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Polysaccharide Storage Myopathy (PSSM)
Dr. Cat Ruksznis
Let's face it: no one wants to go to work on Monday morning. In the days where 'horse power' really did refer to the draft horses pulling the cart, their drivers noticed that even the horses were reluctant to move on Mondays. In fact, this condition was dubbed "Monday Morning Disease" - horses were stiff and slow on Monday mornings after a weekend off while still on full feed. We know this disease by many different names today - tying up, rhadbomyolysis, azotemia, etc. Earlier observations to the contrary, this is a true disease of the muscles (mypoathy), not a coffee deficiency! Although horses may develop this disease sporadically, there are also horses with an underlying genetic predispositions. Polysaccharide Storage Myopathy (PSSM) is one such muscle disease.
What causes PSSM?
There are two types of PSSM: type 1, in which the specific genetic mutation has been identified, and type 2, a category which is essentially a catch-all for horses with PSSM that do not have the known mutation. As the name suggests, these horses have abnormal accumulation of a polysaccharide (a sugar) in their muscle cells. Type 1 PSSM is most common in horses descended from Continental European draft breeds (Quarter Horses, Warmbloods, Appaloosas) and has been found in over 20 breeds. These breeds have a mutation in the enzyme responsible for making glycogen (GYS1). Glycogen is a type of sugar which is normally stored in skeletal muscle fibers and used for energy during the first 20 minutes of exercise. In horses with PSSM, there is a greater amount of abnormally constructed glycogen created, which accumulates in the muscle cells. Although the link between abnormal glycogen and muscle cell damage has not been fully elucidated, we do know that the increased activity of the GYS1 enzyme disrupts the normal muscle metabolism during exercise, leading to muscle damage.
Horses with Type II PSSM do not display this mutation in GYSI, but the muscle cells do display abnormal glycogen deposits (mechanism unknown). It is possible that there are numerous, as of yet undetermined underlying causes that we are currently grouping under this heading.
What are the clinical signs?
Diagnosing muscle diseases can be tricky - they are easily confused with colic, acutely, or a lameness problem chronically. Acute clinical signs include sweating, muscle twitching, muscle stiffness, muscle fasciculations, dark colored urine, unwillingness to move and recumbency. Muscles are most often tense over the hind quarters and the signs worsen with continuing exercise. Although episodes are most often triggered by exercise, these signs are not always perfectly correlated.
As the muscle cells are damaged they release a substance known as myoglobin, which is normally contained within the cells. Myoglobin bears a passing resemblance to hemoglobin; the molecule found in red blood cells that allows them to carry oxygen. However, once myoglobin is free in the body it does more harm than good. The molecule accumulates in the kidneys and, in large enough quantities, can lead to renal failure.
Less severely affected horses with low-level chronic disease may show more subtle clinical signs. Poor performance, a bad attitude, lack of energy, slow onset muscle atrophy or unwillingness to track up may all be signs of PSSM.
How can you diagnose PSSM?
To first diagnose a horse with rhabdomyolysis (tying up), a biochemistry panel is very helpful. This test will show elevations in muscle enzymes (AST and CK) which increase with muscle damage. A chemistry panel will also allow your veterinarian to monitor kidney values, if the muscle damage is severe.
In the case that the patient is a breed known to carry the genetic mutation responsible to type I PSSM, genetic testing can be diagnostic. This requires a blood or hair sample to be sent away for testing. Type I or Type II PSSM can also be diagnosed through a muscle biopsy. A small sample of muscle can be examined with specific stains to look for abnormal cellular features and amylase resistant accumulations of glycogen.
What are the treatment options?
When working with a horse you suspect may be tying up, exercise should be stopped immediately. The horse should be offered water, but no other feed. Veterinary treatment of an acute case of rhabdomyolysis includes intravenous fluid therapy to flush the kidneys, muscle relaxants to stop muscle damage and anti-inflammatory/analgesic medication (NSAID's).
That being said, PSSM is primarily managed through exercise and dietary adjustments. After an episode, horses should be gradual brought back into consistent work with no prolonged period of rest. Regular exercise, being ridden or worked 3-4 days a week with access to daily turn out, is very important to horses with PSSM. Initially, exercise should be light (walk-trot) and they should always be warmed up adequately. Regular exercise is thought to improve energy metabolism within the muscle cells.
