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The Conscience of Thoroughbred Racing

HRI EXCLUSIVE: Mutant Gene Causes Horse Bleeding and Breakdowns

Wednesday, April 03, 2019

By Mark Berner with John Pricci

Everyone at Santa Anita Park looked for a silver bullet, that one thing that caused the recent cluster of catastrophic breakdowns at the Arcadia track. Officials of The Stronach Group, owners of Santa Anita, said it is multifactorial, but they are wrong. The single uniting factor is Warmblood Fragile Foal Syndrome (WFFS), a genetic mutation first discovered in Warmblood horses.

Nena Winand, DMV PhD., a genetic scientist, identified WFFS at Cornell University in April 2011. She believes the mutant gene is present in at least 15% of all Thoroughbreds and may be as high as 30% or more in the US, where lines of bleeders have been highly selected.

WFFS prevents collagen–the body’s most abundant protein and the glue that holds together all living things–from forming properly, thus keeping the protein from doing its job.

Collagen is necessary to form strong cell walls like those that keep blood vessels from bursting under pressure. Collagen also is involved with the creation of strong bones, helping to keep them from shattering under stress. Collagen also forms connective tissue that keeps muscles attached to bone.

Some Warmbloods with this affliction have bones too weak to stand on, skin that falls off upon contact, and vessels too weak to hold blood. Such animals are euthanized at birth.

Thoroughbreds do not suffer to the extent Warmbloods do but they do suffer enough to bleed through underdeveloped blood vessels and suffer broken bones that have not formed properly.

All athletes bleed slightly when the stress of exercise increases blood pressure, causing capillaries in the lungs to burst. Prior to the invention of the flexible endoscope – a device with a camera inserted into the nasal passage that can view the airways and lungs – only bleeders exhibiting epistaxis–visible bleeding from the nostrils–were considered bleeders.

Endoscopes can detect miniscule amounts of blood, which is all the evidence required by racing jurisdictions to qualify a horse to run on Lasix, the anti-bleeder medication legally administered on race day only on this continent. This technology is easily abused by wrongfully identifying horses as “bleeders.” 

Cornell patented a simple DNA test for WFFS in 2011. In March 2018, research at the University of California Davis Veterinary Genetics Laboratory identified a low carrier frequency of the WFFS mutation in Thoroughbreds, and appropriately communicated its findings to The Jockey Club. 

“In reality, there was enough evidence that this was [an] inherited [trait] a year ago to warrant [the] addition of testing to the necropsy protocol that would have shown whether or not [equine deaths at Santa Anita] was caused by the WFFS mutation,” explained Winand. 

“[The Jockey Club has] had every opportunity to educate themselves and haven’t bothered, and there is no mention of any strategy to deal with it in the white paper (The Jockey Club’s recent white paper on its vison for 2050).”

TJC President Jim Gagliano and Executive Director Matt Iuliano said they were unaware of any notification and that it is something not routinely tested for, though Iuliano admitted to seeing a reference to it on the UC Davis VGL website. “We have no authority over the necropsy program,” explained Iuliano.

Subsequent to the previous statement, Iuliano later recalled that his memory was incorrect and that he did receive notification from UC Davis as per contract. 

A test to identify WFFS has been available since May 2018 at the UC Davis VGL at a reasonable cost of $40. Horses that test positive for WFFS should not be allowed to race; they are ticking time bombs.

This is not just a US problem. It exists across all breeds on a worldwide scale. The difference is that laws here allow this problem to be masked by Lasix, effectively treating the symptom but not providing a cure.

As discussed in last week’s HRI column, Bleeders: It’s All in the Families, this goes back to the three foundation sires of the Thoroughbred breed imported to England from the Middle-East, in the late 17th and early 18th centuries: the Byerley Turk (1680s), the Darley Arabian (1704), and the Godolphin Arabian (1729), also from the desert Arabians that preceded them. 

