Equine Protozoal Myeloencephalitis (EPM): Update on treatment

Twenty years ago when I first ventured into EPM research, the standard course of treatment was pyrimethamine (Daraprim®), a common anti-malarial drug, in combination with trimethoprim/sulfadiazine. We used a fairly low dose, and treated for only a few months. However, upon following up with some of those early cases, we discovered that this treatment was not sufficient. Researchers in Oklahoma (Clarke, 1992) found that a much higher dose of pyrimethamine is required to achieve drug levels in the cerebrospinal fluid sufficient to kill the protozoa. After these findings, we adjusted our recommendations to a combination therapy of pyrimethamine (1.0 mg/kg daily), in combination with sulfadiazine (20 mg/kg daily). It turns out that 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. It's been a long time since I patented that discovery, and there are many other options available now. This disease is absolutely curable, and if you stick to a program of appropriate treatment, you will be rewarded with a healthy horse.

Treatment for EPM has since taken many turns, and hopefully, new products will continue to be added to our arsenal for this disease.

• Pyrimethamine/sulfadiazine is still the most common treatment, because compounding pharmacies have made it very affordable. This is a product which interferes with nucleotide synthesis and therefore the production of DNA. Horses require treatment for 6 to 8 months on this drug combination, and sometimes much longer. The biggest problem with this medication is that the long duration of treatment makes compliance difficult. Many horses are taken off the medication too soon, resulting in relapse of clinical signs.

Side effects are most commonly bone marrow suppression which is manifested as anemia and leukopenia (low white blood cell count). This product is not safe in the third trimester of pregnancy, resulting in foals with profound bone marrow suppression and kidney damage. A less common side effect of this product is a neurologic syndrome of ataxia and facial nerve paralysis, which is usually reversible when the drug is discontinued.

• Ponazuril (Marquis®) is marketed as a paste formulation and has been available for over ten years. The label dose is 5 mg/kg for 28 days, but the relapse rate is high (35%) with this dose. Some studies have shown a higher efficacy with 10 mg/kg (or a double dose).

Minimal side effects are seen with ponazuril, although the safety studies indicated that with extremely high doses uterine edema is seen.

• Diclazuril (Protozil®) is marketed as a daily pellet feed top dress at 1 mg/kg for 28 days. This is a difficult product to recommend, since the company's own research had only a 42% efficacy rate. We had reasonable efficacy in the 1990's when we studied a dose of 5 mg/kg, but the Protozil is very expensive at that dosing rate.
• Nitazoxanide (NTZ) was approved right after Marquis in the early 2000's, but was taken off the market when Idexx dropped their pharmaceutical line. NTZ is very effective for EPM at 25 mg/kg for the first four days and then 50 mg/kg daily for 24 days. This product is highly soluble in fat, so added fat in the form of corn or other oil improves the absorption of the product. This product is only available as the human label tablets (Alinia®).

NTZ, while highly effective, has a number of serious side effects. Much of the product is not absorbed in the small intestines, and passes to the large colon, where it can alter the normal colonic flora. The end result can be absorption of endotoxins and in some cases diarrhea. Among the effects of the endotoxemia can be laminitis or founder. While uncommon, this possible sequela should be carefully watched for in the NTZ treated horse. In most horses, the concomitant administration of oil results in improved bioavailability, which results in less drug passing to the large colon, and a lower rate of side effects.

• Decoquinate has recently been suggested as an EPM treatment in combination with levamisole as an immunomodulator (Oroquin-10®) for a 10 day course of treatment. Decoquinate is extremely inexpensive in the form of Deccox premix, a poultry coccidiostat which is added to poultry feeds to prevent coccidia. At the recommended dose of 0.5 mg decoquinate/kg, 4 g of Deccox premix is sufficient for each daily treatment. In cell cultures, decoquinate is highly effective against the rapidly dividing merozoite stage of the EPM organism. The question remains as to whether the decoquinate actually crosses the blood-brain barrier to get to the parasite. Hopefully, further investigation will add this inexpensive treatment to our arsenal.

Oroquin-10 is a new treatment and as such there is no safety data available. The primary anti-protozoal ingredient, decoquinate, is very safe at high doses in horses. Levamisole has many potential side effects in humans, and has not been studied in horses.
• Oxytetracycline is effective against many protozoa in this class. The problem with this drug is that protozoa become rapidly resistant, so it may work for a short period, but treatment doesn't result in a cure. The advantage of this drug is that it can be used intravenously, and in the case of a horse that cannot swallow oxytetracycline provides a way to get treatment into the animal.

In general, oxytetracycline is a commonly used antibiotic in horses for a myriad of conditions, and is relatively safe. In rare cases, oxytetracycline can cause diarrhea.