Horses with PSSM should be fed a diet low in nonstructural carbohydrates (starch/sugar), with a compensatory increase in fat if necessary to meet caloric requirements. There are many commercial options for low starch/high fat diets currently available. Restricting dietary sugars (NSC) from grass or hay is more difficult, but can be achieved though use of a grazing muzzle and/or soaking hay prior to feeding.
Even with excellent management, horses with PSSM will always be predisposed to developing muscle soreness. However, most will show improvement in clinical signs.
Seat Bones from the Rider's Side of the Saddle
By Nancy Wesolek-Sterrett
Dressage Department Head, Meredith Manor International Equestrian Centre
“Sit straight!” I cannot count the number of times I say these words to a student only to get the response, “But I am sitting straight.”
When I first started instructing, it was perfectly clear to me as an observer whether a student sat straight or crooked in the saddle. Crookedness in a horse or a horse unwilling to turn or stay on the rail was often a dead giveaway that the rider was crooked in the saddle. However, what I SAW the rider’s body doing and what the student FELT her body doing in the saddle did not match. There was a disconnect between where the rider’s brain told her ‘straight’ was and the reality I viewed. It took a lot of observation and experimentation to figure out what was going on and how to fix it.
Sitting up straight is a critical skill for riders. At the halt, the rider’s ears, shoulders, hips and heels align when viewed from the side. The small of the back is neither arched nor rounded. Viewed from the front, the horse’s neck, withers and spine form a straight line and the rider’s nose, chin, breastbone, belly button align with the horse’s spine. Viewed from the rear, the rider’s head and spine align with the horse’s spine.
When the rider sits up straight, she puts equal weight in both seat bones. This is fundamental to clear communication with the horse. Understanding how it feels to have equal weight in both seat bones precedes learning to modify those pressures in nuanced ways that communicate information about direction, bend, speed and more to the horse. When the rider has control of her seat bones, she can accurately influence the horse.
Everyone has problems with sitting straight on equally weighted seat bones at one time or another, mainly because we all have a weaker side and a stronger side. Riders tend to draw up their stronger leg therefore putting more weight on the opposite seat bone. Riders who have been ballet dancers or gymnasts may make the easiest transition into the saddle. To walk on a balance beam or move gracefully across the floor, they learned to keep their shoulders balanced over their hips. This is a very important aspect of riding straight in the saddle.
Most riders, however, bring poor postural habits with them when they mount up. They assume the classic ‘computer posture’ with chin jutting forward, shoulders slumping and lower back rounded. This posture removes weight from the seat bones. Some riders slouch off to the left or right placing their hips, shoulders, and head out of alignment. This puts more weight on one or the other seat bone, puts more weight in one or the other stirrup, puts the saddle off center on the horse, or creates any one of several other off balance scenarios.
Take the example of the rider who sits over to the left with more weight on her left seat bone. At the extreme when I view this rider from in front or behind, I may see the saddle pulled off center, the left stirrup hanging lower than the right, and the rider’s ribcage collapsed on the right. Her left shoulder may be higher than her right and her head may be tipped to the right so her ear points at her shoulder. Without putting my hand between her seat and the saddle, I know that she has more weight on her left seat bone than on her right. Or more weight to the left side of the horse then to the right side of the horse.
When someone rides crookedly for years, that crooked position feels normal. Correcting the problem literally requires retraining their brain to understand what straight and balanced, relative to gravity, feels like. It is not easy. Riders with good body awareness (think ballet, yoga, gymnastics, any martial art) can sometimes be talked through any crookedness. I sometimes use my hands to align a rider’s body so that she can feel what it feels like to be straight. But either method can have its drawbacks. If I tell a rider to drop her left shoulder, she may drop her head to the left at the same time. She feels balanced but she is not straight. If I take her knee to push her hips over so they are centered in the saddle, the rider invariably collapses her ribs on that side rather than equalizing the pressure in her seat bones.
Many people sit off to the left in the saddle because they are right handed. Their whole right side is stronger than their left so they draw up the right leg and push themselves to the left. Depending on their personality, some horse will tolerate their rider sitting as much as 2 inches off center before they get annoyed. Most horses begin to show some form of resistance long before that. Riders who sit off to the left usually find their horses do not bend easily to the right, for example.
