To avoid tragic accidents, put only one horse in a stall at a time. Photo © EQUUS

This is a story of a stupid mistake---one that led to a terrifying accident that could easily have cost my horse’s life. I still get anxious thinking about what happened that day, and part of me would like to forget it entirely, but I think it’s important to share my story. My goal is to remind people not to fall into bad habits or to forget that horses---even those you know and trust---are large, powerful and unpredictable animals.

My husband, Kurt, and I own a few acres in Columbia, Missouri, that gives us just enough space to keep a small herd for our family to enjoy. Our setup isn’t fancy, but it serves us well.

For my birthday one year Kurt built me a small but cozy barn that included one very large 10- by 20-foot stall and a smaller 10- by 10-foot stall. The walls are four feet of tongue-and-groove boards topped with vertical metal bars. The gaps between the bars are small---only 2  inches---but they allow plenty of light and air to flow through.

At the time of the accident we owned three horses: Cloud, a registered Quarter Horse gelding; Britches, a 12-year-old Haflinger gelding; and Jiffy, a 3-year-old Welsh pony cross. I’d bought Cloud just a year before; I’d been looking for a smallish, well-trained, unflappable horse, and he was a perfect fit. He was years younger and only slightly taller than Britches, so I didn’t anticipate my new horse would have any problems settling in. I was right. Britches took an immediate liking to Cloud, and they became good friends.

During the day, the three horses could come and go into the barn and stalls at will. I’d often find Cloud and Britches dozing together in the larger stall. To accommodate them at feeding time, I hung grain tubs at opposite ends of the larger stall and one in the smaller stall, for Jiffy, and I’d let Cloud and Britches eat their meal together.

Occasionally, I’d lock the two of them in the stall together for short periods of time--never longer than it took to receive a hay delivery or mow the fields. Neither horse had ever shown any aggression toward the other, and the stall-sharing arrangement worked well.

Until one day, it didn’t.

One Saturday morning in September 2009 I went out to await a shipment of hay. To get the horses out of the way I dumped a handful of grain into each corner feeder. Just as he always had, Cloud walked into the large stall and went to the far corner to
eat. Britches ambled in after him and went to his own corner, while Jiffy headed into the small stall. I then closed both doors.

Moments later I heard a horrible ruckus, and I spun around just in time to see Cloud kicking out at Britches with both hind legs. The kicks were high and powerful. There was no doubt he meant business. As Cloud backed up to take aim again, the pony scooted out of his way.

Cloud’s next kick missed Britches and landed squarely on the stall bars, four feet above the floor. His left rear hoof struck the metal with such force that it bent the bars just enough to allow his foot to slip through. His leg immediately dropped to the surface of the wooden wall, leaving Cloud standing on three legs, with his left hind stretched backward and upward, his hoof trapped between two thick metal bars. It happened in a split second.

Cloud panicked. He lunged forward and back, trying to pull his hoof free. With each attempt to back up, he pushed his leg into the adjacent stall almost to his hock. Then he’d scramble forward, scraping his skin down to the fetlock. Each time he lunged, it seemed he could rip his foot right off. It was horrifying to watch, and I was sure he was going to break his leg.

Two factors probably saved Cloud that day. One was that I had my cell phone in my pocket, and the second was that Kurt was home. He came running from the house as soon as I called him. I opened the stall door to let Britches out and tried to calm Cloud from a distance, but I didn’t want to get too close. He was wild-eyed with fear and pain.

With one glance at the situation Kurt sprinted to the garage and came back with a pry bar to widen the gap for Cloud’s foot. But he couldn’t get the leverage he needed to bend the bars.

Cloud’s panicky, crazed lunging continued, and his leg was becoming a bloody, raw mess. I feared he was stripping his flesh to the bone.

Kurt then ran into the adjacent stall and grabbed Cloud’s trapped hoof. I have no idea how he managed to hold onto it as Cloud continued to struggle, but he did. Arm muscles bulging, he lifted the gelding’s hoof high enough to reach the slight gap where the bars had been bent by the impact of the kick. Lifting the leg to such a steep angle must have caused Cloud intense pain. But with a mighty shove, and aided by a final lunge forward, Kurt forced Cloud’s hoof back through the bars.

The leg had been trapped for maybe 10 or 15 minutes.

Damage done
Cloud stood alone in the large stall, holding the injured limb in the air, his blood streaming down and pooling on the stall floor. With shaking hands, I called our veterinary clinic, and within 15 minutes Tawna Purcell, DVM, arrived at the farm.

Purcell listened carefully to our account as she examined Cloud’s leg. Then she gave him an injection of a sedative, xylazine. If his leg was injured and he placed his full weight on it in a fit of panic, he could make the situation much worse.

Within a few minutes, Cloud relaxed and rested the hoof gingerly on the ground. Purcell gave him an injection of phenylbutazone to control his pain and the inflammation, then she palpated and flexed his leg, looking for any indication of fracture, such as an area of extreme swelling or tenderness. Nothing made her immediately suspect a bone or joint injury, although that didn’t mean he didn’t have one; if he did, it just wasn’t obvious.

Next she began cleaning Cloud’s wounds, which, it turned out, looked worse than they actually were. In fact, most were just superficial abrasions that hadn’t removed any more than the top layer of skin. One deeper cut midway between his hock and fetlock gaped open and bled freely, but no bones or tendons were visible.

By the time Purcell was finished, Cloud’s leg looked much better, and he was bearing weight on it, but we were not yet out of danger. Cloud showed signs of pain as his fetlock joint was flexed, which, Purcell explained, might indicate some fractures in the area. Another possibility was that he avulsed a collateral ligament of the fetlock joint---in other words, pulled the ligament free from the bone. She took a series of radiographs of his pastern, fetlock and cannon bone to view later at the office.

Purcell covered Cloud’s wounds with Thermazene, a silver sulfadiazine-based antibiotic wound cream, and wrapped his leg from hock to hoof. Then, to protect his lower leg in case he had sustained serious bone or tendon injury, she used layers and layers of padding to create a thick Robert Jones bandage. She also applied a standing wrap to support Cloud’s uninjured right rear leg--sometimes, horses who injure one leg and are forced to bear a disproportionate amount of weight on the opposite side may develop laminitis in the “good” foot. Purcell left me a tube of phenylbutazone with instructions to continue administering it over the
coming days.

Rest and recuperation
Within an hour Purcell called to say that the radiographs showed no evidence of fractures or avulsions. That was wonderful news. But she did warn me that Cloud might have strained his ligaments by pulling so hard with his leg locked in such a high position. She suggested I keep him in his stall and leave the bandage on until she returned on Monday morning. I was to remove the bandage only if I saw any swelling of the leg in the region above the wraps.

Cloud was miserable confined to his stall. I spent most of the next day with him, brushing his beautiful coat, combing his tail, feeding him carrots, and wondering whether he would recover. I examined the leg above his hock so many times, I think I burned the image into my retina. The more I looked at it, the more I imagined it was puffing up. But Kurt, who came out to check on us four or five times that day, reassured me that the leg was not swollen.

Purcell removed the thick bandage when she returned on Monday morning, which was a bit dicey because the gauze pads were stuck to the wounds, but Cloud didn’t put up much of a fuss. I then walked him carefully around the exam area. To everyone’s relief, he was reasonably sound, considering what he had been through.