In addition to the anti-protozoal treatment, immunomodulators like levamisole are warranted. In addition to levamisole, there are several approved immunomodulators, including EqStim ®, Equimune ® and Zylexis ®. I investigated EqStim in the 1990s as an adjunctive treatment for EPM with pyrimethamine/sulfadiazine and found that horses on average required two months less treatment before clearing the EPM antibodies from the cerebrospinal fluid (negative CSF test). Any immunomodulator may be effective, but less is known about levamisole, so my preference is to stick with the approved products like EqStim.

Anti-inflammatory treatments are an essential adjunctive treatment for EPM. More damage is caused by the inflammation surrounding the protozoa than the protozoa themselves. 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, a condition which I termed a “treatment crisis” twenty years ago.

Important supplemental therapies are the addition of neuroprotective supplements, such as vitamin E, folic acid and thiamine.

Now that I've explained the different options, I'll tell you my personal recommendations for the treatment of an acute EPM case. I'm not interested in messing around with unproven treatments, unless I have a chronic, relapsing horse with EPM. My standard recommendation is double Marquis (10 mg/kg) for 28 days, followed by pyrimethamine/sulfadiazine for four months. Unfortunately, even with the higher dose of Marquis, some horses will relapse, making the four months of pyrimethamine/sulfa necessary.

Many of the clinical signs associated with EPM are caused by inflammation rather than the parasites themselves. Therefore, almost all of my EPM patients receive DMSO and a short course of flunixin (Banamine ®) to reduce inflammation. I also recommend daily Vitamin E and folic acid. My preference for immunostimulation is EqStim, which I use at the label recommendation of days 0, 3 and 7 and then twice monthly after the initial series.

Equine Protozoal Myeloencephalitis (EPM): Back by Popular Demand

There is no end to the requests that I get to repost my EPM website.  In response to the requests, I have revamped the site and decided to post it here.  This current installment is the introduction, and clinical signs, diagnosis and treatment will follow over the next few weeks.  Keep checking back for the next installment.

He may stumble once or twice. At first you didn't think much of it, but now it's getting worse. He's not lame, just not the same. Or your yearling colt seems to be really clumsy. He drags his hind toes, but maybe its just a stage he's going through. Maybe your trail mare is starting to be a little unsure over the terrain. Or worse, your horse is stumbling, tripping or falling, worse behind. It could be the development of a lameness, or it could be something else.  

Equine Protozoal Myeloencephalitis (EPM) is an infection of the brain or spinal cord of horses that is most commonly insidious in onset with nebulous clinical signs. However, because the organism can affect any part of the central nervous system, clinical signs can vary widely. The neurologic signs that it causes are most commonly asymmetric incoordination (ataxia), weakness and spasticity, although they may mimic almost any neurologic condition. Clinical signs among horses with EPM include a wide array of symptoms that may result from primary or secondary problems. Some of the signs cannot be distinguished from other problems, such as lameness. Airway abnormalities, such as laryngeal hemiplegia (paralyzed flaps), dorsal displacement of the soft palate (snoring), or airway noise of undetermined origin may result from protozoa infecting the nerves which innervate the throat. Apparent lameness, particularly atypical lameness or slight gait asymmetry of the rear limbs are commonly caused by EPM. Focal muscle atrophy, or even generalized muscle atrophy or loss of condition may result. Secondary signs also occur with neurologic disease. Upward fixation of the patella (locking up of the stifle) is among the most common findings among horses with neurologic disease. Another common side effect of EPM is back soreness, which can be severe. Even typical racing injuries may ultimately be caused by EPM, because horses which are uncoordinated are much more likely to "take a bad step" in racing or training. Therefore, any horse with these signs should be carefully evaluated by your veterinarian for the presence of neurologic disease.

EPM was originally identified as a fatal neurologic disease of horses by Dr. Jim Rooney in the 1960s, who saw the characteristic inflammatory lesions in the spinal cord of horses. Protozoa were first identified in the lesions of affected horses in 1974. The protozoa was identified as being similar to other members of the genus Sarcocystis by Dr. JP Dubey, a senior researcher at the USDA, who named it Sarcocystis neurona in 1990. In 1996, my research identified the opossum as the definitive host and source of infection to horses of S. neurona. Over the next several years, I worked with several pharmaceutical companies worked to develop anti-protozoal treatments.

Like other species of Sarcocystis, S. neurona has a two host life cycle. The definitive host (opossum) consumes the muscle tissue of the intermediate host (skunks, raccoons, armadillos) containing protozoal cysts. The protozoa enter the intestinal cells and undergo sexual reproduction in the intestinal cells of the definitive host, forming the infective sporocysts which are passed in the feces of the definitive host. These sporocysts are ingested by the intermediate host, where they hatch in the intestines and pass into the bloodstream. In the intermediate host (skunks, raccoons, armadillos), the protozoa undergoes asexual reproduction in the blood vessels of the liver, lungs and muscles and then encysts in the intermediate host's muscle tissue, without traveling to the central nervous system. When this tissue is eaten by the opossum, the organism undergoes sexual reproduction in the intestinal cells, and forms the infective sporocysts, which are passed in the feces. The opossum does not become sick, but may shed the parasites for months.