Riders can play with a number of exercises to help them find ‘straight:’
* Sitting on the horse in front of a mirror or with the help of an observer, note if the horse’s neck, withers and spine are straight and if the rider’s nose, chin, breastbone, belly button, and spine all align with the horse’s center. Correct any rider misalignment and note how the horse’s alignment changes. Use the horse’s alignment to help the rider see and feel what adjustments in her position straighten the horse.
* At the halt, stand up in the stirrups. Are they equal length? Is there equal weight in each one? Is the saddle centered over the horse’s spine? Is the rider’s spine centered over the horse’s spine? Are the riders’ hips level? Are the shoulders level? Does the rider fall forward, backward, collapse the ribcage on one side, arching her back or round her back in order to stay ‘centered’ over the horse? Do this in front of a mirror (or a barn window) if a ground observer is not available for feedback.
* If the rider tends to put more weight in one stirrup than the other, she will push her weight onto the seat bone on the weaker side. Instead of pushing weight into the stirrups, think of pressing the knees to the ground as though kneeling on the ground. This not only helps to equalize the weight in the seat bones but also helps align the heels with the hips.
* Have the rider sit on a swivel chair or large balance ball with her hands underneath her seat bones. The seat bones are the bottom of the bony pelvic bowl. The bony projections we call our ‘hip bones’ are actually the top of this bowl. The actual hip joints are located in the bend between the upper body and thighs where the balls at the top of the thigh bones fit into the sockets of the pelvis. Keeping shoulders, ribcage and hips as level as possible, move weight from one seat bone to the other. Note what a small movement of the hips is required to do this. Shift weight forward and back without arching or rounding the lower back. Keeping the hips as level as possible and the shoulders over the hips, put the seat bones at a slight diagonal and shift weight from one to the other. Play with these movements with the chair facing forward, then swiveling right or left as though turning. These are the subtle movements that a horse feels and responds to.
* Retrain the brain. Right-handed riders should do everyday things with their left hand, vice versa for lefties. Do exercises that make the arms or legs or both cross the body’s midline to help balance the brain’s signals to both sides of the body. Strengthen the weaker side and stretch the stronger side of your body.
* Trust and use the horse’s feedback. Riding on the buckle, make a left turn, a right turn, circles, a serpentine, a half turn on the haunches and observe the horse’s answers to requests from the seat bones. If the responses are not what the rider thought she was asking the horse to do, she can experiment with changes in how she centers herself and weights her seat bones. Her horse will tell her when she gets it right.
*Temporarily ride with the stirrup longer on your stronger side or shorter on your weaker side. If possible, ride without stirrups on a quiet horse. Focus on keeping your shoulders over your hips and your hips centered over your horse’s spine. Note, this may feel uneven or unbalanced to someone who has been riding crooked for a long time.
The only way to give the horse clear, meaningful communication is to start by ‘sitting straight’ then using strong but flexible core muscles to weight and unweight the seat bones for directional guidance and speed control. This is the ‘independent seat’ that a rider must achieve in order to truly influence the horse. Without it, the rider is still influencing the horse. But until she develops a true feel for ‘straight’ in her own body and in the horse’s body, communication with the horse will be unclear, inconsistent, or, worse still, incorrect.
Omega Fatty Acids
Why all the talk about Omega Fatty Acids in horses diet? Unsure of how to supplement your horses diet appropriately? Read on for some insight into why horses are being supplemented to help you make the best educational choice for your individual horse!
What are Omega Fatty Acids?
Omega fatty acids are not produced directly by the horse’s body, which means they are considered “essential fatty acids”. This fact creates the need for a balanced diet to obtain the appropriate ratio. Without getting too scientific and to describe a complex pathway in the simplest of forms, Omega -6’s are originally from Linoleic acid (LA) while Omega-3’s stem from alpha-linoleic acid (ALA). This fact is important because horse’s require a balanced ratio of Omega 6 (LA) and Omega-3 (ALA) fatty acids in their diet to maintain the proper amount of inflammatory modulators. Once ingested, ALA’s (Omega 3’s) can convert to eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), which are intermediates in the formation of eicosanoids. Eicosanoids are important because they have potential to reduce inflammatory responses, support immune function, and enhance fertility. The proper ratio of ALA (Omega 3) to LA (Omega 6) at this time is not yet perfected and further research is being performed to determine the appropriate ration.