After examining the leg again and watching him move, Purcell said she doubted Cloud had sustained any serious injuries to his bones, ligaments or joints. His slight lameness, she said, was most likely the result of lingering pain from sore muscles he’d sustained during his struggle against the bars.

Still, we weren’t entirely out of the woods. As Purcell rebandaged Cloud, she said that we would have to wait to see if he developed a bony sequestrum. Sometimes, she explained, significant trauma bruises and kills a portion of a bone, which separates from the parent bone. The body treats that fragment of dead bone as a foreign object and tries to get rid of it--the signs are a horribly swollen leg and lameness that develops anywhere from one to three weeks after the initial injury.

The only treatment for a sequestrum is to surgically remove the dead bone fragment. Although Purcell assured me that the procedure is fairly straightforward and usually successful, we both hoped to avoid this complication.

Full recovery
Cloud was unhappy the next day, Tuesday. He’s not accustomed to confinement, and he paced in his stall all day. I gave him all the good-quality hay he wanted, but I could see that he was already losing weight.

Purcell came back on Wednesday to change the bandage. She had offered to show me how to do it myself, but I was too afraid I’d miss something, or wrap him too loosely or too tightly. The visit went smoothly, and Purcell told me I could begin hand-walking Cloud twice a day, which would help him cope with stall confinement.

She returned again late the next day and was pleased when she removed the bandage---the abrasions were healing nicely. She rewrapped both hind legs with plain standing wraps and turned Cloud loose in the ring for the first time since his accident. He cantered and bucked and had a great time. He was still noticeably lame at the trot, but Purcell said that was not surprising. He was probably still sore.

It was now up to me to take on cleaning, medicating and rewrapping Cloud’s leg every day. His wounds continued to heal well, and he was getting sounder, although I worried he was getting depressed because he couldn’t yet join his herdmates.

Purcell returned for a follow-up check when Cloud’s injury was two weeks old. The skin was nearly healed, but he had developed a two-inch horizontal crack on the outside of his injured hoof. Purcell explained that a cut on the coronary band probably disrupted the hoof growth in that area for a short time. She told us to keep an eye on the crack, but she suspected it would grow out of his hoof without causing any real troubles.

Cloud was still slightly “off,” but Purcell suggested I start light riding so he could stretch and strengthen his sore muscles. That Saturday and Sunday, I got on Cloud bareback and ambled quietly around the ring. On Monday, I trotted him under saddle, and he was sound.

We still had a few anxious weeks ahead of us, waiting for the dreaded sequestrum to appear, but Cloud continued to stay sound. Our farrier kept a close eye on the hoof crack, but it required no special treatment as it progressed down his hoof over the
following months.

Three years later, the only tangible reminder of that terrifying day is a single, very small scar midway down Cloud’s back leg. But we cannot forget what could have happened: If Cloud had slipped and fallen while trapped, his leg could have snapped, or he could have dislocated joints, torn ligaments or stripped flesh down to the bone.

We were very lucky, and for that we remain grateful.

Why did Cloud attack Britches? We’ll never know. But one thing is for sure: I’ll never again make the mistake of putting two horses in the same stall, no matter how friendly they are.

This article first appeared in EQUUS issue #427.

Given the forces that this joint handles day in and day out, it’s not unusual for horses to develop SI pain. The trick is recognizing the problem: SI injuries are notoriously hard to pin down, with subtle and confusing signs, easily mistaken for other physical or even behavioral problems. Even a “hunter’s bump,” a raised area at the top of the croup that’s often thought to reveal SI trouble, isn’t a reliable sign. (For a closer look inside the joint, see the box below.)

How can you tell if your horse develops SI pain? And, more to the point, what can you do to help him if he does? For this article, we asked Kevin Haussler, DVM, DC, PhD, of the College of Veterinary Medicine and Biomedical Sciences at Colorado State University, for help in answering those questions.

Who’s at Risk?
Any horse can injure his SI joint in a fall or some other accident. The injury may leave the joint less stable than it was originally, so it can become a source of chronic pain. Performance horses may develop SI problems through simple wear and tear—and the more mechanical stress the joint comes under, the greater the risk, Dr. Haussler says. SI problems are fairly common. In one recent survey, these problems accounted for more than half of 124 horses presented for back problems at the University of Minnesota equine clinic.

Show jumping and dressage seem to be especially hard on the joint, according to a study carried out by Sue Dyson, FRCVS, and others at the Center for Equine Studies, Animal Health Trust, Newmarket, United Kingdom. That study analyzed records of 74 horses seen for SI pain at the center. Dressage horses and show jumpers accounted for almost 60 percent of the group. Slightly more than half were warmbloods, suggesting that breed may play a role. And horses with SI pain tended to be taller and heavier than average, another sign that mechanical stress is an important factor.

Under stress, Dr. Haussler says, the joint can be injured in several ways. The SI ligaments can tear, just as ligaments and tendons in a limb can give way under stress. And the joint itself, like the hock or any other joint, can become inflamed. Over time, osteoarthritis develops—cartilage wears away and bone remodels. Thoroughbred racehorses sometimes get pelvic stress fractures directly over the SI joint, and those need to be differentiated from SI joint arthritis.

How do you feel and behave when you get out of bed in the morning with tight or painful back muscles? Chances are you move stiffly or tentatively and your range of motion is restricted. Until you get relief, you don’t have your usual enthusiasm for normal tasks.

It’s much the same for your horse when his back muscles are stiff or hurting. He may

• flinch or sink away when you’re saddling him;
• travel with his head elevated and/or his back hollowed;
• canter less freely than usual;
• experience a decrease in coordinated power;
• trail his hind end rather than stepping under himself;
• jump flat rather than with a rounded bascule;
• drift sideways, either on the flat or over jumps;
• resist lateral work.

One thing your horse will not do as a response to back pain or tightness, by the way, is buck. He needs to round or flex his back to buck, whereas his normal reaction to pain and tightness in his back is to move away from the discomfort by hollowing.

What’s Hurting

The longissimus costarum, just below the longissimus dorsi, extends across the horse’s ribs. This muscle assists in extending the spine and in flexing it laterally.

© Jim Leiby

The muscles whose tightness is frequently a cause of these signs are the longissimus dorsi—the longest and largest muscles in your horse’s body and a powerful extensor of his spine—and the longissimus costarum, which lie below the longissimus dorsi across the ribs on each side and are important in lateral flexion of the spine and in breathing (see photos page 66 for the location of these muscles).

As part of understanding how tightness develops in these and other muscles, let’s take a quick look at how muscles work. Every muscle has two ends, each connected to bone by a tendon. One end is the anchor and the bone to which it is connected doesn’t move. The other end is connected to a bone that moves when the muscle is used. The middle part of the muscle, which does the work of moving the bone, is called the belly. It’s composed of hundreds of tiny fibers, each of which has its own blood supply. When a muscle is working normally, it tightens, then immediately relaxes or ­releases. Muscle tightness occurs when the muscle doesn’t release as it should. When a muscle becomes chronically tight, the fibers lie closer together. This constricts the flow of blood through the muscle belly, somewhat like stepping on a garden hose reduces the flow of water. The muscle ­operates less effectively when it’s tight, and it may be painful.

All muscles work in pairs of opposites: As one muscle contracts, its opposite ­releases. When a muscle is tight, the ­release process of the muscle is affected. The back muscles extend the horse’s spine, and tight back muscles can’t release to allow for the spinal flexion your horse needs to, for instance, round himself for a bascule over a fence or a nice collected canter. Tightness in the longissimus ­costarum will also affect your horse’s ability to bend around your inside leg.

