this protozoa was first isolated it was thought to be Toxoplasma gondii, a microorganism which characteristically produces lesions. However, in 1974, J.P.Dubey (1974) was able to culture an organism from an infected horse and found it to be Sarcocystis (Dubey (1974) as cited in MacKay, 1997). This genus is named for its terminal developmental stage, sarcocyst, that is found in the striated muscle (i.e. skeletal muscle) of the intermediate host. The organism was named Sarcocystis neurona due to the fact that it usually develops within the neurons (EPM Seminar, University of Missouri, 1995).

Chinese herbs

For EPM horses and horses with EPM-like symptoms, we now have very encouraging news regarding the use of herbs. Both western and Chinese herbs have brought about many very positive results. Rapid, dramatic turnarounds have been achieved in many cases, even in some that were considered hopeless.

In Albuquerque, New Mexico a pair of holistically minded individuals, Mona Boudreaux, DVM, and Gary Allen, LAc, are teaching the secrets of their herbal success to veterinarians around the country through a course on Chinese herbs and how to use them effectively. Though Dr. Allen, a horse owner and human acupuncturist, and Dr. Boudreaux, a small animal veterinarian who practices only complementary medicine, are not equine specialists, they do know their herbs and are experts in the field of Chinese medicine. That is what they emphasize - Chinese medicine - when they teach their course to small and large animal veterinarians.

Patti Duffy-Salmon, owner and master herbalist of Meadowsweet Acre Herbs, specializes in custom blended herbs for horses, especially for the EPM horse, laminitis, Cushings and PMS mares.

Meadowsweet Acre Herbs Inc© 931-684-8838 email psalmon@cafes.net

Equine Protozoal Myeloencephalitis

Introduction and Etiology: Equine protozoal myeloencephalitis ( EPM) is a progressive, degenerative neurological disease of the central nervous system that has been described in horses for over 30 years. The disease is one of the most commonly diagnosed neurological disorders of horses in the United States. A recent USDA study revealed an incidence of 14 new cases of EPM diagnosed per 10,000 horses per year in the United States. While great strides have been made throughout the last decade in an effort to understand EPM, many questions remain unanswered concerning its etiology, pathogenesis, occurrence, treatment, and diagnosis.

Sarcocystis neurona is by far the most commonly implicated agent in cases of EPM; however, recent investigation implies that the syndrome, in rare cases, can be caused by Neospora caninum and/or Neospora hughesi infections as well. Unfortunately, infection with these other protozoan species is clinically indistinguishable from infection with Sarcocystis neurona. For the purpose of this paper, only infection with Sarcocystis neurona as a causative agent of EPM will be described.

Pathogenesis: The definitive host of Sarcocystis neurona is the opossum. Infected opossums shed sporocysts in feces which are in turn infective to the intermediate host when ingested. Many intermediate hosts are currently recognized in the life cycle of this protozoan, and the full range of hosts has yet to be identified. Current species implicated include cats, armadillos, skunks, raccoons, and sea otters. Once the intermediate host is infected, it goes on to develop sarcocysts in its skeletal muscle. When this muscle is ingested by the opossum, the life cycle is completed.

The horse is considered an aberrant or dead-end host of Sarcocystis neurona. While the horse is presumably infected by ingestion of sporocysts in contaminated feed and water, there are many unanswered questions concerning the pathogenesis of this protozoan once it actually infects the horse. It is suggested that sporozoites released from the ingested sporocysts are able to penetrate the intestinal wall and enter arterial endothelial cells. Schizonts then develop in these cells until they rupture releasing merozoites into the bloodstream. This stage of the life cycle may be repeated several times producing large amounts of merozoites. At this point, the infection can be cleared leading to seropositivity but no clinical signs or the protozoan can progress to the central nervous system. It is unknown how S. neurona enters the CNS in horses. It has been suggested that merozoites enter the CNS via infected leukocytes or through the cytoplasm of endothelial cells. Once the merozoite has gained access, schizonts form in one or more areas of the central nervous system including the cerebrum, the cerebellum, the brainstem, cranial nerves, and/or the spinal cord. Schizonts and daughter merozoites in the neural tissue remain uninfective and, therefore, transmission from the infected horse to other animals is not possible.

Recent studies suggest that anywhere between 22-65% of horses in the United States are seropositive with S. neurona antibodies, depending on the geographic location. Although several theories have been developed concerning why only some horses develop clinical disease, the reason is unknown. Theoretical contributing factors to the development of this disease include stress and other unrelated health events that occur before the onset of clinical EPM. In addition, little is known concerning the incubation period between exposure to the protozoan and development of clinical disease.

