In the fall of 2012, Kay Lynn Schulz was riding high. She had just won the Elite Extravaganza for the second time aboard her home-bred gelding, KS Dox Cajun Bug. 

Chagas2Kay Lynn Schulz shares a moment with her beloved home-bred gelding, KS Dox Cajun Bug. Photo courtesy Kay Lynn SchulzThe dental hygienist and mother of two had the support of her family—husband, Steve, and their two boys, Mason and Sterling. Schulz made arrangements with her employer for extended time off as she and “Cajun” took off on her dream quest— trying to qualify for the Wrangler National Finals Rodeo. 

Yet Schulz’ plans began to unravel at a barrel race on New Year’s Eve. Her once steady partner ducked a barrel. Like any good horsewoman, Schulz gave Cajun the benefit of the doubt, taking him to the veterinarian to see if something was wrong. 

Although the problem seemed simple at first, Cajun progressively got worse, and the possible causes grew increasingly complex and perplexing. What began as a journey to return Cajun to top form soon became one to save his life. 

Best Laid Plans

When advancing arthritis in a knee ended the career of Schulz’ rodeo mount Lady Bug Bug in 2002, she decided to breed the granddaughter of Bugs Alive In 75. 

“I wanted to breed her to Sun Frost, but he was a little beyond my budget,” Schulz said. “I talked with Tigh Cowan and decided on PC Dox Cajun.” 

Cajun was foaled in 2003, and Schulz’ entire family had a part in his training and competitive career. He began his career in the fall of 2007 at local jackpots near Schulz’ San Antonio, Texas, home. 

His first national appearance came at the Barrel Futurities of America World Championship derby in Oklahoma City. He placed twice, once with Schulz in 2008 and once with her sister, Jennifer Crawford, who rode the gelding most of 2009 due to Schulz’ pregnancy. 

In 2010, Cajun carried Schulz to the Women’s Professional Rodeo Association Rookie of the Year title in the Texas Circuit, and they made their first appearance at the Texas Circuit Finals Rodeo in Waco, Texas. 

“Before I went to the circuit finals, I made the decision that if I didn’t win it and qualify for the National Circuit Finals Rodeo, I would turn him out for 2011 to concentrate on the toughest year of dental hygiene school,” Schulz said. “I would resume running him once I finished school in May 2012.” 

Cajun didn’t miss a beat after his vacation, running a 16.9 on a WPRA standard pattern at the American Novice Horse Association Shootout in Waco. They went back to Waco two months later and won the 1D at the Elite Extravaganza in 2012. Schulz planned to win enough money in 2013 to qualify for the lucrative winter rodeos so she had a better chance at making the NFR in 2014. 

Then Cajun ducked the first barrel on New Year’s Eve. 

The Unexplained 

Schulz took Cajun to her regular veterinarian, Robert Ball, DVM, of Bracken Equine in San Antonio. After diagnostic nerve blocks to Cajun’s front foot made him sound, Schulz opted for an MRI to make sure it wasn’t something serious. Cajun had his coffin joint injected on January 14, 2013. 

“I rode him periodically to give the injections time to work,” Schulz said. “He was fresh and frisky. I took him through the poles one day. He flew through them, but turning the right pole, he lost his hind end and fell.” 

On the barrels, Cajun still worked his second and third but “turned his first really wrong.” The first weekend of February, Schulz took Cajun to a jackpot and he ducked the first barrel in the warm-up pen. Two days later she was back at Bracken Equine. 

“He palpated sore to his left stifle,” Schulz said. “We had to wonder if his front feet were that sore that he was making his backend sore, or was it from when he fell at the house.” 

After several weeks off, Cajun looked worse despite the rest. In mid-March, it was back to the vet for a neurologic exam. 

“His hind end wasn’t right walking around,” Schulz said. 

Cajun exhibited ataxia—failed coordination—in both hind limbs, with the right hind worse than the left, which fell in line with his right-hand turn issues. 

A spinal tap to retrieve cerebrospinal fluid was performed and sent to the University of California-Davis to be tested for antibodies against Sarcocystis neurona (S. neurona), the most common cause of equine protozoal myeloencephalitis. Unfortunately, the mere presence of the antibodies doesn’t guarantee a diagnosis, as researchers suspect as much as 60 percent of the equine population has had exposure to S. neurona but may not be symptomatic for EPM. 

