Donald Walsh’s introduction to laminitis was abrupt and tragic.

A third-year veterinary student at the University of Missouri some 40 years ago, Walsh was looking forward to his first day in the equine clinic. He’d grown up on a large horse farm in Missouri, and he knew his future would involve treating large animals.

By chance, the first appointment of the day was a laminitic pony owned by a good family friend. The supervising clinician, seeing that the vet student and the client had a personal relationship, felt it only natural to pull Walsh aside and ask him to deliver the news: “The coffin bone is about to extend through this pony’s foot, and I want you to tell them we need to put it down.”

Walsh was shocked. He had to tell this to one of his best friends on his first day?

“Are you sure we have to put the pony to sleep?” he asked. Surely there was some other treatment. “It’s the only thing we can do for him,” the clinician said.

Today, at age 61, Walsh still remembers the day he learned to hate laminitis. He has a successful four-vet practice that treats 2,500 horses in and around St. Louis, Mo., and he was lucky in his first 12 years of private practice. He didn’t really see too many bad cases of laminitis at first, but then they hit the clinic like a firestorm. Such cases where owners spend thousands of dollars and still have to put their horses down, Walsh said, are as much of a rite of passage for veterinarians as falling off is for any respectable equestrian.

“I got very frustrated by the lack of knowledge and the lack of research regarding laminitis,” Walsh said from his clinic, Homestead Equine Hospital. He’s sitting on the front porch of a cabin near the clinic’s main barn, and over the next two hours he reflects on his life dream of preventing laminitis –a dream that led him to develop a non-profit foundation that has become one of the most sustainable funding sources for laminitis research. A dream that moves him–through frustration, determination and glimmers of hope–and keeps him thinking that one day before he dies, the triggering mechanism for laminitis will be understood and public education will be the only barrier to making the disease 100 percent preventable.

Barbaro: The Poster Boy?

It would be fair to say that laminitis is one of the most confounding diseases in the equine world. Defined as an inflammation of the sensitive laminae, or the plates of soft tissue that hold the coffin bone to the hoof wall, the disease is thought to be equivalent in pain to what a human might feel if one shut one’s fingers in a car door and then supported the weight of one’s body with those bruised digits.

Because the inflammation stops the laminae from properly supporting the coffin bone, the bone floats away from the external hoof wall and is driven by the horse’s weight down into the animal’s hoof capsule, shearing off veins and arteries. The coffin bone begins to rotate, but in the worst cases it sinks and can actually pierce through the sole of the horse’s foot. The unrelenting pain makes these animals extremely lame and hesitant to put weight on the toes of their front feet, the most commonly affected limbs. This crippling change in the horse’s anatomy is known as chronic laminitis, or founder.

After colic, laminitis is the second leading cause of death in equines, as the pain often progresses to a point where the only responsible action for horse owners is to euthanize their animals. On Oct. 4, 1989, Triple Crown winner Secretariat was destroyed after he developed a severe case of laminitis. Seventeen years later in 2006, Kentucky Derby winner and Triple Crown hopeful Barbaro developed the disease in his uninjured left-hind leg after fracturing his right hind during the Preakness (Md.). With his broken leg doing quite well last summer, Barbaro’s veterinarian at the University of Pennsylvania, Dean Richardson, removed a large portion of the colt’s left hind hoof wall because it was no longer connected to the coffin bone. Richardson then reported that the horse was a “long shot” for survival. This was, of course, after the champion patient had endured a shattered leg and dislocated fetlock, surgery to put it back together with 27 pins and a metal plate, and then various fiberglass casts to keep it that way during his recovery.

Fran Jurga, of the Hoofcare And Lameness quarterly journal, said she had hoped that Barbaro would be the poster horse for bringing attention to the need for more laminitis research.

“I thought splashing Barbaro all over the papers would have a positive effect on researching the disease, but I’m not sure that it has,” she said, adding that few people were acknowledging the irony behind the fact that the highest level of veterinary care in the country couldn’t prohibit the colt from developing a disease that has been around for almost a century.

Of course, all the vets knew that Barbaro was at risk. “They tried to take precautions with special shoes and other measures,” Walsh said, “but with all we think we know, we couldn’t even prevent Barbaro from getting the disease.”

Granted, the promising colt probably developed laminitis through weight-bearing stress, which is rare. The most common predisposing factors for laminitis–which some estimate play a role in close to 75 or 80 percent of cases–include obesity and over-indulgence in rich, turn-of-the-season grasses.

