TVG interview with champion Thoroughbred Paynter's owner Ahmed Zayat of Zayat Racing, taped the morning of September 19, 2012, explains the timeline of Paynter's illness and suggests the severity of the colt's illness.
All types of laminitis are similar in two ways: First, the epithelial cell system in the foot’s interlaminar zone is damaged.
Second, that damage causes horses great pain. The common analogy of standing and bearing weight on a ripped toenail is an apt one.
But the most common types of laminitis are rooted in the horse’s endocrine (hormone-producing) system.
Hormonal imbalances are aggravated by environment, diet, exercise and seasons. Damage to the laminar junction may be slow but steady, with varying intensity.
With this type, horse owners are stunned when told their horses have laminitis...and that they have had it for months or even years. It just didn’t cause enough pain for the horse to be noticeably lame.
The farrier may have noticed a stretched white line or hoof wall ridges, or that a normally-quiet horse is irritable while being shod. The rider might have thought the horse wasn’t as free-striding as he once was.
A horse that once was hard to catch is suddenly an easy catch. But the owners don't sense that these horses are lame--until they are. Then the subtle signs and the loss of performance start to make sense.
How can this be?
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| The progressive stages of programmed cell death, or apoptosis, in a human cancer cell. (Image courtesy of Wellcome Images library) |
Cellular death in endocrine-related laminitis is by the process known as
apoptosis. Cells in the lamininar zone are under assault. Some may contract and die. Some may stretch and deform. Some may be unaffected and remain attached. One by one, the cells die.
The horse is more lame one day, less lame the next. The blood supply may be disrupted and the diseased hoof grows abnormally and loses its form. As the seasons change, the horse is better, or worse. Low-grade chronic laminitis can go on and on for months or years.
Another form of cell death is seen in the horse that has received a severe insult to its body’s system from the inflammation, shock and dehydration of colitis. Instead of the drip-by-drip influx of insulting factors into the foot, a flood arrives and the result is the traumatic cell die-off process known as
necrosis.
Apoptosis and necrosis are flip sides of the coin of cellular death. Both are associated with the process known as laminitis, but one is a systematic death of cells, while the other is swift and deadly and immediate. One text described apoptosis as cellular suicide, and necrosis as cellular homicide.
The recent case of top three-year-old colt Paynter has been captivating the racing world. Paynter has been in a veterinary hospital in upstate New York near Saratoga since Labor Day weekend. His condition has improved but his owner reports persistent fever and diarrhea bouts, and the colt was diagnosed with laminitis in three of his four feet.
Equine podiatry specialist Dr. Bryan Fraley from Lexington, Kentucky went to New York to work on the horse; his feet are now in casts, which have been reported to be successful. Reports after the first week were that there was no rotation or sinking in the feet. The casts are due to be changed later this week.
Many of us have been there...and done that, when it comes to watching a horse struggle with the severe colitis and resulting dehydration of colitis. Too many of us have lost horses swiftly and tragically in the days following a successful survival--not to colitis, but to the severe laminitis that so often follows.
What is colitis?
Colitis: inflammation of the colon, usually due to infection. Diarrhea, colic pain and rapidly progressing dehydration are usually the result. Treatment focuses on relieving symptoms and preventing dehydration and shock while identifying and treating the underlying cause, if possible. (Definition: American Association of Equine Practitioners)
To understand colitis-related laminitis better, we turned to David Hood DVM, PhD of The Hoof Diagnostic and Rehabilitation Clinic, a laminitis research and treatment center outside College Station, Texas.
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| Dr David Hood during a panel discussion at the Sixth International Equine Conference on Laminitis and Diseases of the Foot in 2011. (Dick Booth photo) |
One of the world's most highly respected laminitis researchers, Dr. Hood’s focus is on understanding the process of laminitis and, in particular, how the foot tissue is damaged by the disease.
Dr. Hood explained that the difference between apoptosis and necrosis is central to understanding why a horse has such a sudden and devastating form of laminitis after colitis--and why the laminitis doesn’t occur until the diarrhea has stopped.
