Stallion with suspected DSLD

[JoanneM]

There was a well known WB stallion local to me who sired a LOT of foals, and now that I’m in the market for a new horse I keep coming across them for sale. A lot of his babies look exactly like him! The stallion passed a few years ago.

I really liked the stallion but saw him when he was aged and he was very much down in the hind fetlocks, and I was told he retired with soundness issues.

Is there any way to know if this guy had DSLD, short of asking the stallion owner (who I would expect to be less than pleased to be asked…) I don’t want to name the stallion, in case I’m wrong about his issues.

Are there any major German WB registry lines known to carry this defect?

Are there any other diseases/injuries that could give the appearance of DSLD, without being DSLD?

[Marla_100]

I believe this has been discussed here before on COTH. Maybe try a search for DSLD. It’s been a while though and I can’t recall the name of the horse. Maybe also do a search using stallion’s name.

[JoanneM]

I did a search and nothing for that name + DSLD came up, and the threads on DSLA mention unrelated lines.

Are there any other diseases/injuries that could give the appearance of DSLD, without being DSLD?

[Libby2563]

Having had to euthanize my young Hanoverian with DSLD just over a year ago, I would run away from offspring of a stallion “down in the hind fetlocks.” Either he has DSLD or he has crappy conformation. One sunken pastern could be an injury but both sounds systemic. I could be wrong but I wouldn’t take the risk.

Mine was by Bugatti, FWIW. The breeder had another one by him who ended up having DSLD too.

[4horses]

Agreed. Any horse that is dropped in both hinds or both fronts, is best avoided. If you want an athletic horse, dsld will cut short any career. At best you end up with an expensive pasture pet. DSLD can onset at any age. I really wish there was $$$ to invest in developing a genetic test, as the longer I’ve been in the horse industry, the more often i see the problem, in multiple breeds.

My old mare has the condition and has been retired for 10 years- think of the money i have put towards her feed and care during that time. That is a significant investment in a lame horse. But she was my first horse as a child and I love her. She is full of personality - always in my way, trying to get my attention. She loves her life despite it’s limitations. For hoof trimming, she will lay flat on the ground while you trim. She has complete trust in me.
I used to ride her over jumps without a bridle. As a child, i just assumed every horse will do that with good training… I know the day is coming where our partnership will end. We have been lucky the disease didn’t progress fast, and her pain has been manageable with medication. How much longer i can maintain her and keep her comfortable, i don’t know.

If you can afford to retire your horse for a significant time, or euthanize, you can take that gamble. As some horses don’t develop the disease until later in life, and can have a decent career before the disease manifests, if it manifests at all. For example, Mr Prospector had the disease in late life, some of his offspring developed the disease, but many did not, otherwise his name would not be so prominent in racing bloodlines. Of course, if the disease doesn’t show until an older age, it’s hard to say how many eventually developed it.

Without knowing how it is inherited, it is difficult to predict which offspring will get the disease, which won’t, or at what age.
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The thesis on Peruvian Pasos looking for a genetic link suggested a recessive mode of inheritance, but the Angel Fire site suggests dominant inheritance.

[Marla_100]

What I don’t understand is why isn’t there a dna test where the genetic markers can be identified, even before symptoms show up?

I just did an Embark DNA test on my rescue dog and for an extra fee they run a health test for 180 genetic health problems. This is so helpful to know what to expect in their future and since my previous dog passed from DM, I wanted to know if my new dog was a potential carrier. She isn’t.

But why can’t something similar be done in horses?

[Marla_100]

Here’s the thread I was thinking of about Furstenball, early on several mentioned his soft hind pasterns at the championship and some years later it was mentioned he had the condition. See post 84 for update.

https://www.chronofhorse.com/forum/forum/discussion-forums/sport-horse-breeding/260982-furstenball-opinions/page5

[JB]

@Marla 100

What I don’t understand is why isn’t there a dna test where the genetic markers can be identified, even before symptoms show up?

I just did an Embark DNA test on my rescue dog and for an extra fee they run a health test for 180 genetic health problems. This is so helpful to know what to expect in their future and since my previous dog passed from DM, I wanted to know if my new dog was a potential carrier. She isn’t.