What Causes It
Back muscle tightness can result from a number of factors. Some of the most common are

• the strain and exertion of repetitive schooling, such as working much more on one canter lead than the other;
• footing that is very deep or too hard;
• an ill-fitting or out-of-balance saddle;
• a very imbalanced rider (whose horse will attempt to compensate for her ­one-sidedness);
• poor saddle placement (for instance, too far up on the withers, which drives the cantle into the back muscles);
• too many pads under a correctly fitted saddle. Contrary to some riders’ belief, this does not reduce pressure on the horse’s back but is more like cramming two pairs of socks inside your shoes.

Tight back muscles can also signal a deeper problem such as hock or ankle issues, weak stifles or ligament problems. How can you know whether you’re dealing with simple muscle tightness or with something more serious? If your horse’s discomfort is not relieved after you have done the massage and exercise sequence I’ll describe on the next two pages a couple of times, you need to involve your veterinarian. (As a general rule of thumb, in my 20 years of practice as a massage therapist, if I find persistent tightness in the forward area of a horse’s back, it may indicate a deeper problem in his front end; if the muscles remain tight in the area near his haunches even after massage, there may be a bigger problem in his hind end.)

Just like people, horses can be far- or nearsighted. © EQUUS

Q: I’ve read that horses can be near- or farsighted. Given how important good eyesight is for social interactions and performance in some sports, do horses ever receive corrective vision surgery? Many people with poor eyesight are treated with laser eye surgery; is that possible for horses? Or do those with poor eyesight simply compensate with their other senses?

A: Horses, like people, can suffer from a variety of optical aberrations that affect visual acuity. The common eye problems you allude to that can affect the eyes of both people and horses are refractive errors, such as nearsightedness (myopia) and farsightedness (presbyopia), and astigmatism, which affects the eye’s ability to focus. A veterinary ophthalmologist can perform retinoscopy to assess a horse for abnormal vision.

Fortunately, most studies report the majority of equine eyes are nearly normal in function. A horse with normal vision (emmetropia) can see almost 360 degrees around with just two small blind spots: The first begins at the forehead and comes to a conelike point about three feet in front of his body. The other is right behind his head, reaching over his back and directly behind his tail.

When refractive errors occur, images are not focused properly on the retina, the light-sensitive tissue in the back of the eye’s interior that transmits signals through the optic nerves to the brain. Other significant factors that can affect a horse’s vision include infectious and noninfectious corneal disease, uveitis and cataracts. These diseases can be treated successfully medically and/or surgically, but scarring and inflammatory changes can result in permanent refractive errors.

So, in answer to your question, yes, horses can have refractive errors and abnormal vision just like people, but as a matter of anatomical and other considerations, LASIK surgery and corrective eyewear are not practical for use in the horse. In general, many horses can adapt and compensate

quite well with visual adversities and are able to lead normal lives, so we rarely intervene with corrective measures. An exception might be following cataract surgery, when an artificial or intraocular lens is placed in the lens capsule to improve the patient’s refraction.

Early detection and intervention increases the chances of successful treatment of eye diseases that could result in refractive errors, so have your veterinarian address any suspected eye problems promptly.

Brendan G. Mangan, DVM, MS, DACVO
University of Florida
College of Veterinary Medicine
Gainesville, Florida

This article first appeared in EQUUS issue #426.

Moving closer I spotted a swelling on his chest, in front of his left shoulder. I stepped through the gate and ran my hand over the protuberance: It was firm but not hot, and it covered his left front chest and extended down between his front legs.

“What happened, Wes?” I asked, rubbing the star on his forehead. “You get kicked?”

Wesley is pastured with two other geldings, and these boys do get rowdy. My horse Zeke had once been kicked in the chest, and the injury had produced a hematoma, a blood-filled swelling, the size of a grapefruit. That must be it, a hematoma, I thought.

I slipped the halter over Wesley’s head, and we headed toward the barn. He was moving sluggishly, reluctant to bear much weight on his left front leg.

My brow furrowed. This could be more than a hematoma. Was it a shoulder fracture? A tumor? I’d lost my first mustang to an aggressive sinus cancer, and I am forever fearful of seeing equine cancer again. Taking a deep breath, I reassured myself that it was probably not cancer and Wesley would be OK. I stroked his neck and encouraged him to come along.

I put Wesley in a stall with hay and water and gave him two grams of phenylbutazone (bute), which I stock for my arthritic horse, to control his pain. In the meantime, my husband hitched up the trailer so we’d be ready to take Wesley to our local veterinary clinic first thing in the morning.

Wesley’s swelling looked about the same the next day, and he had trouble climbing into the trailer because his shoulder and leg made the step up painful. But he’s a good horse, and once he was loaded, we drove to see Steve Shideler, DVM.

Not so simple
“That looks like an injury. Could be a hematoma,” Shideler said as Wesley backed off the trailer. Walking slowly to accommodate Wesley’s pain, we led him to the treatment area.

The veterinarian palpated the swelling, then he cleaned the center of the mound and inserted an 18-gauge needle to see if he could aspirate (draw out) any fluid. Nothing. Shideler said Wesley had probably experienced some trauma. He administered a dose of penicillin in case some infection was present and prescribed daily warm compresses and continuing the bute as needed, but he said he would expect the swelling to go down over time as the injury healed. Relieved, we loaded Wesley and returned home.

Alone in a paddock, Wesley stood quietly for the application of warm compresses. He’s a mild-mannered horse, and he appreciated the attention and the head rubs. We gave him two grams of bute for three days and then tapered him off of it by day five. Bute can cause gastric ulcers, so I didn’t want to keep him on it too long.

But once the bute was stopped, Wesley’s pain seemed to increase. And, instead of shrinking as we expected, the swelling on his chest grew bigger. Now his head bobbed when he walked, a telltale sign of how painful weight-bearing had become. I put him back on the bute.

The Monday after Thanksgiving, I called Shideler to report that Wesley wasn’t feeling better and the swelling was getting worse. We discussed alternative diagnoses. The possibility of cancer came into the conversation; my heart sank. Shideler recommended taking Wesley to the university clinic, where a specialist could ultrasound the swollen area to get a better idea what lurked beneath that ballooning skin.

A different diagnosis
Worried, I emailed a photo of Wesley to Alison Eddy, DVM, at Mississippi State University’s College of Veterinary Medicine; she’s treated our other horses before. Eddy replied that, although she couldn’t diagnose the problem without examining the horse, she thought the swelling looked like pigeon fever---an infection that causes large pus-filled abscesses under the skin. Also called dryland distemper or false strangles, pigeon fever gets its name because the swellings, which often appear on the front of a horse’s chest, mimic the bulging profile of a pigeon’s breast.

She explained that pigeon fever is caused by the bacterium Corynebacterium pseudotuberculosis and is more common in arid regions of southern California and the Southwest. However, she added, they’d been seeing more of this infection in Mississippi this year than they had in the past. Eddy assured me that pigeon fever isn’t usually life threatening, but it does require treatment. I made an appointment at the university for the next morning.

