“Your horse looks like he is goose-stepping!”
Those words, spoken by one of the teenagers clustered around the gate of the arena as we warmed up our horses for our Tuesday night lesson, signalled the beginning of a long road of illness and recovery ahead for Annapolis. At that time, in 1993, not many of the general horse-riding public were familiar with Equine Protozoal Myeloencephalitis, or EPM. Although I didn’t know it, I was about to become the local expert, whether I wanted to or not.
We spent the next 15 minutes trotting Annapolis up and down, watching his bizarre, leg-jerking, goose-step-like gait and debating what could be causing it. Our speculations ranged from stringhalt, a condition which some of us were familiar with and in which the horse exhibits a similar goose-step, to (and you can tell we were clutching at straws here) a urinary infection of some kind, causing discomfort and resulting in the peculiar gait. But the truth remained, we didn’t really have a clue what was causing it. It was time to call my vet.
My vet at the time did a thorough work-up on Annapolis, in front of a crowd of interested spectators at the barn. He too suggested that it looked like stringhalt, but opined that not all the symptoms matched and that for a more definite diagnosis he would refer Annapolis to the Large Animal Clinic at Texas A & M University. Due to work conflicts and the fact that I had to convince a trailer-owning girlfriend to transport us up there, it was almost a week before we checked in to see Dr. Cliff Honnas.
About six or seven veterinary students filed into the examining room as Dr. Honnas was giving his initial examination. They all followed us out to the parking lot so that Annapolis could be trotted up and down in front of everyone. There was much snickering when he first broke into a trot, his hind legs jerking up and sideways up level with his stifle. Looking back, I will admit that it did look funny, but at the time I was not particularly amused.
Annapolis was subjected to all kinds of tests. He was turned in tight circles, he was given flexion tests of both hind and forelimbs. He was injected with a radioactive substance and a nuclear bone scan was done, which turned out to be inconclusive. As Dr. Honnas talked to the students, one of them lifted one of Annapolis’ forelegs and placed it down to the side of where it had been. Annapolis stood rock still and didn’t attempt to move it back. Proprioception is the ability of the horse to tell where his legs are. Annapolis was exhibiting proprioceptive deficit, as evidenced by his not moving his foot back underneath him. That gave Dr. Honnas a clue as to what we were dealing with.
Because of the nuclear bone scan, I was not able to take Annapolis back home that day and arrangements were made for him to stay a few days at the University until I could arrange to get him transported back to the barn. In the meantime, Dr. Honnas conferred with another of the vets at Texas A & M, Dr. Chafin, because the fact that Annpolis had not moved his leg back to its original postition led him to believe that there may be some nerve damage. As Dr. Chafin’s area of expertise was the equine nervous system, he essentially took over Annapolis’ case.
During our first telephone conversation with Dr. Chafin, I first heard the words Equine Protozoal Myeloencephalitis. At the time the cause was unknown. All that was known about it was that a microscopic organism, a protozoa, somehow invaded the spinal column and caused varying degrees of nerve damage. When I asked if I would be able to ride Annapolis again I was told the chances were 50/50. He performed a spinal tap to draw some spinal fluid which was sent to University of Kentucky, Equine Parasitology where extensive testing was being done on EPM. Although there was no definitive test for EPM, if titres (antibodies)were found in the spinal fluid, it was an indication that the horse had been exposed to the organism. There were titres in Annapolis’ spinal fluid.
Dr. Chafin didn’t want to get my hopes up and wanted me to be aware that the possibility of permanent nerve damage was very real. He immediately started Annapolis on the prescribed medication at the time, Trimethoprim-sulfamethoxozole and Daraprim. I had to compound these three times a day with karo syrup and syringe them into Annapolis’ mouth. Needless to say, Annapolis began objecting to this procedure within a couple of days. With at least three months ahead of us, possibly six, I had to find another way. In the end we discovered that Annapolis had no objection to us grinding the pills up and sprinkling them on his feed. He did not pick around the white powder or flip his feed out of the feeder as some horses are prone to do. In fact, he licked his feeder completely clean at every feed, leaving not one single oat grain to be seen.
Dr. Chafin advised me that it would be at least three weeks before I saw any improvement in Annapolis’ gaits, if I was going to see any at all. I had Annapolis confined to his stall for the first week, but I could tell it was not good for him mentally so I began turning him out in his familiar pasture with his buddies. I dared not look for any improvement for at least three weeks but one day, as he trotted away from me towards the other horses, I had to call one of the other boarders over and ask her to tell me I was not imagining things, that Annapolis’ hind legs really were not jerking up as high as they had been before. She agreed with me and we excitedly watched him as he trotted into the distance.
After three months I began riding Annapolis quietly, always concious that he may not have full control of his limbs. I confined my riding to the arena, with its level footing and it was many weeks before I felt confident enough to allow him to canter, even though he regularly galloped about the pasture with the horses without any problems. I continued the treatment at the full dose for three months and then at a minimized dosage for another three months. During that time he returned to full work and was, to all appearances, completely recovered. I was very lucky. We apparently caught the problem before extensive nerve damage was caused.
Since that time, in 1993, I have met horse owners who have also had experiences with EPM. Not all were as fortunate as I. A lady who boards her horse where I board Annapolis in fact had a mare euthanized because the mare’s nerve damage was so bad she was unable to rise. Her occasional stumbles and dragging her feet were attributed to bad shoeing or laziness. EPM was never suspected until it was too late. After talking with her extensively, I will never again ignore or explain away a horse’s stumbling or apparent laziness without getting the horse thoroughly checked by a veterinarian.
Since this article was first written, in 1997, research has shown that Equine Protozoal Myeloencephalitis is most probably transmitted by the possum. Articles in EQUUS magazine and Practical Horseman explain the life cycle of the protozoa and how it is introduced into the equine system. Ohio State University has also done extensive research and published papers on the disease.