Given the difficulty of confirming a definitive EPM diagnosis while the horse is alive, Cajun was immediately started on Marquis (ponazuril)—a 28-day oral paste treatment—March 18, 2013, without waiting for the EPM test results. 

When all of Cajun’s test results came back negative for EPM, Schulz decided to finish the Marquis treatment anyway. The clean test results led Schulz to believe maybe something else was causing his neurologic problems. 

At the beginning of April 2013, Schulz took Cajun to noted equine chiropractor Daryl Elliot, who suspected it was EPM. To further rule out any skeletal problems, Schulz went to Chris Ray, DVM, at Equine Sports Medicine & Surgery in Weatherford, Texas. 

“He had a bone scan, and it was clean,” Schulz said. “We continued to treat him for EPM. He still looked great. He hadn’t lost a pound. In a circle, he couldn’t function, but other than that, he didn’t look like a horse that had EPM.” 

Meanwhile, Schulz tried another EPM treatment, Oroquin 10. The 10-day treatment is a combination of levamisole, an anthelmintic (de-wormer) used in cattle, sheep and pigs, and decoquinate, an anti-protozoal. A tapering course of the corticosteroid dexamethasone was administered along with the Oroquin 10. A second course of levamisole, by itself, was also administered. 

Schulz even took Cajun to Janek Vluggen, DVM, a German osteopath who practices and teaches out of the Whole Horse Veterinary Clinic in San Marcos, Texas. The osteopath confirmed a neurologic blockage in Cajun’s lumbar spine was causing the ataxia in Cajun’s hindquarters, but Vluggen said he didn’t think it was EPM. 

In her last desperate attempt to find answers, Schulz took Cajun to her alma mater, Texas A&M University in College Station, Texas, in July 2013. 

Veterinarians found nothing remarkable on a standing musculoskeletal exam, and unlike most EPM horses, Cajun lacked any muscle atrophy. During the moving exam, Cajun had difficulty turn- ing on his hind limbs and swung his rear legs in wide arcs, a motion called circumduction by veterinarians. He had trouble with uneven surfaces and low obstacles, like curbs. 

When veterinarians pulled his tail while standing still, Cajun had adequate strength but was easily pulled off balance while walking. His right side was still worse than his left, with the right being a 4 out of 5 and the left being 3 out of 5 on the lameness scale. 

Radiographs of his neck and back were normal. Ultrasounds of his spine, sacrum and pelvis—performed both transcutaneous (over the skin) and transrectal (through his rectum)—yielded no abnormalities. His blood work was normal. 

“They did every test imaginable—X- rays, ultrasounds,” Schulz said. “Several thousand dollars later, I still didn’t have any answers.” 

Schulz took Cajun home, announced his retirement from competition and hoped to keep him comfortable for as long as she could. On his good days, Cajun had a little turnout time to graze and play with the other horses over the fence. 

Watching Cajun’s spark diminish was one of the hardest things Schulz has ever done. 

“He continued to decline,” Schulz said. “He started to get depressed. He’d stand at the fence and watch the other horses. He wanted to play, but he couldn’t move.” 

Knowing her only hope for answers was a thorough post-mortem exam, Schulz made arrangements to send Cajun back to Texas A&M. 

“When I talked to A&M again, I said I wanted them to check everything again and compare notes,” Schulz said. “The problem is, you can only diagnose so much while they’re alive. I had to put him down to find out what was wrong with him.” 

She said goodbye October 13, 2013. Cajun was just 10 years old. 

The Unexpected 

Per Cajun’s necropsy report, the cause of his severe ataxia was EPM. Changes found in his spinal cord were “compatible with protozoal meningomyelitis, with the most likely agent being Sarcocystis neurona. . . . Rare protozoa are observed in a few sections.” 

The necropsy report concluded, “It is unknown why he did not improve with anti-protozoal treatment, but studies have shown approximately one third of horses with EPM resolve neurologic deficits with treatment, one third of horses improve to some degree with treatment and one third of horses didn’t improve. It appears Cajun’s case was refractory to treatment.” 