With Eddy’s permission, I gave Wesley two grams of bute one hour before loading to help reduce his pain, and he gamely climbed back onto the trailer. Eddy and the other equine veterinarians were waiting and ready to examine Wesley as soon as we arrived at the hospital. All his vital signs were normal---no fever---and he was bright and alert. His only sign of trouble was the classic hallmark of pigeon fever: pectoral swelling and pain from that king-size abscess. All of this pointed toward that diagnosis---most horses with pigeon fever eat well and have no fever. Eddy told us that an ultrasound of the swelling, to look for the pus pocket, would help confirm their diagnosis.

The swelling was shaved for the ultrasound, and Wesley’s dark-tipped ears flicked forward momentarily with concern as the equipment was wheeled toward him. He stepped back, but after being allowed to sniff the apparatus, he sighed and settled.

A hypoechoic area--one that is dark on the monitor, because it isn’t solid like normal tissue--was found two centimeters (almost one inch) below the skin. This was the abscess. The good news was that draining the pus would start Wesley on the road to recovery. But there was some bad news, too: The abscess didn’t appear to be well encapsulated; that is, it was ill defined and spread out somewhat. If it were opened, the pus might not drain completely, and the abscess would only return. If instead the abscess was left to mature, or “ripen,” the body would wall off the infection into a distinct area that would drain more readily. They couldn’t fix my horse that day.

Eddy estimated Wesley’s abscess might be ready to open in two or three days. Because draining an abscess is a routine veterinary procedure, we had the option of taking our horse home and letting Shideler take care of it when the time came. However, Shideler was heading out of town, so we chose to leave Wesley at the clinic, where he could be monitored until the abscess was ready for lancing.

Crash course
I knew nothing of pigeon fever, so Eddy took a few minutes to explain it to me. Caused when C. pseudotuberculosis enters cuts or wounds as small as fly bites, pigeon fever can take three forms. About 90 percent of the time, the disease causes abscesses, most often on the chest but sometimes under the belly or in other areas, usually near the lymph nodes. In a second type of pigeon fever, the bacterium is carried to the liver, lungs, kidneys or other organs and internal abscesses form; these cases are more likely to be fatal. A third type, called ulcerative lymphangitis, affects the lymphatic system on the lower legs and is much more serious and slower to heal. This type is extremely rare in the United States.

I gave thanks Wesley had the most common and treatable form of pigeon fever. But I wondered how my horse had contracted this infection. Eddy said that C. pseudotuberculosis resides in the soil, and it thrives in arid or droughty conditions. The bacteria enter the skin either directly, when a horse with a cut or abrasion lies down, or indirectly, when he is bitten by a fly carrying
the pathogen.

The disease is common in California and the Southwest because the bacteria flourish in the hot, dry climate. Eddy commented that Mississippi had seen an increase in cases over the past two years. Most of the South has been parched from reduced rainfall those years, and large swaths of the Midwest have been experiencing droughts; in fact, the whole country has seen warmer temperatures. These conditions have enabled pigeon fever infections to sweep eastward and northward in recent years, and veterinarians who had never seen a case in their careers are now treating horses with the illness.

We left Wesley munching horse treats offered to him by the staff. Eddy called me the following evening. The overstretched skin covering Wesley’s voluminous abscess was threatening to split. The veterinarians now believed the lesion was mature enough to make the procedure successful. I gave the go-ahead.

Well-mannered Wesley required no sedation, only the local injection of anesthetic (Carbocaine) to numb the area. Eddy told me that while the process of draining a pigeon fever abscess may be relatively straightforward, it is an extraordinarily messy spectacle. After piercing Wesley’s skin where it was stretched so tight an exudate was beginning to ooze, the veterinarians had guided a 14-gauge catheter into the abscess until pus was aspirated. With the abscess location confirmed, a scalpel was guided alongside the catheter to drain the abscess.

Copious amounts of tan, odorless exudate spilled from the opening; this characteristic appearance of the pus helped confirm the diagnosis of pigeon fever. Because the abscess wasn’t quite fully encapsulated, the veterinarians made a second incision to open another pocket of infection. Wesley fared well during the procedure, and with the wounds left open, he was ready for discharge.

Healing at home
I had to work the next day, so my husband picked up Wesley and received our discharge wound-care instructions. Because the drainage from his wounds might be able to infect other horses, we were advised to isolate Wesley until all the exudates appeared to have exited and the swelling had diminished. Some experts even recommend burning all bedding or hauling it to a landfill, then bleaching all hard surfaces in the stall and any tack that’s come in contact with the horse.

More recent evidence and expert opinion suggest that isolation of a horse with pigeon fever and disinfection of equipment may not be necessary. However, we decided it was just good hygiene to keep this horse with a draining wound away from the others. We also wore disposable exam gloves to treat him and washed our hands after touching him.

Wesley’s daily wound care involved inserting a soft rubber catheter into the open cavities and flushing the pockets with a saline solution. Eddy told us how to make our own saline, using distilled water and table salt. She also advised us to coat Wesley’s chest area below the wounds with petroleum jelly to help protect his skin from the oozing exudate.

Ever the stoic gentleman, Wesley tolerated the treatments well. In less than two weeks, his wounds healed, the swelling resolved and he was released to return to his herd and his duties as a riding horse. We did elect to disinfect his halter and the stall, and I washed the saddle pad

I’d been using on him, too.

Pigeon fever has been around for a long time in the Southwest, yet I’d never heard of it happening here. However, cases have been on the increase in Texas and the South, and the disease has appeared as far east as Florida and Kentucky. The hot, droughty summers we’ve seen in recent years could make the infection more common in states where it had never been before. I hope that my experiences help you recognize the signs of pigeon fever sooner should the infection appear in your area. Finally, Wesley and I are off for that ride.

For more information, see “On Watch for Pigeon Fever” (EQUUS 368).

This article first appeared in EQUUS issue #426.

The term “colic” is very broad, encompassing any pain in a horse’s gut, regardless of the cause. When diagnosing individual cases and devising treatments, however, veterinarians will use more specific language. Here’s a quick look at four common colic descriptions and what they mean.

In strangulating colic, the blood supply to a portion of intestine is cut off. This can happen when a section of small or large intestine shifts and becomes entrapped in an abnormal location; when a lipoma, a mass of fatty tissue suspended on a stalk, gets wrapped around the intestine; or when a section of bowel twists upon itself, like linked sausages. The strangulated section of intestine eventually dies and the horse is typically in extreme and obvious pain with elevated heart and respiratory rates.

The blood flow to the intestine isn’t compromised in nonstrangulating colics but these situations can still be serious. These include gas colics, which occur when accumulation of gas causes painful distention in the bowels, as well as enteroliths, sand accumulations and food impactions, caused when a concentrated mass of dry feed can’t pass beyond a portion of the gut. These colics tend to be less painful, or the pain is transient. Horses tend to be restless, lying down and getting up frequently and staring at their sides.

Medical colics are cases that the veterinarian suspects may be treatable without surgery. These treatments may include painkilling medication and intravenous fluids. In many cases, medications and supportive care can resolve the situation quickly, but even a mild medical colic that does not improve over the course of a few hours is likely to be referred to a larger clinic.

Surgical colics are, as the name implies, those that the veterinarian suspects will require surgery to treat. Virtually all strangulating colics fall into this category as do blockages that do not resolve with medical treatment. Numerous studies have shown that the more quickly a severely colicking horse is referred to a surgical facility, the greater are his chances of survival, so don’t be surprised if your veterinarian makes this decision very quickly.