Horses represent an aberrant host of S. neurona. Sporocysts are ingested, but never encyst in the tissues of the horse. Instead, they migrate to the central nervous system, where they continue to undergo asexual reproduction intracellularly in neurons, without forming tissue cysts. Horses cannot transmit the organism to other horses, or even to opossums. Horses probably eat the opossum sporocysts inadvertently while eating grass, hay or grain.

In one of my research studies, I was able to reproduce the disease by feeding opossum-derived sporocysts to horses. The horses had detectable serum antibodies at about 3 weeks after infection, and all of the horses that ultimately developed EPM had spinal fluid antibodies about a week later. Those that did not develop EPM never had antibodies in the spinal fluid, even as long as 4 months later.

This disease may be preventable by some simple measures. Anything that may attract opossums into barns should be tightly covered, or put away, especially at night. This includes cat food, garbage and grain. Opossums are particularly fond of cat and dog food. Feed should not be left out at night for the morning, or even during the day to attract birds. The opossum population should be kept under control on farms and stables, where possible. Mesh wire or chain link fencing with "hot wire" around the outside may keep opossums out, since they can climb, but they do not dig. The processes of steam-crimping and pelleting grain kills off the sporocysts, so using processed grains can also decrease the exposure to EPM.

Exposure of horses to EPM occurs at an average rate of about 50%, but approaches 80-90% among some groups of horses. It is impossible to predict which exposed horses will develop fulminant disease. Some horses with active disease may be able to clear the organism without treatment. Currently, the only approach to control of EPM is early detection of incoordination, gait or other abnormalities, definitive diagnosis of the disease by cerebrospinal fluid (CSF) analysis, and appropriate treatment. The disease probably requires a minimum of two weeks and up to two years to develop from the time of exposure to the development of marked clinical signs. Exposure rates (but not disease rates) for different farms or training facilities may vary from zero to 100% of the horses at a given location. Premises with very high seroprevalence appear also to have a high prevalence of clinical disease. Most horses probably ingest the sporocysts, mount an immune response, and clear the organisms before they reach the central nervous system. Alternatively, they may be persistently infected in the central nervous system, but are able to combat the organism sufficiently to prevent the development of clinical signs. There is no "dormant" stage, and there is no "remission.".

Developmental Orthopedic Diseases and Nutrition

Long name, sounds complicated.  "Developmental Orthopedic Diseases (DODs)" sounds difficult to understand and probably doesn't apply to me.  How could it have anything to do with my horse or foal?  Fact is, in young horses, DODs are extremely common and, if not managed properly from an early age, may lead to chronic unsoundnesses in the horse as he grows.  Most importantly, many of these conditions are preventable and/or treatable with nutritional management.

What are DODs?


DODs are exactly what the name implies.  As the foal/young horse grows, abnormalities of growth cause orthopedic problems to develop.  These may show up as tendon contractures, where the knees or ankles buckle forward when the foal is standing, physitis, where inflammation and pain occur in the growth plates, or osteochondrosis (OCD), where the normal ossification of cartilage is disrupted.  All of these conditions can result in chronic lamenesses or crooked legs or both.  These are conditions that develop in young foals to yearlings and primarily during phases of rapid growth.

What Causes DODs?


Normal growth and development depends upon a delicate balance of mineral availability, vitamin cofactors, normal hormone balance, exercise and injury prevention.  The easiest method of preventing DODs is to provide proper nutrition and regular exercise.  This sounds easy, but is actually more complicated than it sounds.  There are several points to consider. 


(1)  Major minerals such as calcium and phosphorus must be present in the diet of foals and adolescent horses in a ratio of 2:1.  Imbalances in these major minerals result in abnormal growth.  While it's fairly easy to make sure that the grain fed to a horse has the right ratio of minerals (because the feed companies make them that way), hay can vary widely.  In particular, alfalfa hay can have a calcium:phosphorus ratio of anywhere from 4:1 to 8:1, making balancing the minerals in the complete diet almost impossible, unless you have the hay analyzed.


(2)  Trace minerals such as zinc and copper, as well as vitamin cofactors are key elements of enzymes that build the cartilage and convert cartilage to bone (ossification) during growth.  All of the minerals must be present within a certain range of total intake and balance, because too much of one mineral can result in deficiencies of the others.  Just a mineral block is not enough, because horses don't know when they need minerals.