But why can’t something similar be done in horses?

There’s no test yet because it hasn’t been figured out yet. I don’t know if there’s not enough money to research it, or not enough interest, but I’d bet the interest at least is growing.

Dogs generate enormous income for suppliers of “things”. 9 million horses in the US, vs 89 million dogs. (according to a quick search)

As for @JoanneM’s question “Are there any other diseases/injuries that could give the appearance of DSLD, without being DSLD?”

Yes, though without seeing, it’s hard to impossible to know which it is. Simply having longer pasterns predisposes the horse to a weakening suspensory structure and, if the work is hard enough for enough years, you can get suspensory ligament desmitis even in both hinds. SLD here is not the same as DSLD which is degenerative. It’s also more correctly called ESPA now, equine systemic proteoglycan accumulation, as we know it’s a whole-body disease, affecting all ligaments, which is why the common and best test, outside of tell-tale signs in an ultrasound (if there is enough damage), is to do a nuchal ligament biopsy.

[Edre]

@Marla 100

Here’s the thread I was thinking of about Furstenball, early on several mentioned his soft hind pasterns at the championship and some years later it was mentioned he had the condition. See post 84 for update.

https://www.chronofhorse.com/forum/forum/discussion-forums/sport-horse-breeding/260982-furstenball-opinions/page5

While I think there has been a lot of outside talk about Furstenball, as far as I know, if he has been actually tested for it those test results have not been released. Until a stallion owner has done this, I can’t really say with comfort that a stallion “does/doesn’t” have it. (And while the nuchal biopsy exists and there has been wonder about Furstenball for years, I strongly believe that Schockemohle will either never have the test done or if he does and the results are positive, will never release them. Based on his response to the FFS - Fragile Foal Syndrome - changes, it took the breed organizations instituting rules to force his hand. Perhaps I’m sour on the man, but I genuinely feel like he never does anything that might damage his bottom financial line rather than making choices based on what’s good for horses.)

OP: Not all “DSLD-appearing” things are DSLD, although JB has a better response on that than I could formulate so I’ll just go “What they said.”

Not all long/weak pasterns are DSLD (and not all DSLD cases actually have long pasterns). Unfortunately, while the nuchal biopsy test exists, that’s an invasive procedure so pretty much the only people I know of who do it are those owning horses whose horses are starting to present with symptoms and wondering if it’s what they’re dealing with - not something that can be done on, say, a PPE or that is done to advertise results on stallion pages. I eagerly await the day that they can figure out how to do a genetic test for it… so much heartbreak could be avoided.

One thing that is unique to DSLD/ESPA is the bilateral or quadrilateral presentation of lameness. It doesn’t help you with the stallion not right in front of you, but that’s one of the distinct earmarks of the disease.

There have been family lines implicated for DSLD/EPSA, but the progenitor sires themselves have not been tested/come out and said it, so you’re just left tracking who has had horses conclusively diagnosed with it & then finding out what those pedigrees were, if people are willing to share. To date I cannot think of a single public space where people have really come forward and put down “my horse was diagnosed with this and euthanised as a result and this is my horse’s pedigree”…it seems more of a hush/hush thing. Hopefully with growing awareness, that is beginning to change.

[Scribbler]

I understand that with the Impressive line of QH, the subclinical presence of HYPP apparently helped contribute to the bulky muscular appearance sought in the QH halter class world.

Is there a similar phenomenon with dressage horses and subclinical DSLD? Does the degeneration of the ligaments produce for a while looser, bigger, movement?

Obviously in both these cases the disease will catch up with the horse in a terrible fashion. But it could explain why these horses become popular stallions and why folks are reluctant to weed them out of the gene pool.

The QH industry is a good example of how long it took for breeders to face up to a genetic disease that had a clear genetic marker.

There are many hereditary conditions in both humsns and animals that don’t have a clear genetic marker and can’t be easily tested for. The disease might be a combination of several genes or it might have an epigenetic component.

