DSLD and ESPA: are they the same?

[keysfins]

DSLD = Degenerative Suspensory Ligament Desmitis.

ESPA = Equine Systemic Proteoglycan Accumulation.

What is is the latest thinking on these two conditions? Is DSLD considered one manifestation of ESPA? Is Nuchal Ligament biopsy considered the gold standard for confirming ESPA?

From some basic reading, it seems that some breeds are more likely to develop DSLD, such as Peruvian Pasos, Saddlebreds, QHs, TBs and some Warmblood breeds. Does this suggest a genetic component? And is there any test, beyond a biopsy, that could help identify an affected horse, before seeing symptoms?

Has anyone here managed an affected horse, and what was the outcome? Treatments or therapeutic shoeing that seemed to help? Successes in dealing with discomfort/pain? Can a horse be comfortably pasture sound?

Thanks for any info or reading suggestions. Just want to learn more about this, as the condition seems to have an evolving definition. I actually came across the “new” name when it was cross-referenced in a blurb about Ehlers-Danlos syndrome in humans.

[JB]

What used to be called DSLD is now referred to as ESPA, because more research revealed that what results in DSLD is actually a systemic issue which can, and often does, affect more than just the suspensories - it can affect the connective tissues in general. The fact that the nuchal ligament can be biopsied is telling.

It is absolutely hereditary, which is why it’s found much more frequently in certain breeds, as you listed. It is a progressive, systemic disease, cannot be cured, only managed. Some horses are affected earlier and/or more severely, some progress faster than others. This means some horses can be pasture sound, or even light riding sound (like child pony rides) for years, while others are PTS at an early age.

I believe an ultrasound of the suspensories will show the disease if it’s actually to the point of causing issues.

Jiaogulan is a Chinese herb that Dr Kellon is doing some work with that is at least showing some promise in helping these horses. Some are reporting increased pain relief, some are reporting actual healing. I have not looked into this enough to see how valid these anecdotes are, as in, are they good enough to be considered reliable, or are there simply coincidences? Regardless, there’s enough interest in some results for it to still be currently pursued, which is encouraging.

I have a friend with EDS, and funny that it never occurred to me the potential relationship. There are a couple different types of EDS and afaik, ESPA is ESPA

[keysfins]

@JB

What used to be called DSLD is now referred to as ESPA, because more research revealed that what results in DSLD is actually a systemic issue which can, and often does, affect more than just the suspensories - it can affect the connective tissues in general. The fact that the nuchal ligament can be biopsied is telling.

It is absolutely hereditary, which is why it’s found much more frequently in certain breeds, as you listed. It is a progressive, systemic disease, cannot be cured, only managed. Some horses are affected earlier and/or more severely, some progress faster than others. This means some horses can be pasture sound, or even light riding sound (like child pony rides) for years, while others are PTS at an early age.

I believe an ultrasound of the suspensories will show the disease if it’s actually to the point of causing issues.

Jiaogulan is a Chinese herb that Dr Kellon is doing some work with that is at least showing some promise in helping these horses. Some are reporting increased pain relief, some are reporting actual healing. I have not looked into this enough to see how valid these anecdotes are, as in, are they good enough to be considered reliable, or are there simply coincidences? Regardless, there’s enough interest in some results for it to still be currently pursued, which is encouraging.

I have a friend with EDS, and funny that it never occurred to me the potential relationship. There are a couple different types of EDS and afaik, ESPA is ESPA

JB, I am so glad you responded, thank you.

The parallels of ESPA and some of the types of EDS are what grabbed my attention. Then I went clicking around related links and had to look back in my browser history to find one of the things that I wanted to ask about.

http://www.ckequinehospital.com/page…-Desmitis-DSLD

From the article:

Wear and tear associated with normal regular exercise causes small “microtraumas” that occur in the suspensory ligaments. Normal horses produce more cells that lay down additional collagen fibers to repair the ligament. In horses with DSLD, these cells do not lay down collagen, but convert to a type of cell that produces cartilage instead.

((I also started thinking that there could be situations where producing cartilage might be beneficial for humans, such as in arthritic knees. ))

Some sources suggest MSM supplementation may be beneficial. Thoughts on that, or other therapies? Or is it mostly a matter of maintaining comfort?

[JB]

MSM has proven anti-inflammatory properties, so in whatever situations excessive (which is relative to the scenario) inflammation can be minimized, it’s a good idea. Some inflammation is good and necessary. Too much is when things get into trouble. I don’t think there’s any information out there that points to normal uses of MSM reducing inflammation beyond what is healthy, causing its own set of issues. So to me, in any situation where there might be inappropriate inflammation, MSM isn’t a bad idea.