(3)  Glycemic index is a term that is gradually working its way into the common vernacular.  A feed with a high glycemic index causes a spike of blood glucose and insulin in the body.  A feed with a low glycemic index is not associated with this insulin and glucose response.  The reason that this is important is that these wildly variable fluctuations in glucose and insulin contribute to the abnormal cartilage growth that results in physitis and OCD.  Therefore, low glycemic index feeds are ideal for feeding young horses.


How do I prevent DODs?


Fortunately, all this research is not just available to you and me, it is also available to the feed companies.  Therefore, most feed companies that produce horse feed, and specifically specialty feeds for growing foals and young horses provide minerals in the correct balance in their feed already.  There are only a few additional things that we need to closely watch to make sure that there are no mistakes.


(1)  Seems counterintuitive, but DON'T allow foals to eat from the mare's feed.  Mare feed is designed for high calories in order to support milk production.  The gastrointestinal tract of foals is not able to properly digest grain until at least 3 months of age.  The only thing the grain will accomplish is to produce the dreaded high glycemic response.  Foal creep feeds such as Foal Starter and Creep (Progressive Nutrition) which are milk based feeds with cooked oats or barley are designed for the intestinal tract of the foal.


(2)  Feed grain mixtures that are designed to be fed with grass hay to growing horses.  If you must feed alfalfa hay, then get it analyzed and consult the nutritionist for the feed company to have a specific grain mixture recommendation.  It is critical that the calcium:phosphorus ratio is correct for growing horses, or tendon contractures, OCDs and physitis will be inevitable.


(3)  Diet balancer mineral products are perfectly balanced in minerals for your growing horse, but the quantity may vary depending upon the age, weight and how fast the horse is growing.  Fortunately, there is almost a standard formula for these products across feed companies.  Similar products are available from most feed companies (M30, Stamm 30, Grow N Win, Purina 32); my personal favorite is Proadvantage (Progressive Nutrition).  A "unit" of balancer turns out to about a pound, or a pint volume of feed, no matter which company's product you are using.  Progressive Nutrition makes a handy chart for the horse owner to use to determine how much diet balancer you need for a growing horse in his stage of growth (http://www.prognutrition.com/pdf/GrowthChartDailyFeedPlannerLT05.pdf).

How do I treat DODs?


I've discussed how to prevent DODs, but how are they treated?  Some of the conditions are more easily treated than others.  Many physitis cases and tendon contractures respond to nutritional therapy.  These conditions are associated with rapid growth, likely because the mineral intake is imbalanced, and bone growth requires a different set of minerals than tendon or cartilage growth.  If the minerals can be properly balanced and any deficiencies corrected, synchronous growth of all the structures can be restored.

In order to restore mineral balance, I will typically feed these young horses 1/2 to 1 pound more diet balancer than the recommended quantity for their stage of growth.  If they are on alfalfa hay, it has to be discontinued and replaced with grass hay.  In suckling foals, mineral supplementation can be achieved by administering a paste or drench mineral supplement, such as Rejuvenaide (Progressive Nutrition) or Foal Aide (Buckeye Nutrition).  Again, for foals that already have a DOD showing up, I administer 15 - 25% more than the label recommendation.  Fortunately, in suckling foals, contractures will respond within just a few days to this mineral supplementation.  Physitis may take longer to respond, because the bony enlargement associated with physitis doesn't go down; it just stops getting bigger, and the foal grows into them.

If trauma or concussion is contributing to the DOD, such as can be the case with physitis, some exercise restriction is recommended.  Generally, the young horse should be restricted to a small paddock with one other buddy, so that excessive concussion from "running with the herd" is avoided.

What about non-nutritional treatments?

Physitis:  Many people advocate the use of poultice to help remove heat from inflammation of the growth plate.  This may help, but the majority of the heat and abnormal cartilage is deep within the growth plate and unaffected by the poultice.  Topical anti-inflammatory treatment with Surpass may also help, but again will only affect the superficial parts of the growth plate.  If the young horse is actually stiff or lame with the physitis, systemic anti-inflammatory medication is warranted, preferably Equioxx for 2-3 weeks.  Other anti-inflammatory drugs such as bute can predispose to stomach ulcers, so should be used with Gastrogard.

If the physitis is actually causing asymmetry of growth such that the legs are becoming crooked, then some other intervention is required.  Non-invasive therapies include trimming the feet lower on the side of the physitis to encourage growth on that side.  Shock wave therapy of the affected side may decrease the pain associated with the inflammation, increase blood flow and decrease inflammation, thereby stimulating growth of the affected side of the physis, and ultimately straightening the leg.  Some people are also advocating internal or external blistering of the affected side of the growth plate, also to increase the blood flow.