While other risk factors include carbohydrate overload–as in what happens when a horse breaks into the grain room and stuffs himself–a retained placenta, colic, insulin imbalances, repeated concussion on the legs, Cushing’s disease, obesity and access to lush grass are such common predisposing factors that Jurga said the disease is all the more tragic because many owners have the ability to prevent it.

Focus On Prevention

Initially, Walsh thought he could figure out laminitis by himself.

He started the Animal Health Foundation in 1984, a non-profit that encouraged owners to donate their laminitic horses to the clinic in exchange for a tax credit. Slowly, Walsh built up a herd of 22 or so horses in various stages of the disease. But after several years, he realized that while studying a herd progress through a death sentence was enlightening on some levels, he wasn’t equipped to engage in the kind of groundbreaking, microscopic research that was needed at the acute and developmental stages of the disease.

“The most important conclusion we could make back then was that obesity was a large predisposing factor,” Walsh said. “And that was 20 years ago. Today we have fatter horses than ever, which might be why cases have been steadily increasing.”

At national laminitis research conferences, Walsh turned his efforts toward scouting out researchers his foundation could support. Highly aware of the time-consuming grant writing process and of how it often impeded researchers from pursuing a long-term laminitis study, Walsh was determined to find someone with a long-term goal. In 1995, he found it in Chris Pollitt, a scientist from the University of Queensland who is now regarded as one of the leading researchers of the disease.

“Chris didn’t jump in and start where everyone else was,” said Walsh, who first thought the scientist was a hoof anatomist. “He started from scratch. When I met him he was making vascular casts of horses’ feet and basing all his work on observation. He didn’t accept anyone else’s theories as right or wrong, or let himself get compromised in any way. He’s a great scientist, he’s got the laboratory and the broadest outlook on what laminitis research needs.”

Such a combination is not easily found in the laminitis research world, which spends a lot of its time arguing about theories rather than making great strides toward breaking new ground. The reasons why, Walsh said, are numerous: First, few people want to study the disease because the nightmarish recreation of it requires horses to be induced and then killed so you can study the insides of their feet. Second, few young veterinary scientists who want to see results from their work see the value in pouring their efforts into researching a disease as frustrating as laminitis. Third, because nobody yet understands exactly what internal mechanism triggers the onset of laminitis, research conferences often end up with scientists and vets split into different camps, arguing about whose theory is correct.

Blood flow is one of the big issues, except that people can’t decide whether the increase or decrease of it might be triggering laminitis. Scientists generally support one of two theories: vascular or enzymatic, the first of which deals with blood flow as the trigger and the latter which suggests enzymes go haywire in a horse’s basement membrane, which holds the folds of the laminae together, and cause the material to break down and subsequently pull the laminae apart. Others argue that a third triggering theory involving mechanical factors can’t be discounted, or else you have no way to explain what happens to horses like Barbaro in a weight-bearing condition.

“The thing is, we’re probably all right,” said Walsh. “What we probably have to figure out is which takes place first.”

The idea is that a greater focus on the developmental stage of the disease will more quickly yield the answer to preventing it, so treatment will never be necessary. So far, Pollitt has uncovered the only proven technique for preventing laminitis after a grain overload. In the study, Pollitt induced horses with carbohydrates to simulate a grain overload, then iced some of the subject’s legs immediately. In the legs that received cryotherapy at about 41 degrees, the cooling slowed blood flow to the hoof and laminitis did not develop. And, the enzymes that have been theorized to overreact and cause the basement membrane breakdown were recorded in much lower concentrations in the cooled legs versus the untreated limbs, he writes.

Walsh tells owners who find their horse has broken into the feed room to ice all of the horse’s legs, up to the knees, for 48 hours straight.

“People come up with all types of ways–four buckets of ice water, ice pack wraps, blue jeans strips sewn up to hold bags of ice around a horse’s legs–it doesn’t matter,” Walsh said. “But what has been proven through Pollitt’s research is that for every horse who was induced with a carbohydrate overload and then subsequently iced, laminitis did not develop.”

But despite such advances and a greater understanding of the engineering marvel known as the equine foot, nobody has been able to pinpoint the exact laminitis triggering mechanism. Furthermore, Walsh said, in most laminitis studies there are horses that never develop the disease, which so disrupts scientific result gathering that such subjects are simply disregarded. For the ones that do develop the disease, other inexplicable variations take place: some get it worse than others, and in each horse, one limb is usually affected more than another.