I don’t know that that applies to the normal micro-tears in tissue that results from normal exercise. Microtears are a fact or exertion, and that’s why the DSLD/ESPA horses are not candidates for forced exercise, or at least nothing more than very minimal

[Angela_Freda]

I do not think DSLD/ESPA [yes same thing] are hereditary in that it is attributable to breed, but instead to some lines of some breeds.

And even then only potentially. There are no absolutes there either… just because a horse is related to a line that has had some with DSLD/ESPA, does not mean ALL of that line will ever show symptoms of it. IMO it is a latent potential that expresses in some, but not all. In my horses case it was due to stress/ulcers that his DSLD/ESPA expressed.

Think HYPP and Appendix QHs. Not all Appendix QHs have HYPP. But if you have an Impressive bred horse you might have HYPP.

[keysfins]

@Angela Freda

I do not think DSLD/ESPA [yes same thing] are hereditary in that it is attributable to breed, but instead to some lines of some breeds.

And even then only potentially. There are no absolutes there either… just because a horse is related to a line that has had some with DSLD/ESPA, does not mean ALL of that line will ever show symptoms of it. IMO it is a latent potential that expresses in some, but not all. In my horses case it was due to stress/ulcers that his DSLD/ESPA expressed.

Think HYPP and Appendix QHs. Not all Appendix QHs have HYPP. But if you have an Impressive bred horse you might have HYPP.

Sure, your example of HYPP makes sense, as far as heritability. I hope a genetic marker will be found that will allow less-invasive testing for ESPA.

It seems that right now, diagnosis comes after an injury or lameness, based on how the body begins to heal the suspensory ligament(s).

I also wonder if other injuries or chronic issues may have this condition as the cause/basis, since it is systemic. Perhaps more answers will come.

[Angela_Freda]

@keysfins

Sure, your example of HYPP makes sense, as far as heritability. I hope a genetic marker will be found that will allow less-invasive testing for ESPA.

It seems that right now, diagnosis comes after an injury or lameness, based on how the body begins to heal the suspensory ligament(s).

I also wonder if other injuries or chronic issues may have this condition as the cause/basis, since it is systemic. Perhaps more answers will come.

Aortic ruptures are one related problem.
Because of the tissue in which the Proteoglycan is known to accumulate in, ie the veinous system is susceptible and ruptures are potential issues… but how many of those occur and are diagnosed, and were in horses known to have DSLD/ESPA to begin with?
The problem is, as you suggested, that often the diagnosis is too late and done via process of elimination*
There are lots of other symptoms that suggest DSLD/ESPA beyond the very obvious, classic dropped fetlocks that I encourage people to be aware of and keep an eye out for.

http://dsld-vet.blogspot.com/p/symptoms.html

*my horse never got u’sounds or had the nuchal ligament test.
He had many of the most classic symptoms that he was able to tolerate and live a decent QOL after diagnosis using supportive care, which all pointed to DSLD/ESPA.

[keysfins]

^^^^^ AF, May I ask what supportive care you were able to provide your horse?

[Guilherme]

@Angela Freda

I do not think DSLD/ESPA [yes same thing] are hereditary in that it is attributable to breed, but instead to some lines of some breeds.

And even then only potentially. There are no absolutes there either… just because a horse is related to a line that has had some with DSLD/ESPA, does not mean ALL of that line will ever show symptoms of it. IMO it is a latent potential that expresses in some, but not all. In my horses case it was due to stress/ulcers that his DSLD/ESPA expressed.

Think HYPP and Appendix QHs. Not all Appendix QHs have HYPP. But if you have an Impressive bred horse you might have HYPP.

The tendency to the disease is clearly hereditary but that doesn’t mean every horse with the tendency will develop the disease.

G.

[keysfins]

@Guilherme

The tendency to the disease is clearly hereditary but that doesn’t mean every horse with the tendency will develop the disease.

G.

So the chicken and the egg question.

How would you know if a horse has this, if conformation still looks fine, performance is good, and no symptoms apparent? Is the disease only recognized after the fact, such as an unusual healing/non-healing of a suspensory injury, or degradation of the suspensories?

I’m also interested in the possible role this may have in some cases of Kissing Spines.

[JB]

@Angela Freda

I do not think DSLD/ESPA [yes same thing] are hereditary in that it is attributable to breed, but instead to some lines of some breeds.

And even then only potentially. There are no absolutes there either… just because a horse is related to a line that has had some with DSLD/ESPA, does not mean ALL of that line will ever show symptoms of it. IMO it is a latent potential that expresses in some, but not all. In my horses case it was due to stress/ulcers that his DSLD/ESPA expressed.

Think HYPP and Appendix QHs. Not all Appendix QHs have HYPP. But if you have an Impressive bred horse you might have HYPP.