What are the sources of Omega 3 & 6?
Omega 3’s (ALA) are found predominantly in leafy plants, which obviously are the more traditional components of equine diets. Linseed oil (flaxseed), fish oil and canola oil are also a rich source of omega-3 fatty acids. EPA and DHA are a great source of omega 3’s, however they are derived from fish, which we all realize is not the normal equine diet, therefore creating the drive for supplementing Omega 3’s in the equine diet using plant material and or fish oil.
Omega-6 fatty acids originate from the oil of cereal grain and seeds. Examples of feedstuff containing higher omega 6’s are corn oil, safflower oil, rice bran and sunflower oil. Studies have shown that horses are able to absorb fatty acids when they are supplemented in the diet regularly. High performance horses and horses that are hard keepers tend to need more grain/concentrate rations (higher in Omega 6) then forage sources (naturally higher in omega 3). This is important because horses need both sources of Omegas, however a diet with a higher Omega-3 to Omega 6 ratio appears to be more desirable.
Why are Omega Fatty Acids important for the equine diet?
Once ingested, fatty acids are metabolized (broken down) by the body to produce prostaglandins (inflammatory mediators). Prostaglandins are hormones that participate in strong physiologic effects throughout the body. They play a large roll in promoting and inhibiting parts of the inflammatory cascade. Knowing this fact, researchers have evaluated horses that were supplemented with Omega 3/6 to determine if there is a change in the level of inflammation, which eventually leads to osteoarthritis. Research and supplementing has shown that Omega Fatty acids have appeared to improved coat and skin health, hoof quality, boosting immune systems, helps aid in reproduction, helping hard keepers maintain their weight along with protecting horses with EIPH (exercise induced pulmonary hemorrhage), lowering overall heart rates and protecting RBC (red blood cell) membrane fragility. A study performed by Kentucky Equine Research showed that 60 ml/day of fish oil supplementation increases serum and RBC EPA and DHA in horses. (Pagan, Lawrence, Lennox). (Remember that EPA and DHA, which are a source of Omega-3’s help aid as anti-inflammatory modulators).
What’s the future of Omega Fatty Acids?
Researchers are continuing to determine what the best ratio is for Omega 6 to Omega 3 supplementation for horses are. They are also continuing to do research on the best form of supplementation.
What are some drawbacks to supplementing Omega Fatty Acids?
Horses that are easy keepers may not do well on a fat supplement mostly due to obesity. Horse’s that are overweight should be on a high forage diet with minimal concentrates (grain), which will help increase their Omega 3 amounts!
Treatment Options for Kissing Spine
Lori Smolkovich, DVM
Overriding dorsal spinous processes, better known as "kissing spine" is a condition that many horse owners fear, because, until recent years, treatment options were very limited. In this article, the anatomy of the horse’s back, clinical signs, and treatment options will be discussed.
Individual bones called vertebrae fit together to form the spine. The vertebrae are named for their location. Starting at the head and moving toward the tail, the equine spine consists of seven cervical or neck vertebrae (#1 in image), 18 thoracic vertebrae (#2 in image), 6 lumbar vertebrae (#3 in image), 5 sacral vertebrae (#4 in image), and approximately 20 caudal or tail vertebrae (#5 in image). When discussing kissing spine, the area of interest is the thoracic and lumbar vertebrae (#2 and #3).
As you can see in the picture, there are bony "protuberances" that project dorsally (or up) along the spine. These "protuberances" are part of the vertebrae called dorsal spinous processes (DSPs). There are ligaments that are in between each DSP called the interspinous ligament, and a ligament and several muscles that run over the top of the DSPs. These muscles and ligaments make up the top line of the horse and help support the vertebrae to give it strength. Kissing spine occurs most frequently when the dorsal spinous processes come in contact with each other because the back muscles are weak and do not provide the support the spine needs. When the DSPs "kiss", or touch, the repetitive rubbing causes inflammation and bony changes. As a result of inflammation, the horse develops back pain. The bony changes in the DSPs can be easily diagnosed with radiographs.
Radiograph #1 illustrating normal DSPs
Radiograph #2 illustrating kissing spine. Notice the lack of space between the DSPs and the increased bone density where the rubbing and pressure has occurred.