Clinical Pathology and Necropsy Findings: No characteristic changes are seen in the hemogram or serum chemistries found in horses affected with equine protozoal myeloencephalitis. Cytological examination of cerebral spinal fluid typically does not reveal significant changes. Gross pathological changes are apparent in the affected portions of the brain and spinal cord, and include multifocal areas of hemorrhage and malacia or both grey and white matter. Gross changes of muscular atrophy may also be seen in the skeletal muscle of affected horses. Histological examination of affected nervous tissue reveals neuronal necrosis and loss in addition to marked mononuclear perivascular cuffing. Infiltration of monocytes, lymphocytes, some eosinophils, and rare neutrophils can also be observed. Direct visualization of the organism is often not achieved because they are often present in very low numbers. This is especially true if the animal has been previously treated with antiprotozoal medications.

Diagnosis: A definitive diagnosis of EPM in a live horse is challenging. Simple seropositivity toward S. neurona antigen is inadequate for diagnosis since the protozoan must enter the central nervous system from the systemic blood circulation in order to cause the disease. In other words, a seropositive horse has been exposed to the organism, but may or may not have EPM. While there are several tests available to diagnose EPM, all of them are problematic.

The most recent major advance in diagnosis is the introduction of the immunoblot test for detection of IgG antibodies against Sarcocystis neurona.

Antibodies detected in the cerebral spinal fluid (CSF) provide support for a diagnosis of EPM. However, if the CSF is accidentally contaminated with blood during the procedure, a false positive can result. For this reason, it is recommended that only CSF samples with less than 50 RBCs/μL be submitted for immunoblot testing. It has also been suggested that limited antibody movement into the CSF can occur without the presence of CNS disease. This could also result in a false positive immunoblot test result.

Although the immunoblot test is reported to have a sensitivity and specificity of 89%, a recent study by Daft et al determined that the specificity of the Western blot test (a type of immunoblot test is between 44-60%. These results, as well as the risk of a false positive test, suggest that the use of immunoblot analysis is most useful in ruling out EPM rather than diagnosing the disease.

Other diagnostic tests for EPM include polymerase chain reaction (PCR) testing, the albumin quotient test, and the IgG index test. While PCR testing can detect minute amounts of protozoan DNA, the rapid destruction of DNA in the CSF environment and the possibility that DNA may not be present in the CSF makes the sensitivity of this test questionable. The albumin quotient test was developed to detect contamination of the CSF sample with blood. Unfortunately, the test does not decipher whether the contamination is iatrogenic or a simple “leakage” of protein through the blood-brain barrier. The IgG index test was developed to detect the production of IgG in the CSF. However, subsequent studies have found little difference between index values of EPM-affected horses and normal control horses.

The detection of characteristic lesions on necropsy is considered the gold standard of diagnosis by some. Due to the small number of organisms needed to cause the disease, however, the diagnosis can be missed even with a full neurologic necropsy. In general for the live animal, a clinical diagnosis is best established in horses with neurological disease consistent with EPM and a positive immunoblot test or an uncontaminated CSF sample. Another clue for diagnosis is an improvement of clinical signs in response to treatment of EPM. Overall, it is imperative that the diagnosis be based not only on test results, but in conjunction with a thorough diagnostic examination that rules out other causes of neurological disease.

Treatment and Prognosis: Treatment of equine protozoal myeloencephalitis is expensive, and even mildly affected horses can require prolonged therapy. The standard treatment for many years has been combinations of antifolate drugs including sulfadiazine and pyrimethamine with or without trimethoprim. The use of folic acid supplements in conjunction with this therapy has been recommended by some in an effort to reduce the risk of folic acid deficiency. A recent case report showed that supplementation failed to prevent the development of folic acid deficiency, however. The use of nonsteroidal anti-inflammatory medi-cations in conjunction with traditional therapy has been routinely used for many years. Supplementation with various vitamins has been recommended by some as well as the use of acupuncture in an effort to treat EPM; however, the efficacies of these practices have not been proven in clinical trials.

The most recent breakthrough in the treatment of EPM is the development of triazine-derivative drugs. These medications were initially developed as herbicides and have historically been used as coccidiostats in poultry and swine. Ponazuril (Marquis™) is a member of this family, and is the first approved medication for the treatment of EPM. Other drugs in this class include diclazuril and toltrazuril. Ponazuril is a primary metabolite of toltrazuril, and has shown anticoccidial activity against several parasites, including Sarcocystis neurona. Treatment regimen requires once a day dosing for 28-56 days. While studies show ponazuril can effectively rid horses of S. neurona, it does not improve the CNS damage that occurs before treatment begins.