HYPP is attributed to a breed. It does not exist in other breeds. It ends up in QH crosses, which then puts it into “breeds” that use QH as a cross.

I’m not sure how that means “I don’t think ESPA is hereditary”. Of course it is.

That doesn’t mean it exist in the entire breed, since not every horse in a breed with a disease is related to the horse with the original mutation. But it’s absolutely hereditary.

It’s just not known what sort of genetics are at play, though I think not thought to be autosomal dominant like HYPP is. My guess is it’s a multi-factor set of genes. I don’t discount the notion that some event could trigger it, but when it’s so prevalent in a given breed like the Paso, that seems to be an exception rather than a rule.

[sdlbredfan]

Yes. Only the name changed.

[JB]

@keysfins

So the chicken and the egg question.

How would you know if a horse has this, if conformation still looks fine, performance is good, and no symptoms apparent? Is the disease only recognized after the fact, such as an unusual healing/non-healing of a suspensory injury, or degradation of the suspensories?

You don’t know until you have ligament tissue that looks the part, either via a biopsy if you’re suspecting it because of pedigree and the horse is also starting to feel off, or the characteristic enlarging of the suspensory even before there’s any dropping or lameness

I’m also interested in the possible role this may have in some cases of Kissing Spines.

ESPA is a connective tissue disease. KS I suppose could be a symptom of some connective tissue failing, but I’ve never seen anything that suggests KS is generally the result of connective tissue failure.

[Paige777]

I have a TB mare with DSLD. She was diagnosed about a year and a half ago after ongoing lameness that lasted for about a year; I’d rehab, get her back up to about 2 minutes of trotting, and she’d go lame again. Shortly after the diagnosis, you could see her hind suspensories start to change - one leg is worse than the other.

She’s pasture sound, in that she goes out and plays and jumps around quite comfortably, but she has a hitch when she trots due to the worse hind leg. She’s retired and living out life in my backyard. The vet advised me there’s nothing that can be done, but giving her plenty of turnout and room to move around helps. (She has a run-in stall with access to a larger pasture.) She seems happy and is doing well for the time being, but I also know that I don’t have too much longer with her.

[keysfins]

@JB

You don’t know until you have ligament tissue that looks the part, either via a biopsy if you’re suspecting it because of pedigree and the horse is also starting to feel off, or the characteristic enlarging of the suspensory even before there’s any dropping or lameness

ESPA is a connective tissue disease. KS I suppose could be a symptom of some connective tissue failing, but I’ve never seen anything that suggests KS is generally the result of connective tissue failure.

Now I will have to search back in my browser history again, JB, to see where I read about that connection.

[Angela_Freda]

@JB

HYPP is attributed to a breed. It does not exist in other breeds. It ends up in QH crosses, which then puts it into “breeds” that use QH as a cross.

I’m not sure how that means “I don’t think ESPA is hereditary”. Of course it is.

Which is what I wrote before you split hairs by only looking at half of that sentence you quoted:
‘I do not think DSLD/ESPA [yes same thing] are hereditary [B]in that it is attributable to breed, but instead to some lines of some breeds.’

Not all TBs get DSLD/ESPA. It has been seen primarily in certain lines of TBs.
Just like HYPP is not seen in all QHs, but in those with Impressive lines.[/B]

[Angela_Freda]

@keysfins

^^^^^ AF, May I ask what supportive care you were able to provide your horse?

Yo was 23 when diagnosed. He started out dropping weight, lots of weight in a very short period of time.
That we later attributed to ulcers, thanks to him being relocated next to a stud-ish food aggressive horse.
Shortly after the weight loss started, the fetlocks dropped and appeared ‘coon footed’.

I moved him to a retirement home, he was out as much as possible [days in winter, nights in summer] in a field with portions that were slope-y.

He got anti-inflammatories* was put on an IR diet, and got special shoeing to offer him support through raised heels of the hind legs that were effected. My farrier, amongst the rest of the fabulous crew, was so thoughtful about how to deal with his shoeing, he was a Godsend.

• he got joint supplements that contained MSM, which is contraindicated with the Jaiogulan/arginine potion the DSLD/ESPA group leader Bunny sells. I chose that option because while he was a horse with DSLD/ESPA he was also a horse with other issues that needed alleviation as well [arthritis, etc].
  I had to treat the whole horse, not just the DLSD/ESPA, and for me/for Yo that meant not doing the herbs, but other treatments that addressed the other issues as well as the symptoms of the DSLD/ESPA

He was retired for 6 years, from 23-29 and was put down due to colic.

If you look at the link I shared, there are many symptoms that might precede the ligament issues that you can keep your eyes out for… but also can be attributed to other things as well… hard to know, until you do. Sadly.