There are two broad categories of treatment for kissing spine; medical management and surgical intervention. Medical management commonly consists of shockwave therapy, bisphosphonates, corticosteroid injections, and physical therapy. Shockwave therapy is utilized to modulate pain and discomfort. Bisphosphonates and corticosteroid injections treat and quiet inflammation. Physical therapy is required to strengthen the back muscles and build the top line so that the DSPs have more support and are less likely to contact each other. If medical treatment is not able to manage the horse's clinical signs, surgical intervention is often the next step.
There are several ways to surgically approach kissing spine. Two of the more common procedures will be discussed in this article. One surgical option is a subtotal ostectomy of the impinging dorsal spinous processes (SODSP). This means that a portion of the DSP is removed to create a wider gap between the DSPs thus preventing them from touching or "kissing". This procedure has been performed under general anesthesia and on horses standing with heavy sedation. The decision to perform the surgery standing or under general anesthesia is often dependent on which DSPs are affected, surgeon's preference, and risk factors specific to the individual horse. The other surgical option is an interspinous ligament desmotomy (ISLD). Unlike the SODSP, which is a surgery that removes a portion of bone, the ISLD approaches “kissing spine” by altering the soft tissue structures around the affected DSPs. As previously discussed, in between each DSP, there is a ligament called the interspinous ligament. In an ISLD, those ligaments are incised or cut, allowing the DSPs to not be held so tightly together. As a result the DSPs can spread apart and therefore do not “kiss”. The ISLD is surgery that is performed standing under heavy sedation so general anesthesia is not required.
Regardless of the surgical procedure that is utilized, physical therapy plays an integral role in the success of the horse following surgery. Once the DSPs are no longer kissing, the back must be strengthened to ensure the DSPs are supported as much as possible so that the condition does not reoccur. Physical therapy often begins after surgery with carrot stretches, later on, the horse is worked on a lunge line in a chambon, Pessoa, or other rig to encourage the horse to use his body and back properly while not adding the weight of a rider. Once the horse is ready, under saddle work that encourages engagement of the back and hind end is necessary to continue to build strength and to maintain the back muscles.
Kissing spine is a painful condition for horses and a frustrating one for riders. Fortunately there are many ways to help your horse achieve relief. If you think your horse may be affected by kissing spine, have your veterinarian evaluate him and discuss which options may be best for you and your horse.
Jacklin, B.D., et al. (2014). A new technique for subtotal (cranial wedge) ostectomy in the treatment of impinging/overriding spinous processes: Description of technique and outcome of 25 cases. Equine Veterinary Journal, 46, 339-344.
Brink, P. (2014). Subtotal Ostectomy of Impinging Dorsal Spinous Processes in 23 Standing Horses. Veterinary Surgery, 43, 95-98.
Coomer, Richard P.C., et al. (2012). A Controlled Study Evaluating a Novel Surgical Treatment for Kissing Spines in Standing Sedated Horses. Veterinary Surgery, 41, 890-897.
Catarina Ruksznis, DVM
Despite its relatively small size, the equine eye is a complex organ which can go very seriously wrong, very quickly when injured. If your horse comes in from the pasture with his eye swollen shut, take no chances- have your vet take a look as soon as possible. These clinical signs could be due to anything from a bump, to a foreign body, to a disease process within the eye. One of the more common problems we see are corneal ulcers. In order to understand this problem, let's first think about the anatomy of the eye.
In its most simple conception, the eye is a round structure divided into two compartments: the anterior ("forward") chamber and the posterior ("behind") chamber. The two compartments are separated from one another by a divider made up of the iris and lens. The anterior chamber lies between the cornea and the iris/lens, while the posterior chamber lies behind the iris/lens and the back of the eye. The cornea is the clear "window" at the front of the eye through which light enters and we can see. It is made up of different layers of cells like layers of a sandwich. The bread is formed by epithelial layers and the contents by the stromal layers, which form the majority of the corneal thickness. In total, the thickness of the equine cornea is only about 1 mm. The cornea is by necessity a very specialized tissue (it's clear!) and contains various mechanisms through which water is excluded from the stroma and transparency is maintained. The remainder of the outside of the eye is covered with a fibrous layer of white tissue (the "whites of the eye"), which is called the sclera.