If the angular limb deformity ("crookedness") is severe, then surgery, where a screw is placed across the growth plate on the less affected side is indicated.  A screw is used to slow growth on the faster growing side of the physis and then allow the more affected side to catch up.  When the leg is straight, the screw is removed.

Contracture:  Caught early, nutritional treatment should correct most cases of contracture.  If allowed to progress, then complex splinting procedures, or even surgery, where tendons and ligaments are cut may be necessary.

OCDs:  OCDs can be prevented, but not treated with nutritional therapy.  Most researchers agree that the very beginning of OCD occurs in utero, so adequate mineral balance in the pregnant mare, and particularly in third trimester is critical.  The early signs of OCD in the young horse usually becomes evident from 8 - 12 months of age.  Treatments in this age group range from adminstration of Adequan (polysulfated glycosaminoglycans) or Legend (hyaluronic acid) to feeding calcium containing supplements.  As previously discussed, imbalanced high calcium or high phosphorus diets can cause OCDs, so additional supplementation should probably be avoided.  Shock wave therapy to stimulate blood flow to cartilage may be useful.  Platelet Rich Plasma (PRP) has also been advocated because of the growth factors that may be present in the PRP.  Equine Growth Hormone also stimulates the presence of local growth factors in cartilage that may return normal function to the cartilage.  Finally, surgery to inject corticosteroids into the lesion or remove the abnormal cartilage may be necessary.

Conclusion:


If your equine interests include foals or young horses, then developmental orthopedic diseases should be at the top of your list of concerns.  The most important factor that you can control is the nutrition.  Do not allow your foal to eat from the mare's feed tub, and provide a creep feed designed for the foal's digestive tract.  Make sure that your young horse has good quality grass hay and feed a diet balancer that is designed to be used with grass hay.  Avoid high glycemic index grains, like sweet feed until at least 2 years of age.  Allow foals to run in groups and spend at least 8 hours a days in free turnout for exercise.  Follow these simple steps to lay the foundation for a healthy and sound partnership for life.

Everything you need to know about Deworming Horses

Everyone knows how to deworm horses. You buy an inexpensive dewormer from the feed store and give it to your horse. You need to rotate the dewormer every two months to prevent resistance in the parasites. The old method of tube worming isn't used anymore since the newer dewormer compounds have become available.

Actually, recent research on parasite resistance has blown this whole concept of rotational dewormers out of the water. It turns out that (1) eliminating parasites completely from horses is neither beneficial nor desirable, and (2) our diligent rotational deworming program has not prevented resistance in equine parasites, but rather is creating super-parasites.

Historically, animals and their parasites have evolved together, reaching an “agreement” where the animal's immune system keeps the parasites under control, and the parasite agrees not to kill the host upon which it depends. By eliminating all of the parasites, the animals' immune system can go into overdrive, ultimately predisposing the horse to develop allergies, and possibly autoimmune diseases. So, in reality, a low level of parasitism functions as an “immune optimizer” for the animal. It turns out that a fecal egg count of 0-500 reflects a low level of parasitism, which is optimal for the horse, but unlikely to cause parasite related disease. Over 500 epg indicates a possibly disease causing infestation.

The more disturbing concern is the possible production of super-parasites. Resistance to every major class of dewormer has been identified.  In the case of the most common equine parasite, strongyles, eggs are passed in the feces, they are not infective to the horse. They must hatch and develop into stage 3 larvae (L3), a process which is weather dependent. They do not develop at all below 46F or over 100F, making April – November the prime time for parasite transmission in most of the United States, including Kentucky. It turns out that a solid deworming after the first hard frost in the late fall with moxidectin will take care of the parasites for the rest of the winter. Once the weather starts to break in the spring, a fecal on all the horses at a farm is indicated to determine which horses are shedding. Since 20 % of the horses shed 80% of the parasite eggs, the key is to identify those horses and treat them regularly to keep the overall worm burden on the pastures down. The 80% of horses which are low shedders should be allowed to maintain this lower worm burden, and shed eggs that are not subjected to the selection pressure of rotational dewormers. This way, only a small number of the eggs on the pasture belong to the potential “super-parasites.”

After the first spring fecals and treatment of all horses with fecal egg counts over 500 epg, the fecals should be repeated on those treated horses in 4 weeks to determine if the worms were sensitive to dewormer used. If the counts are still high, that indicates that the worms on that farm are no longer sensitive to that dewormer. This resistance is now permanent for that farm, and it is of no value for use on that farm. Worms on specific locations have been tested as long as 20 years after resistance develops, and they are still resistant on that farm. The ineffective dewormer should be permanently left out of the dewormer rotation for that farm