Studies estimate that clinical improvement can be seen in 70% of treated horses, but fewer than 25% return to original function. Relapse of disease occurs in approximately 5-28% of horses when treatment is discontinued. The mechanism of this relapse is unknown, but reemergence of a latent stage parasite, persistence of a small focus of infection despite treatment, and reexposure to S. neurona have all been proposed.

Prevention and Control: Due to the lifestyle and eating habits of the definitive host of Sarcocystis neurona (the opossum), prevention and control of EPM are potentially problematic. Current recommendations include preventing access of opossums to hay, grain, pasture, and water sources. This may be difficult, especially if food and water are in short supply for the opossum. The most reasonable and simple precaution for horse owners to take is to deny access of stored hay and grain bins to the opossum.

The opossum is considered a scavenger and will consume whatever is available to it, including road-kill. Recommendations to prevent EPM commonly include picking up road-kill in the immediate area. This suggestion may be somewhat ineffective, however, since there are likely many other unknown intermediate hosts that are perpetuating the lifecycle.

A killed vaccine against Sarcocystis neurona has been developed using merozoites. No clinical evidence supports the efficacy of the vaccine and little research has been completed to date, however. Overall, there are few suggestions to aid in the prevention of Sarcocystis neurona exposure.

-by Katherine Gilmor, Class of 2004

-edited by Dr. Theresa Boulineau, ADDL Graduate student

Equine Protozoan Myeloencephalitis (EPM) ¹

James Rooney, a recently retired Doctor of Veterinary medicine from the University of Kentucky, identified a mysterious neurologic condition in 1964 that later gained the name Equine Protozoan Myeloencephalitis. The name literally means Horse disease caused by a protozoan (organism) that affects the muscles of the central nervous tissue. Ten years later research teams recognized the protozoa and learned the extent of distribution of what was once thought a rare disease.

The organism, Sarcocystis neurona, a single celled animal, can cause a neurological disease in equines of any age, sex, and location throughout the USA. The parasite cycle involves two animals: birds eat both plants and other animals of prey that carry the sporocysts of the organism. The opossum, the host responsible for ultimately carrying the protozoan to the horse, eats birds killed by the effects of the disease. The organism reproduces sexually in the opossum and is passed out in the feces. The horse picks up the organism by eating opossum feces dropped in feed or hay. The horse is a dead-end host, meaning the horse is non-contagious.

A growing problem? Many scientists and veterinarians alike have come to a realistic idea that this disease has been present for longer than twenty years, while considering the rise of incidence. In the start of the infection horses will display asymmetric incoordination (or incoordination on one side of the horse or the other), and loss of proprioception (or loss of sense of awareness of the position of the limbs). People may confuse this with a lameness . Not all horses exposed to EPM will show signs and some may develop an immunity and fight off the disease. Variations of the clinical signs depends on how much tissue damage is done, and may include various levels of seizure, muscle atrophy (leading to loss of ability to use muscles), and facial paralysis.

Antiprotozoal drugs are used in treating EPM, which drugs which kill the protozoan. The most common is trimethoprim-sulfamethoxazole, an antimicrobial. Anti-inflammatory therapy is recommended and supplements of vitamins E and folic acid may aid in treatment. The prognosis is variable. Approximately 60% respond to the therapy. Some undesirable effects of treatment may occur, and depending on the amount of nerve tissue damage, there is no reversibility with treatment.

The best preventative to EPM is to control the contact between opossums and your horses in and around your barn. Keeping all food covered and out of range is an essential practice (especially if there is cat food around). Any person with a trained and precise eye should consider EPM when evaluating a lame horse. The key is to catch the disease early in order to effect a full recovery. There is also a higher incidence in stressed horses; for example, a race track may have an 80-90% occurrence rate. It is helpful to know that the disease takes a minimum of two weeks to two years from exposure to time it shows signs. There is presently no vaccine, and labs estimate 20 years before an effective vaccine is available.

I have a spectacular Holsteiner gelding - Sergent Pepper - who has EPM and is not completely reponding to treatment.

This blog is to collect information and to make contacts to have my lovely man be healthy again - and hopefully support the same for other horses.

This is an epidemic issue and my local veterinary community, led by the vet school don't recognize it, treat it or consider it.