[mvp]

The first horse I ever saw with those remarkably horizontal hind pasterns was a KWPN stallion who did or had belonged to a well-known dressage pro (from MA?) and stood at Cornell University. I have seen DSDL horses diagnosed since and I’d bet money this horse had it. PM me if y’all want the name.

[JB]

@Scribbler

I understand that with the Impressive line of QH, the subclinical presence of HYPP apparently helped contribute to the bulky muscular appearance sought in the QH halter class world.

Is there a similar phenomenon with dressage horses and subclinical DSLD? Does the degeneration of the ligaments produce for a while looser, bigger, movement?

I won’t speak to any specifics as it’s been a while since I paid closer attention to this, but I have several friends who are very gait-oriented in their analysis of horses, and they have noticed a pattern - in hindsight - with quite a lot of horses they know ended up developing ESPA. Not bigger movement, just…odd? I wish I could remember their insights. But also, because it was all hindsight, it wouldn’t be fair to even remark “these are the traits they saw”, because IIRC, all of those things could be the result of something else.

Obviously in both these cases the disease will catch up with the horse in a terrible fashion. But it could explain why these horses become popular stallions and why folks are reluctant to weed them out of the gene pool.

In this case it would be closer to something like HERDA, where something like 30% of the top Cutting horses are carriers. Are they high performing, and therefore popular, because of an effect of being a carrier of HERDA? We know there is some extra stretch and snap to the tendons, as seen in studying the structures themselves, but so far no work has been done to see if that actually translates to better acceleration or stops or anything that might give them a competitive advantage. And who’s to say that HERDA wasn’t just a come-along and has nothing to do with the quality and performance of those stallions who have passed it on?

[4horses]

Does the degeneration of the ligaments produce for a while looser, bigger, movement?

I would say yes it is entirely possible that the initial stages of the disease produce better movement. I have some old pictures of my mare at liberty and she has extraordinary movement.

When looking at dressage stallions, I would not consider any that don’t offer pictures of the horse without leg wraps, or don’t have the horse stand square so you can evaluate the hind limb conformation. Ideally I would look for older stallions and try to see recent videos. One thing about DSLD is that it tends to manifest in later life. By limiting your breeding to older stallions and getting current pictures or video, or even seeing the stallion in person, can help eliminate the disease from at least the stallion side. I would also look for a horse with a lengthy career. Unless or until there is a genetic test, breeding to older stallions is probably your only preventative option. Even better if you are using a broodmare over 15 years old. You can’t do much about unaffected carriers, but you can avoid breeding to horses with the disease.

Of course this isn’t ideal, so until there’s a genetic test, it will be a difficult fault to remove from the gene pool. All you can do is try to be educated breeders. If you have an affected horse, share the bloodlines.
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[charlieTBD]

@Marla 100

What I don’t understand is why isn’t there a dna test where the genetic markers can be identified, even before symptoms show up?

I just did an Embark DNA test on my rescue dog and for an extra fee they run a health test for 180 genetic health problems. This is so helpful to know what to expect in their future and since my previous dog passed from DM, I wanted to know if my new dog was a potential carrier. She isn’t.

But why can’t something similar be done in horses?

Is it for sure all a genetic disease or is it auto-immune where the environment might make it manifest in some horses but not all? Many connective tissue diseases are not genetic or solely genetic.

I think the movement of a horse with soft tendons and ligaments is there to be seen many years before the disease is diagnosed. I have often seen it in the hind end - I would describe it as floaty and imprecise movement of the feet. I think tests like backing up or cavaletti work can show if the horse is young and careless or is making big moves of the hind feet because they have to. Of course many things can cause a disconnect to the back legs but it can be seen if looked for carefully.

[JB]

@charlieTBD

Is it for sure all a genetic disease

It is all but certain to be genetic. There’s a reason certain breeds are well-known for being predisposed to it - Paso Finos for example

or is it auto-immune where the environment might make it manifest in some horses but not all? Many connective tissue diseases are not genetic or solely genetic.

AI is genetic in many ways. In others, it develops because of other issues, but that begs the question - does the genetics have to be there in the first place for the environment to trigger it?