This article first appeared in

EQUUS issue #426.

You go to catch your horse for a ride and there it is—a big, ugly laceration right in the middle of his chest. You panic when you see blood running down his leg, and it looks like he’s cut right down through the muscle. Now what?

Breathe. Relax. Believe it or not, even a big, deep laceration in your horse’s chest is likely to heal quickly, and without much trouble. Why? Because it’s an area with large muscles, good blood flow, and few critical structures at risk of being damaged. But if you find a tiny little puncture at the back of your horse’s pastern, that’s another story. Even the smallest, most benign-looking wound in that area could mean trouble.

In this article, I’m going to help you understand what makes a wound more serious, and why. First, I’ll give you a quick rundown of the five critical factors to evaluate when faced with any wound. Then, I’ll give you some real-life scenarios so you can decide whether that wound is a nightmare or a nuisance—and what you should do about it.

Factor 1
Location, location, location. The location of a wound is one of the most important factors in determining its severity. If it’s over a well-muscled area of the upper body like the chest or croup, you’re in luck. There’s good blood supply and few critical structures to complicate healing. It’s likely to heal well, even if it’s big and deep.

The same is true for wounds on the head. They often heal quickly and well with few complications, even if they look horrifying at the start.

Wounds on the lower legs, especially those below the hocks and knees, are typically more difficult. Blood supply may be limited, and there’s little extra tissue between the skin and the more critical underlying structures. A wound that’s directly over a joint or tendon sheath is the scariest of all because penetration risks infection of one of those critical, closed-off structures—a potentially life-threatening complication.

Factor 2
Other signs. Is it “just a wound,” or is there some other symptom that could mean something more? Most commonly, excessive bleeding may be cause for concern, and might happen any time a large vessel is disrupted. If blood is bright red and spurts in pulses, that’s the most concerning of all, as it means a high-pressure artery is likely to be involved.

Lameness is another sign that a wound might be serious. If your horse is lame with a wound, a critical structure such as a joint, tendon, or ligament might have been damaged. Severe lameness might also mean a more serious injury, such as a broken bone.

Finally, if the wound is on your horse’s face, signs such as squinting or tearing might mean his eye’s been damaged. Blood from his mouth, or difficulty chewing, could point toward an injury to his teeth or jaws. Anytime a wound is accompanied by another problem, it’s likely to be more serious, and to require special care.

Factor 3
How deep? The depth of a wound is important for helping you decide just how serious it is, and whether it needs sutures.

To determine just how deep it is, try to separate the edges by putting pressure on either side. (It helps to clean the wound with cold water from a hose before this step.)

If the wound is fresh and you can pull the edges apart, it’s likely to have penetrated the full thickness of the skin and would heal best with sutures (unless it’s a puncture wound; see page 2). If you can’t pull the edges apart, chances are it’s just an abrasion and sutures won’t be necessary.

Keep in mind there are areas on your horse’s body where the skin is up to one-quarter-inch thick, meaning a deep abrasion can look much more frightening than it is. Most non-full-thickness injuries will heal without much trouble.

Finally, a very deep wound, even if it’s small, might end up as the most nightmarish of all, due to risk of penetration of more important deeper structures—taking us back to location as a crucial factor. A tiny but deep wound over a joint may turn out to be a much bigger issue than a huge abrasion over a well-muscled area.

Factor 4
How big? If all other factors are equal, size does matter. A wound that’s less than one-half inch in length typically won’t need sutures, even if it’s a full-thickness deep through the skin. A wound that’s between one-half and one inch might heal better with a stitch or two, and a wound that’s longer than an inch will almost always heal better if it’s sutured.

Again, though, location plays a role in this decision. A longer wound on the well-muscled upper body is likely to heal even if it isn’t sutured, while a shorter wound on the lower legs will be much more problematic if left to heal on its own. As a general rule, a call to the vet is an important step for any full-thickness lower-leg wound.

Factor 5
How old? It’s always best if you discover a wound immediately so that you’re able to make a treatment decision right away, while the damage is fresh. Fresh wounds that are attended to immediately are much less likely to become nightmares than are wounds that are days or even hours old.

Excessive swelling or drainage of yellowish/brownish thick fluid are two signs that a wound is older and possibly in need of special care. However, contrary to popular belief, even a wound that’s a day or two old may often still be sutured, and will heal much better as a result.

Now that you know the five basic factors to evaluate on any wound, let’s take a look at some common wound scenarios and whether the wound in each will become a nightmare or a nuisance.

On-again, off-again lameness, low energy levels, a cranky attitude—those signs could point to something as simple as overwork. But Lyme disease could produce all those problems, and it may be a growing problem for horses in parts of the United States. Lyme disease can have long-term complications that include damage to your horse’s joints, skin, nervous system and even vision.

A bacterial disease spread by tick bites, Lyme is a problem for people, dogs and other animals, not just horses. As the ticks that carry this disease slowly expand their range, cases and concern are increasing. Is your horse at risk? If he develops Lyme disease, how will you know, and what should you do? Can you protect him? This article will help you make sense of the threat.

Who’s at Risk?
Lyme disease takes its name from Lyme, Connecticut, where it was first identified in the 1970s. It’s now the most common vector-borne disease in the United States, according to the US Centers for Disease Control, which tracks human cases. The disease has popped up in ­almost every state, but CDC figures show that most cases occur in the northeastern, mid-Atlantic and north-central states, with pockets in Pacific and southern states.

While no one collects national statistics on Lyme disease in horses, cases tend to occur in the same areas as human cases, says Thomas J. Divers, DVM, of the Cornell University School of Veterinary Medicine. Those are all places where the disease-carrying blacklegged ticks—mainly deer ticks and Western blacklegged ticks (photo above)—are common. In some areas up to half the blacklegged tick population may harbor the spiral-shaped bacteria, Borrelia ­burgdorferi (Bb), that cause Lyme disease.

The ticks have three life stages (larva, nymph and adult) and need a blood meal ­before they can molt into the next stage. They pick up the bacteria as larvae and nymphs by feeding on the blood of infected mice, and they transmit the infection to their next hosts—human, horse, dog, deer or any passing mammal or bird. They seem most likely to feed on horses as adults. In cold-winter regions, adults typically appear in early fall, spend the winter dormant in brush and leaf litter and come out again in early spring. This makes early spring and fall prime times for infection. But horses can get Lyme disease whenever infected ticks are active.

CDC statistics show a steady increase in reported cases. In some areas, including parts of Maryland and Virginia and northern New England, human case numbers are up sharply. Maine, for example, went from no cases reported in 1988 to 970 in 2009. Maine state veterinarian Don Hoenig, VMD, says that Lyme disease is turning up in new areas as the vectors—deer ticks—increase their geographic distribution. “We have ticks where we had none six or seven years ago,” he says. Several factors likely contribute to the spread:

• Wildlife populations: Deer and other wildlife hosts, including migratory birds, can carry the ticks and move them to new areas.
• Changing landscapes: In many areas abandoned farmland is reverting to forest, and the ticks prefer forest habitat to fields. They’re often found in the brush of the forest understory and forest edge—and suburban yards, which mimic that habitat.
• Warming climate: Warmer winters ­allow ticks to expand their range northward and to spread disease for more of the year, as they are active whenever the temperature is above 40 F.