Corneal ulcers are injuries, abrasions or erosions, to the cornea. While superficial corneal ulcers only involve the outermost epithelial layer (the 'top slice' of bread), deeper ulcers may include loss of the stromal layers and even expose the inner endothelial layer. Any depth of ulcer is painful, and horses may display squinting, tearing or rubbing at the offending eye. You may also see redness, swelling of the eyelids or thick, abnormal discharge from the eye.
When examining an eye, your vet will begin with a careful ocular exam. This will include looking for causes of the ulcer, such as a foreign body stuck in the eye, decreased tear production or the inability to blink. Corneal ulcers can then be definitively diagnosed by staining the eye with a colored dye called fluorescein. Fluorescein stain is not taken up by the normal corneal epithelium, but does stick to the inner stromal layers of the cornea (the filling of the sandwich) in places where the epithelium has been scraped away. While the stain appears yellow/green to the naked eye, it fluoresces green when viewed under a blue light. Ulcers appear as areas of intense green on the cornea. It is important to note that deep corneal ulcers, ones which have gone through all of the stromal layers, will only show a thin ring of stain uptake on the edges of the ulcer. This is because the endothelial layer which forms the bottom of the ulcer does not adhere to the stain but the sides of the ulcer, where the stroma is exposed, do. Other stains may also be used to evaluate the eye, such as rose bengal and lissamine green, to look for viral or fungal infection.
Management of corneal ulcers involves both systemic (oral or intravenous) treatment and treatments applied directly to the eye. Pain from the corneal ulcer is managed with systemic banamine, a non-steroidal anti-inflammatory medication similar to ibuprofen, along with topical atropine. Atropine is an anticholinergic agent which stops the spasmotic contraction of muscles within the eye secondary to pain, allowing the pupil to dilate.
Corneas, like your skin, are constantly exposed to the environment. Once there is a breech in the epithelial barrier, there is an opportunity for infection to occur. Bacterial or fungal infection may cause significant corneal damage and even corneal melting (keratomalacia) as the body tries to respond. Topical antibiotic therapy is therefore an essential part of treatment for corneal ulcers. There are a wide variety of antibiotic choices available, the most common of which is triple antibiotic ointment, composed of three antibiotics (Neomycin, Polymixin B, Bacitracin). This product has a broad spectrum of activity against many of the probable bacterial contaminants and is a good choice for an uncomplicated ulcer. It is essential to remember that this product is composed of only antibiotics and is often referred to as NeoPolyBac. There is a very similar product known as NeoPolyDex, which contains a steroid in addition to antibiotics. Steroids should never be applied to a corneal ulcer, as they inhibit healing. In cases of more complicated or non-healing ulcers, corneal scrapings can be taken to sample the cells and bacteria/fungi within the cornea and to guide antibiotic choice. In addition to an antibiotic, an antifungal is often added to the treatment regime in more complicated cases.
In the case of an uncomplicated corneal ulcer, healing should be complete within 7 to 10 days. If the ulcer does not heal or worsens, more intensive treatments or diagnostics are warranted.
Irby, Nita L. "Ophthamology." Equine Emergencies Treatment and Procedures. Fourth ed. St. Louis: Elsevier Saunders, 2014. 400-07. Print.
Gilger, Brian C., ed. Equine Ophthalmology. Second ed. Maryland Heights: Elsevier Saunders, 2011. Print.
Equine Protozoal Myeloencephalitis: An overview
Equine Protozoal Myeloencephalitis (EPM) is a commonly diagnosed neurologic disease of the horse that has captured the attention of equine veterinarians and horse-owners alike since it was first documented 30 years ago. It is a progressive and degenerative disease of the equine central nervous system, and is caused most commonly by the protozoan species, Sarcocystis neurona. (There have been few documented cases identifying Neospora hughesi as the causative agent, though the two species are clinically indistinguishable from one another.) Recent studies show that approximately 22-65% of horses in the United States are seropositive with antibodies from S. neurona, but only a small portion of these horses will go on to develop clinical disease.
The definitive host of Sarcocystis neurona is the opossum. This is the host in which sexual reproduction of the parasite occurs. Infected opossums shed sporocysts in their feces which are in turn transmitted to the intermediate host when ingested. Intermediate hosts include cats, armadillos, skunks, raccoons, and sea otters, and once infected, they develop sarcocysts in their skeletal muscle. Once this muscle is ingested by the opossum, the life cycle is completed. In the pathogenesis of EPM, horses are considered aberrant, or dead-end hosts, which halt the life cycle of the organism. Horses become infected through ingestion of contaminated feed or water and once infection is established, disease progression ensues.
