Few equine diseases are as frightening--or confounding--as equine protozoal myeloencephalitis (EPM). A neurological condition caused by protozoal parasites, EPM often produces subtle, easy-to-miss signs early on. Yet, left untreated, the disease can cause irreversible damage to the spinal cord and brain. Although great strides have been made in understanding and treating EPM, the average horse owner can be forgiven for spending a bit more time worrying about this disease than most others.
It's little comfort that some of the leading researchers in the field readily admit that they are uncertain as to why some horses contract EPM or which treatments are consistently effective. Even determining whether a particular horse has the disease is difficult, because the standard tests frequently produce inaccurate results.
The diagnostic challenges posed by EPM reflect the complex nature of the disease itself. EPM is caused by one of two organisms, Sarcocystis neurona or Neospora flughesi. As with most protozoal diseases, the horse is not the main host for these parasites but is instead an accidental and rare victim of an agent whose natural host is common in the environment. S. neurona's "home base" is the opossum, which is found widely in the Americas. Horses ingest the protozoa when they consume forage or water contaminated with opossum droppings. Infection with these protozoa does not mean disease, however. In fact, most horses who are exposed to S. neurona or N. hughesi develop antibodies to the organisms without ever becoming ill. Only when the protozoa somehow pass from the bloodstream to the central nervous system and undergo rapid multiplication does the horse develop clinical signs of EPM. Affected horses become increasingly uncoordinated and, in the worst cases, unable even to stand.
There are three basic diagnostic tests for EPM, all of which seek to detect S. neurona infection. (A test for N. hughesi is not yet available.)
The blood test detects antibodies to S. neurona. A negative blood test can virtually rule out EPM, missing only those horses who have so recently (one to two weeks) been exposed to the protozoa that they have not yet produced specific antibodies. A positive test, however, does not necessarily mean a horse has the disease-EPM occurs only when protozoa cross the blood-brain barrier, multiply and damage the nervous system. Experts estimate that in some areas of Kentucky as many as 90 percent of horses carry blood antibodies to S. neurona--and the vast majority show no signs of disease. In addition, some surveys suggest that, nationwide, some 5O percent of all horses carry antibodies to S. neurona. As a result, the blood test alone is generally considered useless in diagnosing EPM, and some veterinarians prefer to by- pass it altogether.
The other two EPM tests require a spinal tap, the withdrawal of fluid from the spinal cord, which is a demanding and slightly risky procedure. The easiest test on the spinal fluid looks for antibodies, a sign that the protozoa have passed from the bloodstream to the nervous system. The presence of antibodies in spinal fluid can be an indicator of disease but only hen a "clean" sample has been obtained-if even a minute amount of blood carrying antibodies contaminates the sample, a false positive reading will result. And getting a clean spinal tap isn't easy, even for experienced veterinarians. A study at the University of Pennsylvania's New Bolton Center found that as few as eight red blood cells per microliter--about one millionth of the concentration present in the bloodstream and far too few to stain a sample pink--was enough to trigger a positive reading. As with the blood test, a negative spinal tap result can pretty well be trusted, but a positive one is not necessarily conclusive evidence of disease. An extremely low level of antibodies in the spinal fluid is more likely to indicate a sample's contamination than a horse's illness.
The other diagnostic analysis done on spinal fluid is the polymerase chain reaction (PCR) test, which uses gene amplification technology to detect the presence of the S. neurona organism itself in spinal fluid. When PCR tests were first put into use a few years ago, expectations were high that they would revolutionize EPM testing. In practice, however, the tests have proved to be unreliable.
In light of the uncertainties surrounding current EPM testing techniques, it's clear that the notion "better safe than sorry" does not apply to EPM testing. A horse who stumbles occasionally or takes a few more missteps than usual is not a prime candidate for testing. Nor is it wise to see darker implications in minor lamenesses and niggling training problems that might once have automatically been attributed to overwork or rider error. But in the face of borderline signs of uncoordination, the question of whether to test for EPM is rarely simple. Choose wisely and you can save your horse's life; take the wrong course and you may be treating a nonexistent condition or ignoring another serious problem.
Your veterinarian is your best resource for deciding what to do in your particular situation. But researchers investigating the disease offer the following four guidelines on how to proceed if you suspect that your horse has EPM.
1. Don't do any test if a horse doesn't have distinct signs.
Unlike screening tests for diseases like tuberculosis in people, random EPM testing would cause more problems that it would solve. In fact, says Clara Fenger, DVM, PhD, a veterinarian in Georgetown, Kentucky, who has studied EPM for years, "The worst thing people can do is test a clinically " normal horse just because they are curious." She is especially critical of the practice of including EPM tests in prepurchase exams of clinically normal horses. "There is a very real possibility that you'll be passing up a great horse because you think he has a disease that he doesn't have. Everyone loses - buyer and seller." The tests for EPM are best viewed as only one of many ways to identify horses with te disease, says Fenger. "The test is meant to be a diagnostic tool used in conunction with other signs [of EPM]."