Bartlet’s Childers, nicknamed Bleeding Childers, was one of the earliest champion sires of the breed. A descendent of the Darley Arabian, he sired Squirt, who begat Maske, the sire of the great Eclipse, the dominant sire line of today’s Thoroughbreds. He has a presence in the male-line of about 95% of the breed. He has also sired several foundation mares. 

The other founding ancestor recorded as a bleeder was Herod (1766), who reportedly lost the Great Subscription Purse at York due to breaking a blood vessel in his lungs. 

Herod’s dam was by Blaze, a son of Flying Childers. Anytime Herod and Eclipse crossed in a pedigree, combining Bleeding Childers with Flying Childers, the assumption was that the bleeding had a heritable component, a recessive for that trait. 

Eclipse and Herod, combined with in the first three generations of several early English classic winners, Herod (25%) and Eclipse (13%) are the largest contributors to the genetic make-up of the breed; both with bleeders close up in their pedigree. 

Breeders in North America have perpetuated the problem by continually selecting bloodlines that saturate the gene pool with a genetic mutation that creates a predisposition for catastrophic events. 

With recessive genetic disorders like WFFS, two copies of a recessive gene in Thoroughbreds will result in a foal that will have to be euthanized, just like those Warmbloods mentioned above.

What was not known before and has been discovered by Winand in research since 2011, is that it only takes one copy to be present for the horse to exhibit signs of what seems to be a recessive defect, however WFFS appears to be an unusual dominant mutation. The weak foal phenotype mimics a recessive but there are for the most part sub clinical abnormalities in horses with one mutant gene copy.

“We don’t see it very often, individuals with two copies of it,” said Ernie Bailey of the University of Kentucky. “One copy could weaken a horse.” Bailey is a faculty member for nearly 40 years at the Department of Veterinary Science and Gluck Equine Research Center at the University of Kentucky, and the International Society for Animal Genetics, president (2010-2016).

WFFS, identified in Europe with ballpark estimates of 15% in Thoroughbreds but it could be higher, particularly in the US. As an example, Hereditary Dermal Asthenia, a different connective tissue fragility syndrome that is recessive was selected for in cutting horses where the carrier frequency rose to almost 30%.

Resultantly, there is every expectation that the number of Thoroughbreds in the US will fall within the 15 and 30% parameters but those ranges could be even higher due to selective breeding.

It follows that every year there is a foal crop of 20,000 horses, 3,000 to 6,000 horses are susceptible to catastrophic breakdowns. On the backsides of Santa Anita or Belmont Park alone, there live 300 to 600 horses with bones ready to shatter. 

Significantly, breeding horses with this genetic defect is a death sentence. When combined with bisphosphonates, the horses’ whose bones are exposed to stress are ready to implode at any time.

“I think you have to see what the injuries have in common and what the injuries tell you [to examine],” said Dr. Larry Bramlage, renowned veterinary orthopedic surgeon. “We now have that information to make those determinations.”

“It is not the track that presupposes that a horse is at risk [to] injury. It is the fact that each Thoroughbred must design and build the perfect skeleton for him [or her] to use as a racehorse. This is done with training,” continued Bramlage.

“Yearlings are not born with racehorse skeletons; they have to mold their skeleton into one that will carry their weight and their mechanics competitively around the track. This is done by progressive small episodes of overload [small stress fractures] and then over-repair [and get stronger]. This takes training. 

WFFS prevents this natural cycle to strengthen bone. “A Thoroughbred maintains only the minimum skeleton sufficient to carry it around the track. Excess skeleton is added weight and penalizes speed. So a light skeleton is a speed advantage, unless it gets too light to carry [itself], and then it fails.”

It is imperative, for the future of the breed and the life of the animal itself, that the breeding industry adapt. Buyers will demand proof via DNA testing that foals are negative for WFFS.

Maybe horses possessing this mutant gene should no longer be progenitors. The industry must address this issue and decide if it wants slower, sounder offspring, or faster dead ones.

© Mark Berner, John Pricci,, April 3, 2019

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One Response

  1. This genetic panel should be required for all foal registrations if it can be proven a single copy of the gene causes phenotypic expression.

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