The pre-patent period (time from consuming the infective L3 larvae to adulthood and production of eggs in the feces) of strongyles is about 60 days, so fecals should be repeated on all the horses in 2 months. Again, any horses with 500 or lower epg counts are considered to have low level infestations and do not need to be treated. Horses with over 500 epg have high infestations and require treatment. As a rule, those horses with high egg counts will be the same horses over and over, because they lack the appropriate immunty to control the infestation on their own. Therefore, this subset of “high shedders” require a rotational deworming program. The typical rotational program for this group of horses will sound pretty familiar: Oxibendazole (Anthelcide ®), Ivermectin, and Pyrantel (Strongid ®). The reason that all the horses should not be on the rotational program is that we want to encourage the subset of parasites that can be easily controlled by the horse's own immune system, and not indiscriminately kill off that group. This is the best way to prevent the development of a super-parasite, and also allow the horses to maintain a healthy, small population of worms to properly stimulate immunity.

There are other parasites besides those that produce eggs that can be measured in the feces. Because of these groups of parasites, all the horses in a group should be dewormed twice a year with either ivermectin or moxidectin. Firstly, the large strongyles have a pre-patent period of almost 6 -9 months and the larvae can migrate through the liver, mesentary and other abdominal organs. Therefore, horses should be wormed before the eggs can be detected in the feces.

The second group of parasites that are not typically found in a fecal egg count is the tapeworms. This group of worms has a stage of its life cycle in mites that live on the pasture, and horses actually pick up the infection by eating the mites on the grass. The larvae develop into adults which attach themselves to the mucosa in the region between the ileum and cecum and can cause colic. Tapeworm eggs are not usually found in the feces because they do not float in the typical fecal lab test. In order to keep tapeworms under control, we deworm at least once a year with either praziquantel, which is found in Quest Plus ® (moxidectin with praziquantel), or Equimax ® or Zimectrin Gold ® (ivermectin with praziquantel).

Next are the bots. Bot flies lay eggs on the horses hair, commonly on the neck and inner portions of the front limbs. As the horses itch themselves with their teeth, they pick off the eggs, which hatch in the mouth and travel to the stomach. The bot larvae attach to the stomach lining, causing stomach irritation, including ulcers. Typically we control bots by keeping the bot eggs scraped off the hair to prevent ingestion and also by deworming with either ivermectin or moxidection after the first frost in the fall to eliminate the bots.

Other parasites include habronema, which contributes to summer sores (non-healing wounds on the legs), conjunctivitis and other eye lesions, and onchocerca, which causes skin and eye lesions. Since these parasites don't produce eggs in the feces, twice yearly deworming with either ivermectin or moxidection controls these parasites.

Summary of Deworming Recommendations for Adult Horses:

1. Deworm with moxidection with praziquantel (Quest Plus ®) in the fall after the first frost to eliminate encysted strongyles, bots, onchocerca, habronema and tapeworms. This should control parasites for the rest of the winter.

2. Check fecals on all horses in the group about 4 weeks after the first warm days (7 – 10 days of consistently warm days in a row). Deworm all horses with egg counts over 500 with 5 day double dose fenbendazole (Panacur ®) to eliminate migrating larvae and encysted larvae.
3. Recheck all treated horses again in 10 – 14 days to determine if the fenbendazole was effective. If yes, then the Strongyles on the farm are not resistant to fenbendazole, so it is a good product to keep in the rotation.
4. Check fecals on all horses in the group 8 weeks after the first. This allows a full cycle of infective L3 larvae picked up after the first taste of Spring maturing into adult worms which shed eggs in the feces. Any horses whose immune systems are unable to control their parasites (high shedders) will have egg counts over 500 epg, and should be dewormed with the next compound in the rotation, pyrantel pamoate (Strongid®) . Again, fecals should be checked on those that were dewormed at 10-14 days to determine if the pyrantel was effective. Again, if the parasites are not resistant, this product can be kept in the rotation. Low shedders will have low egg counts (<500 epg) at both times.
5. Now you know which horses are “high shedders” and which are “low shedders.” After the next 8 weeks, all horses should be dewormed with Ivermectin with praziquantel (Ivermectin Gold ®, Equimax ®).
6. At the next 8 week point, deworm the “high shedders” with the next product in the rotation, oxibendazole (anthelcide). Again, recheck the fecals at 10-14 days to determine if this dewormer is effective on your farm.
7. At the next 8 week point, repeat the process, this time using pyrantel again, only if it effective in your location.
8. Next, deworm with Quest Plus after the first frost.

After following this program for a year, you should have a good idea which horses are the high shedders and which are the low shedders. If you have a stable population, then, your program will be similar year after year. All horses coming into the group should be dewormed with Quest Plus before joining the herd.

Foals add a different dimension to the program. Most adults develop immunity to worms, but foals have never been exposed, so deworming is of critical importance. The first worms that foals pick up are Strongyloides (threadworms), which they actually ingest in the milk of the mare. There is some debate about whether Strongyloides causes any disease in foals. However, current recommendations are to dewormed the mares with ivermectin within 24 – 48 hours of foaling to eliminate this parasite.