Dr. Hood mentioned that the chief culprit in colitis is that the horse goes into shock. In response to the inflammation in the bowel caused by colitis, the horse’s system demands that a large volume of fluid be pulled out of cells all over the body. It is pumped to the bowel to replace the fluid lost there but, as a result, the circulatory system is left with a deficit of fluid.
When treated by a veterinarian, the sick horse will receive lifesaving intravenous fluids. The circulation is refueled or rehydrated. But that is the cue for laminitis to begin.
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This plastination specimen illustrates
chronic laminitis and typical hoof
capsule deformity. |
As you can imagine, the dehydrated body system is shocked by the massive and sudden rehydration, which is necessary to counter the loss of body fluid through the diarrhea, but still a shock to the system. The reperfusion of the cells with the fresh fluid is connected to necrosis, or a sudden traumatic death of cells within the laminar interface of the horse’s foot.
It is in the reperfusion stage that necrosis in the foot tissue takes place. This is why the onset of laminitis seems to follow the diarhhea in the medical timeline of the disease.
Not only is laminitis by necrosis sudden and traumatic, the cellular death in the laminar zone causes a collapse of the foot’s ability to support the weakened horse, and severe pain is obvious and extreme.
“By the time you see that it has happened, there’s not much to do except start rehabiliation,” Dr. Hood commented. “It’s like a patient who just had a heart attack: the damage is done, and the patient’s prognosis depends on how much damage was done.”
Dr. Hood noted that post-colitis laminitis is also very different from the third form of laminitis, known as "support-limb" laminitis. “That’s also a slow onset,” he remarked. “And the cellular death is not necessarily necrosis. The foot is almost anesthetized while the horse is standing continually on it. It’s not until the blood flow comes back that the horse begins to show signs of pain.”
Do post-colitis cases tend to demonstrate sinker syndrome rather than the rotation type of coffin bone detachment seen in typical laminitis? “It all depends,” Dr. Hood said, “on the amount of damage and the percent of lamina that have experienced acute necrosis.”
Endotoxin has been implicated as a factor in post-colitis lamintiis but Dr. Hood discounted it. “Research data indicate that while endotoxin can make a horse sick and can cause shock,” he stressed. “it--alone--does not induce laminitis.”
Are there facts that are known about colitis in horses? Dr. Hood agreed that much
is known about post-colitis laminitis and fired off a quick list: horses do survive it. It’s a painful condition. It’s hard to control. Horses undergo rapid and radical damage to their feet. There are different varieties. Rehabilitation of damaged hooves after colitis can take months or even years. The more the foot is damaged, the harder it is to fully rehabilitate the foot.
In endocrine-related laminitis, on the other hand, Dr. Hood said the situation is reversed. The feet are relatively easy to treat. It’s the disease condition that is difficult.
Laminitis, in any of its forms, is a medical emergency and a critical juncture in a horse's medical history and athletic potential.
We all hope that Paynter will continue to successfully fight both colitis and laminitis.
Thanks to Dr. Hood for his time and expertise in sharing and preparing information for this article. Plastination specimen courtesy of Christoph von Horst, DVM PhD.
To learn more:
Dr. David Hood Launches the Hoof Diagnostic and Rehabilitation Clinic in Texas
Paynter Watch: Top Thoroughbred Colt Diagnosed with Post-Colitis Laminitis in New York
Paynter Laminitis Watch: Podiatry-Vet Fraley Amazed at Progress Since Hoof Casts Applied
© Fran Jurga and Hoofcare Publishing; Fran Jurga's Hoof Blog is a between-issues news service for subscribers to Hoofcare and Lameness Journal. Please, no use without permission. You only need to ask. This blog may be read online at the blog page, checked via RSS feed, or received via a digest-type email (requires signup in box at top right of blog page). To subscribe to Hoofcare and Lameness (the journal), please visit the main site, www.hoofcare.com, where many educational products and media related to equine lameness and hoof science can be found. Questions or problems with this blog? Send email to blog@hoofcare.com.
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The conference was made possible by ZinPro Corporation, MLS Nutritional Supplements and Alvin Farrier Supply, along with the support of AgriLife Extension and the department of animal science.