Of course, the clinical signs of EPM are frequently missed or confused with other problems. Acute cases, characterized by severe incoordination and facial paralysis, are easy to spot. Subtle cases are harder to interpret-owners of affected horses have been tipped off by everything from belavior changes to a simple "offness" under saddle. However, Robert Mackay, PhD, a professor of large animal medicine with a specialty in equine neurology at the University of Florida, explains that there are certain clinical signs that are more indicative of neurologic disease-and therefore EPM-than any other disease:
- a tendency to swing the outside hind leg outward when walking in a circle
- a tendency to leave feet in strange positions (base wide or base narrow)
- asymmetric loss of muscle mass
- a lameness that doesn't respond to analgesics, such as phenylbutazone, and cannot be localized with a thorough lameness examination
- frequent unexplained stumbling under saddle
- problems with lead changes in an otherwise sound horse who previously has not had this problem. "The more bizarre this is, the more likely it is neurologic," says Mackay. "For example, if a galloping horse maintains different leads behind and in front."
- pelvis wobbles from side to side when the horse walks
- the hind legs (stifles) frequently lock out backwards despite efforts to get the horse fit.
2. Rule out other diseases.
If your horse exhibits any signs you think might indicate neurological impairment, it's wise to ask your veterinarian to perform a full physical exam and standard diagnostic workup. But don't expect him to do a spinal tap as a matter of course. Before a veterinarian tests for EPM, he will rule other diseases, possibly after consultation with a neurologist or EPM specialist "You always look to the most likely cause first," says Fenger. "And there are many diseases that fall into that category. In particular, eastern equine encephalitis (EEE), equine herpes virus (EHV-l), spinal compression (wobbles) and early orthopedic disease (especially body stiffness or a sore back) can produce the same signs as EPM.
To complicate matters further, says Fenger, a perfectly normal horse can sometimes exhibit slight uncoordination or occasional clumsiness: "Young horses in particular have gawky stages. A Thoroughbred is growing until he is a 2-year- old, and a warmblood can be changing until he is 4. Until then, they may have perfectly normal periods of slight uncoordination. She even advocates waiting three weeks and doing a second neurological exam if the results of the first test aren't clear. "In that time period, mechanical lamenesses will usually resolve themselves, but EPM won't." Fenger says that delaying treatment a few weeks in such early cases won't be harmful to the horse. "In the majority of cases, EPM progresses very, very slowly. You really have time to figure out exactly what is going on before you make a decision."
3. Remember that, in the absence of conclusive test results, treatment can be used as a diagnostic aid.
In cases where a neurologic test is inconclusive or the spinal tap results are in question, one final method of diagnosis is the treatment itself. Various combinations of sulfa drugs and other medications with anti-protozoal actions are currently used to treat EPM. All of these medications, so far, are "off label for EPM, meaning they haven't received Food and Drug Administration approval for use in horses. However, their hazards are known and dealt with in the dosing regimen. The most common treatment is a mixture of sulfadiazine and pyrimethamine, usually made by a compounding pharmacy. Just about all of the drugs available, while moderately expensive, are quite safe.
If laboratory tests are inconclusive, a positive response to treatment may be an indicator that a horse is indeed infected. If, on the other hand, the horse keeps getting worse even as he receives a full course of treatment, he probably doesn't have EPM. A reasonable argument can and often is made that response to treatment is one of the best diagnostic tools available," says Mackay, who starts a horse on a course of anti-protozoal medication when he strongly suspects EPM but can't make an immediate, definitive diagnosis, or when he is awaiting consultation with a specialist. If the horse improves with medication, EPM could very well have been the cause, Mackay says. "You can always stop treatment if something else is uncovered."
4. Continue to look for alternative causes.
Even when you are certain your horse has EPM and he is undergoing treatment for the disease, Fenger advises that you watch for clues that might reveal another source for the problem. "I've seen horses with serious musculoskeletal prob- lems kept in work simply because the owners were convinced that they had EPM. People treat horses for a nonexistent disease and continue to strain another obscure injury that they never really looked for," she says. "Racehorses have been known to break down because early warning signs of skeletal problems are attributed to EPM."
Until more is known about EPM, questions about when to test horses for the disease will linger and debates over how to interpret the results will continue. Beyond the widespread agreement that a clinically normally horse need not be tested, there are no hard and fast rules. A concerned horse owner is best off learning the facts about EPM, discussing the situation with a trusted veterinarian and making a decision based on the horse's individual signs and circumstances.