The next group of parasites that are important to foals are the ascarids, or roundworms. This group is one of the biggest problems groups, because the eggs hatch in the intestines and then burrow through the tissue of the foal and migrate through the lungs. Many foals develop a cough and even pneumonia as a result of the parasites migrating through the lung tissue. For this reason, the first deworming of foals should be with a product that will eliminate most of these migrating larvae. Therefore, this early deworming at 3-4 weeks of age is with ivermectin. Those ascarids that escape the ivermectin deworming will go on to develop into adults, which can then cause generalized unthriftiness and colic. Therefore, at 8 weeks, foals should be dewormed with pyrantel.

The early deworming program in foals is designed to treat for parasites that are not mature enough to produce eggs, so fecal egg counts are not of value. However, once the foals are out to 16 weeks, they should start on the fecal egg count program. Young horses should be checked every two months until after the first frost of their yearling year, after which they join the adult program. Yearlings are still at risk for ascarids, and consequently vigilance should be maintained until they are two-year-olds.

Summary of Deworming Recommendations for Foals:

1. Deworm mares with ivermectin within 24 – 48 hours of foaling to control Strongyloides (threadworms) infections in the foals.
2. Deworm with ivermectin at 3-4 weeks of age to treat migrating larvae of ascarids (roundworms).
3. Deworm with pyrantel at 8 weeks of age.
4. Start checking fecal egg counts at 8 week intervals starting at 16 weeks of age, and use rotational dewormers of oxibendazole, and pyrantel, when counts are high. Respiratory signs without evidence of infectious disease may be associated with migrating ascarids, and may require an additional deworming with either ivermectin or double fenbendazole. Recheck fecal egg counts 10-14 days after deworming to determine if the worms are susceptible to the dewormer product you are using. If the product you are using is not effective, you need to eliminate that product from your rotation.
5. Ivermectin is indicated at the next 8 week point, similar to the adult program.
6. The terms “high shedders” and “low shedders” aren't useful in this age group, because they tend to all have high egg counts, probably because of limited immunity at this age.
7. Continue to deworm at 8 week intervals until after the first frost, when moxidectin with praziquantel (Quest Plus ®) is indicated. Always carefully estimate the foal's weight and dose exactly according to weight to avoid accidental overdose.
8. Young horses join the adult fecal egg count and deworming program 4 weeks after the first break in the weather in the spring, although most yearlings of this age have not developed sufficient immunity to control the parasites themselves, and will carry a high worm burden. This group needs to continue on the rotational deworming program, with spot checking egg counts at 10-14 days post dewormer to determine resistance among the parasites on the farm.
9. By the spring of their two-year-old year, the pattern of “high shedder” and “low shedder” emerges, and you will be able to determine which horses must remain on a high frequency rotation, and which require only ivermectin or moxidectin with praziquantel twice a year.

Management Program to keep Parasitism in Check

Management programs will also help limit parasitism in horses, and are probably a bigger part of parasite control in warm regions of the country, where you cannot count on a hard frost to “reset” the environmental parasite clock.

The most critical factor is pasture rotation. If pastures can be rested for 2 – 4 weeks at a time, the fields can be harrowed to break up the manure piles, and over a 2 – 4 week period (shorter in temperatures over 70F, longer below 70F) the strongyle eggs hatch, and the infective L3 larvae emerge. After a period of time, if they are not ingested by a susceptible host (horses), they die off, leaving the pasture strongyle free. If pastures cannot be completely rested, an alternative species, such as sheep, cattle or goats can be grazed instead, because the parasites do not cross host species lines. If horses are kept in a sufficiently small pasture, an alternative to pasture rest is manure removal. The manure can be picked up and disposed of similar to stall muck. Composting, where the internal temperature of the piles reaches and maintains 165F will also kill off the parasites. Unfortunately, very little kills off ascarid eggs, and these eggs remain viable on pasture for up to 20 years.

This is the current state of the recommendations of the parasite experts at this time in order to optimize equine health and immunity as well as prevent further resistance among the equine parasites. For specific recommendations for your area of the country, contact your veterinarian.

Bleeding in Horses (EIPH)

Your racehorse stops at the top of the lane and slows to a crawl coming home. He may cool out slowly and may not drink water after the race. He may cough or snort and swallow while cooling out. Or he may have fresh red blood trickle out his nose. These are all common findings after a race when a horse “bleeds” from the lungs during a race. We all know that racehorses commonly “bleed,” but eventing horses and other types of speed competition horses like barrel racers also "bleed." Even racing greyhounds and some elite human athletes bleed from the lungs during exertion. For that matter, studies have shown that almost all racehorses bleed, and most event horses bleed.  Have you ever wondered why and exactly what goes wrong when they bleed? What about the best treatments/adjuncts? In this article, I'll try to answer some of your questions about this very frustrating malady.