Reports of Lyme disease have also ­increased as people have ­become more aware of it. “We’re looking for it more,” Dr. Hoenig says. Lyme is now so prevalent in Maine, he adds, that it’s no longer on the state department of agriculture’s list of reportable diseases.

If your horse is in a region where blacklegged ticks live, he’s at risk. But even if he’s bitten, he may not get sick. Even if a tick is packing the bacteria, it generally must attach and feed for more than 24 hours before it transmits the infection to its new host. And even when a horse is infected, he may not develop any signs of the disease. “There must be a distinction between infection and disease,” says Dr. Divers. Infection is common where the disease-carrying ticks are prevalent—nearly half of adult horses in some areas of the Northeast have been infected. “Clinical disease [disease that produces recognizable signs] does not appear to be common in horses, although we do not have data on this,” he says.

When Obie's pupil suddenly became dilated, his owner was immediately worried.

Photo © EQUUS

Obie caught the eye of an excellent eventing trainer seeking a new prospect, and we agreed to deliver him to her farm on July 9th for an evaluation period.

Jason bathed Obie the evening before he was scheduled to leave and then, to keep him clean, placed him in a stall for the night instead of turning him back out in his dirt paddock. Noticing that the flies were bad that evening, Jason went back to the tack room, grabbed the nearest fly mask and put it on our horse.

When I arrived early the following morning, Obie came out of the stall looking great. Even with the barn lights turned off I could see that he was gleaming. He was still wearing the fly mask, and we decided to keep it in place for the trip. My trailer has stock sides, and the mask would provide protection from any debris that might come up off the road. Jason took a quick peek under the mask to make sure Obie’s eyes weren’t gooey, and since everything looked good, we loaded up and left.

We pulled into the trainer’s farm two hours later, and Obie, always a good traveler, came out looking relaxed and regal. It wasn’t until we led him into the barn and took the fly mask off that we discovered a problem: Obie’s left eye looked strangely blue. On closer inspection, we saw that the blue appearance was the result of huge dilation of the pupil.

Although more oval than round, a horse’s pupils function just as our own do: They expand to take in more light when necessary, then constrict to limit the glare in brighter conditions. And, also as in people, both of a horse’s pupils ought to be the same size at the same time. Any noticeable difference between the appearance of the pupils can be a sign of serious trouble.

That was exactly the problem confronting us: Obie’s right eye looked normal, and the left pupil was wide open and completely unresponsive to light.

No clues
My first thought was that Obie must have hit his eye or whacked his head in the trailer. But we found no other signs of trouble---no tearing, swelling, discharge or any marks that would indicate trauma. Obie didn’t appear to be in pain; he let us touch his face all around the eye without protest. In fact, he was acting perfectly normal---interested in his surroundings and even more focused on the possibility of getting some of the hay stacked in the corner. Neither Jason, the trainer nor I---all lifelong horsepeople---had ever seen anything like this.

I was truly alarmed, so we called the trainer’s veterinarian, who arrived within the hour. After her initial examination, she agreed there was no obvious sign of trauma or disease and that Obie didn’t seem to be in pain. She did offer one possibility---glaucoma, an increase of fluid pressure in the eye that is a common cause of pupil dilation. In horses, glaucoma is usually secondary to a disease such as uveitis or a tumor within the eye. If the pressure within the eye remains elevated long enough, the optic nerve can be damaged, leading to blindness. The good news was that Obie didn’t show any other signs of glaucoma, such as pain or squinting.

To get a closer look at the internal structures of the eye, the veterinarian gave Obie a dose of tranquilizer and a local anesthetic. Once the gelding was relaxed and numbed up, she examined the retina more closely and found it to be perfectly normal. She also stained the eye with a fluorescein dye, which would settle into any scratches in his cornea to appear as bright yellow streaks or spots. But the veterinarian saw no evidence of even subtle trauma.

Next, she used a small penlight to check what is known as the “consensual response.” Normally, if you shine a light into one eye, the pupils in both eyes will react in exactly the same way. If they don’t, then the horse may not have vision in the eye being tested. Fortunately, shining the light in Obie’s left eye caused his right pupil to constrict, so he still had at least some sight on the left side. But we still had no clue what was wrong---or if he was in danger of going blind.

As she finished her examination, the veterinarian was unable to make a diagnosis. Based on the clues she had, her best assumption was that the dilation of the pupil was due to some kind of trauma, despite the lack of cuts, bumps or scrapes on Obie’s face. She prescribed a course of phenylbutazone, in case there was any inflammatory process at work, and suggested that, if there was no improvement within a few days, we take Obie to the ophthalmology department at the University of California–Davis for a more thorough workup. As she packed up to leave, she told us to keep a fly mask on Obie to protect the eye---too much sunlight entering through the dilated pupil could damage the retina and create a very real danger of blindness.

A flash of insight
After conferring with the prospective buyer we decided to leave Obie at her place rather than trailer him again with this undiagnosed ailment. We were also hoping that the problem would resolve on its own, as quickly as it had appeared. Unfortunately, after three days there was no change in Obie’s pupil, so my husband and I brought him home.

Back at our place, Obie still seemed completely normal except for that ominous eye. I was worried about the possibility of sun damage, so I made a “pirate patch” by cutting up an old fly mask and sewing two extra layers on top of his existing mask. He accepted this impediment to his vision with his usual good nature. Meanwhile, I went into research mode and read up on every equine eye problem I could find on the Internet. Obie’s single sign of trouble didn’t seem to match up with anything.

I also called the ophthalmology department at UC–Davis and was put in touch with Ann R. Strom, DVM. I explained Obie’s case and asked what they could do that the trainer’s veterinarian hadn’t already done. Strom explained that the UC–Davis clinic had specialized equipment that would enable them to detect problems not visible with the tools available to a veterinarian in the field. If the physical exam turned up nothing, they would start looking for possible neurological causes, such as a brain tumor or a tumor between the eye and the brain, which could best be viewed with a CT scan. Unfortunately, the cost of all this could easily run into the thousands, which we simply couldn’t afford. I had no idea what to do.

My friend Jason had also been racking his brain, trying to think of anything he had seen or done that might offer clues. He was absolutely certain Obie’s eye had been fine after his bath on the evening before the problem was discovered. What he didn’t know was whether the eye was dilated before the trailer ride the next morning
---although he had glanced under the fly mask, it was too dark for him to have noticed any changes in the pupil.

Then Jason had a light bulb moment: He remembered that the last horse to occupy the stall Obie had been in was a mare who was being treated for an eye problem. He dug through the ranch’s medical records and discovered that six weeks previously, this mare had sustained an injury to her left eye. She had been treated with atropine ointment, a powerful and long-lasting drug used to dilate the pupil. Could that horse have rubbed her medicated eye on something in the stall, something that Obie then rubbed on, too, causing him to get some residual atropine into his eye? It didn’t seem entirely implausible.

Jason and I ran this scenario by several veterinarians, all of whom seemed to think the idea was too far-fetched. My own veterinarian, Jen Powers, DVM, of Above and Beyond Animal Care in Redding, California, was also dubious, but she didn’t discount the idea entirely: “I think it’s highly unlikely, but stranger things have happened.”

Powers, like Strom, mentioned the possibilities of glaucoma or a tumor, although she agreed that it would be unusual for a horse to have either condition without showing any additional signs of trouble. She was fairly sure that the dilation was not due to trauma. In her 18 years of experience as an equine veterinarian, she said, she had never seen a traumatic eye injury with a dilated pupil as the only sign. Any blow severe enough to cause the pupil to dilate that much should have caused some other obvious injury to the head or eye itself.