While the pathogenesis of EPM infection is still widely a mystery, it is postulated that the ingested sporocysts are able to penetrate the intestinal wall and enter the cells that line the horse's arteries. The organism develops within the arterial walls until they rupture into the bloodstream where they can spread to other parts of the body. At this point it is possible for the horse to clear the infection on his own, leaving him seropositive, but without any clinical signs or evidence of disease. It is unknown how S. neurona enters the CNS in horses, though once the protozoa gain access they can establish infection in any area of the brain or spinal cord. Horses infected with S. neurona are unable to transmit the disease to other horses.
EPM can manifest itself through a variety of clinical signs, though the most classic are the three As: Ataxia, Asymmetry, and Atrophy. A common appearance of a horse with EPM is one with severe asymmetrical gluteal muscle atrophy. Since the organism can infect any area of the central nervous system, ataxia, or incoordination, is frequently observed in horses with EPM. Moreover, a variety of neurologic deficits can be seen, ranging from cranial nerve abnormalities in the form of a head tilt or facial paralysis to a dull or depressed mentation. Various gait abnormalities may also be seen and can occasionally be mistaken for lameness. The timeline for disease progression is variable, but if left untreated, in its most severe form, EPM can lead to seizures, coma, and even death.
Obtaining a diagnosis for EPM can be challenging, and it's important to know that a truly definitive diagnosis may not be attainable during a horse's lifetime. That being said, tests for EPM in live horses include the Western blot, indirect fluorescent antibody test (IFAT), and surface antigen-1 ELISA test (SAG-1 ELISA). Simple seropositivity for S. neurona antigen is not sufficient for a diagnosis, as that only relays if there are circulating antibodies within the vasculature. All exposed horses should be seropositive, but it takes the protozoan entering the central nervous system from the systemic circulation for the horse to actually have EPM.
To make a diagnosis of EPM, cerebral spinal fluid (CSF) and blood samples should ideally be submitted together for paired testing and analysis. The Western blot test looks for IgG antibodies against S. neurona within the CSF, though false positives are possible, especially if there is blood contamination of the sample. With a specificity of only 44-60%, it is likely that the immunoblot tests are best to rule out the presence of EPM, rather than provide a diagnosis for the disease. The IFAT test has shown comparable sensitivity, better specificity, and it is less affected by blood contamination. However, this test might give positive results for the protozoa S. fayeri, which might or might not cause disease in the horse. The newest test, the SAG-1 ELISA, looks for the presence of a particular surface protein of S. neurona, but not all strains express this particular protein. Therefore, false negative results are common.
The gold standard for diagnosing EPM in the horse is based on finding characteristic lesions on post-mortem exam within the CNS. However, due to the small number of organisms needed to cause the disease, 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 clinical signs of neurological disease consistent with EPM combined with positive CSF testing. Another option for diagnosis of EPM is looking for improvement in clinical signs in response to treatment. Since test results can take days to weeks to come back, horses are often started on treatment for the disease once they begin showing signs of neurologic disease while other possible causes continue to be ruled out.
Treatment for EPM is generally successful with studies indicating clinical improvement in 60-70% of cases. However, a portion of horses that are treated will have some residual neurologic signs that do not completely resolve with treatment. Relapse of disease once treatment is stopped is possible, though uncommon. There are four drugs that have been approved by the FDA for treatment of EPM: pyrimethamine, sulfadiazine, ponazuril and diclazuril. The most common oral medication used for the treatment of EPM is ponazuril (Marquis). It is administered once daily for 28 days or more depending on disease severity. While studies show ponazuril can effectively rid horses of S. neurona, it does not improve the CNS damage that occurs before treatment begins. Regardless of which medication is instituted, early detection and prompt treatment are essential for a positive outcome and a full recovery.
If you have any questions regarding this article or the health of your horse, please contact your veterinarian or the doctors at New EnglandEquineMedical & SurgicalCenter.
Tessa Lumley, DVM
New England Equine Medical & Surgical Center, 15 Members Way, Dover, NH03820