I fully believe that in at least some horses, ESPA is triggered by something - injury, high enough stress, age-related hormone changes, something. But that’s not always the case, especially when looking at a young 3yo who hasn’t been in work, or injured, or sick, who fairly rapidly develops dropped fetlocks and devolves from there

[JB]

@charlieTBD

I think the movement of a horse with soft tendons and ligaments is there to be seen many years before the disease is diagnosed. I have often seen it in the hind end - I would describe it as floaty and imprecise movement of the feet. I think tests like backing up or cavaletti work can show if the horse is young and careless or is making big moves of the hind feet because they have to. Of course many things can cause a disconnect to the back legs but it can be seen if looked for carefully.

Yes, that jives with what my friends have noticed too. Unfortunately, that sort of movement can be from other things as well, which is what makes seeing that and saying it’s from ESPA is a dangerous thing

I sure hope there is a simple hair dna test developed soon!

[4horses]

To clarify Peruvian Pasos are prone to. The breed was kept isolated in Peru for 400 years. Paso Finos do not appear to be prone to it- the Paso Fino breed was developed in Colombia and Puerto Rico. Completely different breeds with a similar ancestral breed (the Jennet). So while a Paso Fino can get DSLD, it is not that common.

I believe it was the isolated breeding of the Peruvian that makes the disease more common in that breed. I can’t find the website but there was a breeder of Peruvians who had multiple horses develop DSLD and went through the heartbreak of putting them down.

[JB]

https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0167069

“Degenerative suspensory ligament desmitis (DSLD) is prevalent in specific horse breeds, such as the Peruvian Paso, Paso Fino, American Saddlebred, Quarter Horse, and Akhal-Teke [1, 2] and is rare in pony and draft breeds amongst others.”

[beowulf]

It helps no one to keep the name[s] of stallions you suspect may have DSLD hush-hush.

Here are the stallions that have offspring with DSLD/ESPA that have been talked about on this forum that can I remember off of the top of my head:

Furstenball
Bugatti VDL
Waterford
Donnerhall

Whether or not they were the source, we don’t know - stallion owners are not going to test using the nuchal ligament biopsy - it is extremely invasive… until a better test comes out, I imagine it’ll stay this way - frankly, I don’t blame them either; the test is painful, and damaging - and can impact a stallion’s comfort for a long time. One should also remember, every horse has a dam that brings her own influence to the equation.

That being said - JB covered the differences between dropped pasterns, and DSLD/ESPA. The former can be caused by the latter, but not always - however, be wary of broodmares in fields with dropped pasterns, sometimes called slung pasterns and sometimes accredited to the additional weight of carrying foals… Dropped pasterns in broodmares are absolutely not normal. Not all DSLD/ESPA presents early on in young horses either - sometimes it is something that a sickness, or stress of the body, brings about suddenly - such as pregnancy or an illness that makes the disease come out in full force . It’s not very well understood but the consensus by experts in the field is that it is genetic - they just haven’t figured out the mode of inheritance yet.

The strange movements JB touched based on… in general, I’ve seen them present very similar to horses with suspected CA issues. They can have lingering but inconsistent soundness issues behind, usually with a forelimb lameness that acts as a red-herring. They also tend to occasionally present as if their stifles are weak, as if they’re UFP - but it is so inconsistent it’s usually chalked up to weak stifles rather than something else.

The most consistent non-physical symptom is overall body malaise that you have a hard time resolving. Things like continued back-soreness, suspensory soreness, weakness behind especially in canter - with difficulty separating hinds – usually can present as bilateral suspensory soreness… By the time the pasterns drop, you are looking at the accumulated damage of a disease that has already progressed significantly. The disease causes issues well before the pasterns begin to sink.

[beowulf]

I missed the comment about Mr Prospector. @4horses this is genuinely news to me. Can you share, where you heard this? He was straight through the stifle and hock for a TB - when they are significantly aged, this can present as dropped pasterns from accumulated suspensory desmitis - but is not the same thing as DSLD/ESPA.

DSLD is in TBs, but that is not a line I consider a risk. You’re more likely to see it in horses linebred to Grey Dawn, IME. Mr P is so inundated in TBs I’d expect to see it more commonly considering how often he is linebred in TBs.