If exposure to atropine had caused the dilation, Powers said, we would start to see gradual improvement within seven to 10 days of the initial exposure, although it could take a couple of weeks to fully resolve.

Jason then contacted us with another important clue: After consulting with his staff, he discovered that the fly mask he had put on Obie that night was very likely the same one the injured mare had worn during the course of her treatment. We found no sign of any ointment on the mask, but it seemed more plausible that he might have come in contact with residue from the fly mask than from some random spot in the stall.

With this news, my husband and I decided to wait a few more days to see if Obie’s eye showed any improvement. If it didn’t, we were going to have to bite the bullet and haul him to Davis.

Back to normal
To our joy, we found that the dilation of Obie’s left pupil did begin to subside, all on its own, exactly one week after that fly mask was first put on him. The progress was slow, but the eye continued to improve day by day.

On July 19, the 10th day after the trouble began, I emailed Powers a photo of Obie’s eye and asked if she felt it was OK to continue to wait or whether we should go ahead and take him to Davis. She responded, “The amount of dilation Obie shows at this point is not severe, which decreases my fears of glaucoma, tumor or blindness. I think you are fine to wait another week.”

We continued to see improvement with each passing day, and by July 21, his pupil was able to constrict enough that we felt we could safely remove the extra layers of material on his fly mask, and five days later, his eye seemed completely normal again. The entire ordeal had lasted 18 days.

Powers now agrees that atropine was the most likely cause of this strange problem. “Without the stimulation of pain [there was no injury] or light [due to the eye patch], there was no stimulus for the pupillary muscles, so it is possible for the effects of atropine to have lasted this long,” she told me. “The atropine theory is also supported by the resolution course and the story of the fly mask---a good example of why it is important to wash and disinfect shared items!”

I am happy to report that Obie now shows no sign of having ever had a problem with his eye, and he has a wonderful new home.

This article first appeared in EQUUS issue 424.

It's normal for a horse to lay down from time to time, but if he suddenly spends more time than usual down, it's cause for investigation.

Spice was spending nearly all her time lying down. The 16-year-old Paint mare didn’t appear to be weak or in pain---she could readily scramble to her feet when she wanted to. But she simply wouldn’t stay on her feet. For almost a month, she’d get up just two or three times a day to eat, drink, defecate and urinate, then she’d lie down again.

Several veterinarians came out to see Spice that April in 2008, but they found no obvious reasons for her peculiar behavior. She was current on her vaccinations, she wasn’t lame and her vital signs were normal.

Spice’s veterinarian was baffled and recommended a consultation with nearby Colorado State University. But the mare’s owner was afraid that the ride would be too difficult for her or that she would go down in the trailer. So Lutz Goehring, DVM, PhD, a faculty member with the veterinary teaching hospital, made a farm call.

Goehring found Spice lying calmly in sternal recumbency, propped up on her chest and looking as if she just decided to take a brief afternoon nap. “I was thinking I’d find a horse who looked ill or in distress, but she was happy, and it was obvious she had been really well cared for in the time she was down,” he says. “Her owner had bedded her on deep sand in a large roofed area. She looked like a mare who just happened to be lying down and resting.”

Spice also seemed normal as she got up, which she did with just a bit of encouragement. “She had no problem at all standing up. She was very coordinated and strong, with normal reflexes,” Goehring says. But, he adds, once the mare was on her feet, “we did notice something very unusual.”

As she stood Spice’s muscles became stiff and tense. “You could actually see the muscles contracting under the skin,” says Goehring. When she was asked to walk she moved in short, rigid steps. When she stood still, her hind and forelimbs were drawn closer together than normal, giving her the appearance she was standing on a large circus ball. These were all important, but somewhat contradictory, clues.

Process of elimination
Goehring worked through a number of potential diagnoses:
• Tying up (recurrent exertional rhabdomyolysis) causes severe, painful cramping of the large muscles, usually after exercise. When you see muscles contracting as Spice’s were, “you naturally think of tying up,” Goehring says, “but all of her muscles were affected, not just the hindquarters as you’d expect.” Also, horses who are tying up are usually in obvious pain, with profuse sweating and rapid breathing; Spice was not. “To be certain, we also tested her urine and blood and did not see any of the proteins you’d find associated with the muscle damage of tying up,” he adds.
• Hyperkalemic periodic paralysis (HYPP) is an inherited muscle disorder of Quarter Horses and related breeds that causes muscle tremors, weakness and recumbency. But Spice’s pedigree did not include any horses known to carry HYPP, nor did she display the characteristic weakness and collapse.
• Tetanus is a rigid paralytic disease caused when the anaerobic bacterium Clostridium tetani, which normally lives in soil and feces, enters a puncture wound. Tetanus can cause stiffness throughout the body, but Spice was current in her vaccinations against this disease, and she was not displaying any other classic signs of the condition, including the protrusion of the nictitating membrane across the eye.
• Botulism is a paralytic condition that occurs when a horse ingests food or water contaminated with toxins produced by the bacterium Clostridium botulinum. Horses with early stages of botulism often lie down for long periods as the associated paralysis develops. But botulism usually affects the muscles of the head and mouth first. Spice was eating and drinking normally.
• Laminitis, the inflammation of the sensitive soft tissues that connect the coffin bone to the interior of the hoof wall in the foot, can cause horses to stand with an unusual “base-narrow” stance like Spice was showing. But laminitis is extremely painful, yet the mare did not react at all to sole pressure from hoof testers, and radiographs of all four hooves showed no coffin bone rotation.
• Fractures to the pelvis or lower spine can leave a horse reluctant to walk, even if he doesn’t appear to be obviously lame. Goehring ruled out an injury like that in Spice with a rectal exam.
• Neurological diseases, such as equine protozoal myeloencephalitis (EPM) or West Nile encephalitis, can cause a variety of signs, including stiffness, recumbency, weakness and incoordination. To investigate this possibility Goehring performed a full neurological workup on Spice, checking the muscle tone in her tail and asking her to walk forward, backward and in small circles. “In neurological disease, you see some incoordination or asymmetry,” he says. “But we didn’t see any of that. She was moving stiffly but was not weak or clumsy.”

Having exhausted the possibilities for physical exams, Goehring gathered blood samples to follow up with laboratory tests, and he suggested transporting the mare to the University clinic so he could take spinal fluid samples and a muscle biopsy. But Spice’s owner was still concerned about the toll the trip might take on her mare and opted to pursue only tests that could be done on the farm---especially since Goehring didn’t yet have a particular diagnosis in mind.

Working on the assumption that some type of muscle pain was keeping the mare off her feet, Goehring prescribed a course of phenylbutazone and the muscle relaxant methocarbamol, and he asked Spice’s owner to provide him with frequent updates on the mare’s condition up until his next scheduled visit, in two weeks. By then, he hoped, the results of the blood tests would have shed more light on the cause of Spice’s trouble.

One last shot
Spice was getting worse when Goehring returned. Instead of lying on her chest, the mare was now spending most of her time stretched out flat on her side, and she was eating and drinking while down. She was also getting up less often, as little as only once a day to defecate and urinate before stretching out again on her opposite side.