What is “bleeding” or Exercise Induced Pulmonary Hemorrhage (EIPH)?

The lungs are specialized organs for oxygenating blood. The structure of the lungs are like a tree, with the trachea as the trunk, the bronchi as the branches and the tiny microscopic alveoli as the leaves. The tiny sac-like balloons of the alveoli are lined with tiny blood vessels (capillaries). It is across these capillary cells that oxygen enters the body and carbon dioxide is expelled. Each heart beat sends freshly oxygenated blood to the working muscles and the same amount of spent blood to the lungs to be recharged. During breathing at rest, the hemoglobin in the red cells is fully (100%) saturated as it passes through the lungs. During exercise in horses, the blood is traveling so fast that after passing through the lung, the blood is only partially oxygenated. Blood pressure increases both in the body to keep pace with the demand from the exercising muscles and in the lungs to get the same volume of blood through the lungs. This pressure ultimately breaks some of the capillaries causing loss of blood into the alveolar space. When enough capillaries break, the blood drains down the bronchi and into the trachea. The diagnosis is made by looking in the trachea for evidence of blood called endoscopy or “scoping.” EIPH occurs in just about all racehorses at some time or another.

How is EIPH prevented?

The first line of prevention of EIPH is Lasix (Salix, furosemide). Lasix is a diuretic that decreases plasma or blood volume which results in decreasing the blood pressure in the pulmonary (lung) circulation. It is a fine line between losing plasma volume necessary for preventing EIPH and losing so much that critical blood pressure to the muscles is decreased. Recently, Lasix has been proven beyond any doubt to prevent bleeding in racehorses.

The next group of drugs for preventing EIPH are the antifibrinolytic drugs Amidocarb (Amicar) and Tranexamic acid (Tranex). When a capillary breaks, the underlying exposed collagen stimulates platelets to collect and substances in the blood called clotting pro-factors to become activated, forming a clot. Part of the normal process in the clotting cascade is the simultaneous breakdown of that clot, called fibrinolysis. During exercise, both clotting and fibrinolysis are increased, as blood is recruited to sustain blood pressure. Amicar and Tranex prevent fibrinolysis, allowing the normal clotting process to seal the broken capillaries. Recent studies on Amicar actually increased racing times, indicating some interference with performance, which makes it a bleeding drug that should only be used if absolutely necessary.

Kentucky Red (Carbazochrome Salicylate) works by stabilizing the capillary membranes, preventing breakage. This is also the mechanism of action of vitamin C and bioflavonoids (including hesperidin), common supplements used for bleeding.

Estrogens (Premarin, estradial cyprionate or ECP, estrone sulfate) may have more than one mechanism. The primary function of estrogens is to increase platelet aggregation at the site of a capillary breakage. However, estrogen also has antifibrinolytic effects, similar to Amicar and Tranex.

Vitamin K is also commonly administered to prevent EIPH. Vitamin K is an important co-factor for several proteins in the clotting cascade.

Finally, a commonly used Chinese Herbal product called Yunnan Bai Yao can be used to prevent EIPH. This product shortens clotting times, and may have direct effects on platelets, similar to estrogen. There are numerous other herbal treatments, which may be administered daily for the purpose of strengthening capillaries, improving clotting function and oxygen exchange.

Flair ® nasal strips have actually been shown to decrease the severity of bleeding also. These products have the ability to hold the nostrils open, decreasing the work required by the horse to breathe.

My Horse Bled in a race, now what?

Bleeding is the result of capillary damage in the lungs. This is a similar injury to a bruise and can be as serious as a large hematoma. It takes at least 10 to 14 days for a bruise to reorganize and heal, and that is the same time frame that the lungs require to heal. If the horse is raced or does other speed work too soon after a significant bleeding episode, it is the equivalent of reinjuring a bruise or hematoma. The end result is a more significant injury that will take even longer to heal. Repeated trauma to the lungs has the same result as repeated trauma anywhere else: the tissue is unable to heal completely resulting in scar tissue formation. Scar tissue in the lungs cannot contribute to oxygen exchange, and is less flexible, making further episodes of bleeding more likely. Lung rest is the most important factor in recovering from EIPH.

The blood in the airways traps mucous and bacteria, so treatment for a horse that has bled includes bronchodilators to open the airways, most commonly Ventipulmin, and antibiotics to prevent a lung infection. Usually Ventipulmin is administered for 10 days to clear out blood and mucus in the airway, and antibiotics are administered for 7 days to prevent infection. Ideally, after a significant bleeding episode, it takes a full three weeks for a complete recovery.