The report left Schulz frustrated. 

“When the necropsy report came back and said he had EPM, I felt a little jaded. I was thinking maybe I should have given him another year and maybe tried some alternative therapies,” Schulz said. “The week before I put him down, I took a bunch of pictures of him, and he didn’t look like a horse with EPM. He didn’t fit the profile with the muscle atrophy and nerve damage.” 

It wasn’t until Schulz visited with her regular veterinarian some time later that she learned pathologists at A&M had made a startling discovery upon further inspection of the protozoa found in Cajun’s spinal cord. The damage to Cajun’s spine wasn’t caused by S. neurona, the causative agent of EPM. His protozoa were Trypanosoma cruzi (T. cruzi), the agent that causes Chagas disease in humans and dogs. 

Named after Carols Chagas, the Brazilian physician who discovered the disease in 1909, Chagas disease is endemic in Mexico, Central and South America. Cases in dogs and humans have been widely reported in South Texas. Chagas is transmitted by triatomine bugs, namely the kissing bug, because they bite around the mouth and eyes. They are found in 28 states, especially Texas, New Mexico and Arizona. 

Kissing bugs—not to be confused with lovebugs—spread T. cruzi through their feces. When they bite and ingest blood of their victim, they defecate. The feces enter mucus membranes or breaks in the skin. Dogs can contract the disease by eating kissing bugs as well. 

Humans in acute phase of Chagas disease often have flu-like symptoms, with fever, body ache, diarrhea and vomiting. Long-term effects of the disease include cardiac and intestinal complications. 

More common in dogs, Chagas largely goes unnoticed in the acute phases, as the symptoms, which mirror those of humans, often resolve with time. Chronic infection in dogs often results in fatal heart disease. Some dogs die without exhibiting any outward signs of heart disease, much to the puzzlement of owners. It’s only once a necropsy is performed that they find the protozoa present. 

Anti-protozoal drugs benznidazole and nifurtimox are used to treat humans with Chagas disease in Latin America, but they’re not widely available in the United States. They are often obtained from the Center for Disease Control for human treatment in the U.S. 

Although benznidazole and nifurtimox have been used experimentally in dogs, treatment in canines is largely limited to symptom management. How those drugs would affect horses is unknown, as is how the typical EPM treatments used on Cajun may have affected the T. cruzi, if at all. 

Cajun’s case was unique in that he didn’t have T. cruzi present in any other organ systems—only in his spine, not in his heart, such as most canine cases. 


Schulz’ efforts to find answers for Cajun’s neurologic deficit allowed researchers to document the first clinical case of Chagas disease in horses. Given the similarity to EPM, the potential for misdiagnosis is high, especially in areas where Chagas disease is present in the dog population. 

Much more research is needed across the board as far as diagnosis and treatment options, however, having cases to study is very problematic. The cost to diagnose and treat horses with neurologic problems is high, and by the time euthanasia is performed, few horse owners are willing to spend more money on a sophisticated necropsy like the ones performed on Cajun, if one is performed at all. 

“How many people out there are told their horse has EPM, they treat with Marquis and the horse doesn’t respond, so they just put it down?” Schulz said. “How do they know it was EPM if they didn’t have a necropsy done? Nothing is ever going to happen; the diagnostics and treatments are never going to get better if people don’t follow through.” 

Looking back, Schulz says she’s glad she went the extra mile with Cajun. 

“It was good to have closure,” Schulz said. “There was nothing else I could have done.” 

Cajun’s legacy was supposed to be in the arena, not a potentially life-saving discovery. 

“He showed me what it is like to have a horse with heart, desire and love for the sport,” Schulz said. “From the beginning, he wanted to be great—that’s something that cannot be taught. A great horse has no trainer, just a passenger to share the ride with. For that, I will be forever grateful to have had the opportunity to be there with him.” 

For more information on Chagas disease in humans, please visit and in dogs,

For more information on kissing bugs and their control, please visit

Tanya Randall is an avid barrel racer and veteran contributor to Barrel Horse News.
 This article was first published in the February 2017 issue of Barrel Horse News


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