The standard blood work had revealed nothing abnormal, and the tests were also negative for antibodies to the West Nile virus as well as Sarcocystis neurona, the organism responsible for EPM. Spice’s protein and enzyme levels were normal, indicating there was no muscle damage or malfunction, nor did her blood show any sign of inflammation or infection.

Goehring encouraged Spice to rise then spent a few minutes just watching her. He noticed the same pattern he’d seen on his first visit: “She’d walk around for a few minutes, and then you’d notice muscle contractions and a tightening of all her muscles. Then she would lie down in a very coordinated way. She didn’t seem upset or uncomfortable; it was almost as if she got tired, and lying down was her way to cope with the increased muscle contractions and what I assume was associated fatigue and soreness from it.”

The problem had to originate in either her muscles or her nerves---but given that the phenylbutazone and muscle relaxant had had no effect, a neurological explanation now seemed more likely. “If the problem wasn’t with the muscles, it had to be the nerves that control them,” says Goehring.

Yet Spice’s signs didn’t fit into any known neurological pathology. “A traumatic neurological event or a disease process generally affects neurons at one specific location in the nervous system, so you’ll see a horse lose control of his hindquarters or one side of his body. But every muscle on this mare seemed to be involved equally,” says Goehring. “Toxins can also affect a horse’s nervous system, but they tend to target a particular type of neuron and are progressive; eventually you’ll see seizures and other more serious problems.”

That left one area of possibility: an immune-related disease affecting only a specific portion of the central nervous system. “In immune-mediated diseases, the horse’s own body will attack a very specific target group of cells or structures,” says Goehring. “It was possible, we thought, that such a scenario could give us the strange presentation we were seeing. At the time, we had no idea what that specific process might be, but it was really our last shot.”

A one-in-a-million diagnosis
To test that hypothesis, Goehring recommended a course of injectable corticosteroids. “Steroids will suppress the body’s immune system, which can be a bad thing unless it’s the immune system itself that is harming the body,” he explains. If Spice’s condition was an immune-mediated neuropathy, the steroids would lead to improvement.

Goehring was headed to a conference, so a colleague oversaw the treatment, starting with a relatively high dose followed by smaller subsequent doses that tapered off over the course of a week. “At the conference, I discussed this case with several prominent equine neurologists and told them what I was going to try,” he says. “They were interested but maybe a little skeptical. So it was nice when I was able to share the text I got two days later that the treatment was working---the mare was up and moving more.”

Indeed, Spice showed a dramatic improvement: By the end of the week she was standing about 75 percent of the time. That success led Goehring to search the literature for a possible explanation.

He found one disease in human medicine that seemed to fit Spice’s case: Moersch-Woltmann syndrome, also called “stiff person syndrome” (SPS). People with SPS experience fluctuating muscle rigidity, particularly in their trunk and limbs. The first symptom is usually stiffness in the back that can come and go, often triggered by loud noises or stressful events.

Over weeks or months, the disease progresses until the painful spasms become increasingly frequent and involve the entire body, to the point of immobilizing the person for hours. Patients typically have a halting, stiff gait because the muscles never fully relax between spasms. They also report being exhausted by the episodes. SPS is extremely rare---the exact frequency is unknown but it may affect as few as one in a million people. The condition typically develops between the ages of 30 and 50, although babies may be born with it.

SPS was first named in 1956, and in the 1980s, researchers linked the disease with an autoimmune dysfunction after they discovered that the majority of affected individuals were producing high levels of antibodies to an enzyme called glutamic acid decarboxylase (GAD)---that is, their bodies were attacking and destroying this critical enzyme in large numbers. GAD is essential for the production of an amino acid called gamma-aminobutyric acid (GABA). GABA acts as an inhibitory neurotransmitter, meaning it slows down the activity of nerve cells.

“When a horse or person moves, certain muscles have to relax in order for others to contract,” explains Goehring. “For instance, when the biceps [on the front of the upper arm] contracts, the triceps [on the back of the upper arm] must relax [in order to raise the arm]. GABA helps make this happen by blocking nerve impulses.”

In people with SPS, the destruction of GAD, and the subsequent reduction in GABA, causes nerve cells to fire too often and too easily. And so, for example, the biceps and triceps muscles might struggle to contract simultaneously---a situation that produces the characteristic limb stiffness and muscle spasms.

Could horses experience an equine version of SPS? Goehring found one paper published in 2000 that described a Belgian Warmblood who had shown periodic stiffness similar to Spice’s and who had elevated antibodies to GAD, just as in SPS. The authors of the paper dubbed their observations “stiff horse syndrome.”

To see whether Spice might have stiff horse syndrome, Goehring had her blood tested for antibodies to GAD, along with a sample from a normal, healthy mare for comparison. Spice’s blood had a significantly higher amount of the antibodies. This result wasn’t a definitive diagnosis, but it did strongly suggest that the mare might have this rare condition.

Exploring unknown ground
Even though there was little precedent for treating Spice, her owner decided she wanted to try. The mare was kept on the corticosteroids for another month, during which time she gradually improved to her normal self. She was then weaned from the medication, after which she continued to remain on her feet as much as any normal horse. Continuing blood tests showed the mare’s GAD antibodies decreasing over the course of treatment.

“This made me more certain that she had some form of stiff horse syndrome,” says Goehring. “It seemed that we had interrupted the immune system enough for the assault on GAD to end, allowing GABA to be produced and regulate muscle activity.”

Goehring hypothesized that the muscle contractions Spice had been experiencing were simply exhausting the mare, which caused her to lie down more than normal. “What we were seeing wasn’t an inability to stand,” he says, “but an all-over soreness and tiredness that made her not want to.”

Months passed with no further developments, until the following spring, when the mare began lying down more than normal again. “I wasn’t surprised,” says Goehring, “because once the immune system returns to full function, it’s going to start attacking antibodies again. The question is just how quickly and to what extent.”

At that time, Goehring adds, “we looked into officially testing for GAD to quantify just how badly she might be affected, but new testing methods for human samples appeared to not work in horses.” Instead, he started Spice on another course of corticosteroids and, as before, the mare improved dramatically within a few days.

This pattern continued for four years: Every eight to 12 months Spice would begin to spend more time lying down, and a course of corticosteroids would get her back on her feet. To reduce the risk of adverse side effects, Goehring gave Spice the lowest amount necessary to see an improvement. But the mare never showed any other signs of illness or trouble until she died after an unrelated colic earlier this year.

Although stiff horse syndrome is undoubtedly quite rare, Goehring says he suspects it may occasionally go undiagnosed: “I’m certain there are horses out there with this right now, but no one knows. Personally, I see maybe one or two cases a year that come in as an orthopedic problem. The horses aren’t lame; they just have a generalized stiffness that gets worse with work. They have normal muscle enzyme activity, and when you put them through diagnostics like scintigraphy and radiographs you can’t find a problem, and they don’t have any other obvious illness. In these cases I add stiff horse syndrome to the list of considerations and suggest corticosteroid treatments.”

Unfortunately, he says, many owners are doubtful and reluctant to pursue that suggestion: “It’s as if they don’t believe me. But if they try it and the horse improves, we’re that much closer to an answer. And if we can do it before the horse goes down, even better.”

Goehring adds that Spice’s case shows that this condition, although chronic, can potentially be managed long-term with corticosteroids and attentive care: “This mare was watched closely by her owner, who learned what the signs of trouble were and then knew how to care for her. She’s really the reason this mare did so well.”