And if these reasons weren’t enough to keep a researcher from tackling laminitis, the lack of funding certainly would be. Although the Department of Agriculture funded a study in 2000 relating to laminitis, most research dollars come from the well-supported Grayson Jockey Club Foundation, the Morris Animal Foundation and the American Quarter Horse Association. But considering the scope of these organizations, their contributions seem low: According to spokespeople from each group, Grayson has put slightly more than $700,000 into laminitis research since the mid 1980s, the MAF slightly more than $500,000 since 1971, and the AQHA, according to its website, slightly more than $350,000 since 1974.

By contrast, Walsh’s Animal Health Foundation, through independent donors, charity banquets and a benefit horse show, has supplied Pollitt and two other stateside researchers–Philip Johnson who studies endocrine dysfunction in laminitis and Kathryn Watts who studies how the levels of sugar in grass contribute to the disease–with more than $760,000 over the past 20 years. With a sale likely of the old horse show grounds, the AHF board has just voted to supply Pollitt with another $300,000 over the next three years. If that happens, the foundation will have generated more than $1 million for laminitis research.

Treatment Options

Because of slow going in laboratories, day-to-day practice in treating laminitis also suffers from a lack of information. Amy Rucker, a veterinarian from Columbia, Mo., said that more research is needed on the treatment phase of laminitis as well as the developmental phase.

Rucker advocates using venograms to track the progression of cellular changes that are too small for most X-rays to pick up. “With a venogram, you inject a dye into the blood vessels, and you can see how the horse’s pattern of vessels differs from the normal pattern,” Rucker said. “Before the coffin bone is even suppressed, you can see when the tissue starts to alter.”

Venograms are great at tracking the progression of the disease and helping vets determine a treatment path, but they aren’t publicized very much, Rucker added. Because treatment usually means figuring out how to best take the weight off the horse’s toe, Rucker prefers a modified ultimate shoe or a heel wedge. Extreme cases, where the blood supply has been cut off to the foot, can require cutting the deep flexor tendon, applying a pin-cast, removing part of the hoof wall, or euthanasia.

A lot of that can be avoided with early intervention, said Rucker, but the problem is most owners have a “wait and see” attitude about laminitis, especially because it sometimes doesn’t look like the horse is in pain right away.

“Sometimes it works out OK, but if it doesn’t, you’ve missed your golden window to make a difference,” she said. “If people would pony up and do something about their horse right away rather than waiting six or eight weeks, it could make a big difference.”

Some frustrated owners, bogged down by differing opinions and options, have started turning to the “barefoot movement,” which advocates pulling off the horse’s shoes and focusing on proper trimming and diet. While some horses do get better, Walsh said the idea that they are “cured” is false.

“If you smash your fingernails and then let them grow out, they’re just not going to be the same,” he said.

But Walsh does believe in caring about diet and educating owners about not letting their horses get fat, about being wary of the “easy keeper’s” desire to devour everything, and about limiting horses’ access to lush grass until more advances are made in controlling the amount of fructans (sugars) in feedstuffs.

Currently, Walsh is taking his plea for studies needed on grass laminitis research to the government. He met with Missouri senators Mitch McConnell’s and Jim Talent’s staffs last spring, and he’s learning the hard way how slow the process is in getting the government to fund anything, much less something like grass laminitis.

Walsh also approached the new federally funded laboratory at the University of Kentucky, called the Forage-Animal Production Research Unit, about looking at breeding grasses lower in fructans, said lead researcher Jim Strickland. He added that the laboratory would start looking at how the blood changes in horses with chronic laminitis, with the goal of trying to figure out if they could disrupt the mechanism that progresses the disease.

“It may come down to actually making forage [grasses] that are specifically for horses,” Strickland said from Lexington.

Back in Missouri, Walsh is walking back to the clinic, saying that he considers figuring out laminitis his “one big ‘yes’ dream.” It’s dark now, and you can’t make out Walsh’s creased and smiling face anymore or his glasses, but his crisp voice, with a Midwestern nasal twinge, rings out authoritatively in the darkness.

“Twenty-two years ago when we started this organization we called it the Animal Health Foundation because I thought we’d conquer this and move on to something else.

But I want to get rid of this disease. Others can focus on treatment, but we’re interested in prevention so nobody else has to ever go through this. We’re down on a molecular level now. Once we understand that, it’s going to start opening some doors.”