DSLD in warmbloods and crosses

[beowulf]

[QUOTE=Bats79;8840102]
It certainly IS learned in some instances - if the factors are right (and assuming they are referring to wind sucking not wood chewing).

In 40 years of breeding horses with the same mare lines we have had a total of 2 foals become windsuckers. Different bloodlines, different environmental situations - the ONLY constant between the 2 was that we had a couple of mares (not related to the foals) but in the same paddock and they sucked wind.

Since then (18 years ago) I have not allowed a wind sucker near my young horses and I have not had another foal learn to suck wind. I’m not saying that there isn’t an inherited predilection to the behaviour but I’ve definitely not had a foal become a wind sucker (and we bred full siblings to both the foals that learned to suck wind) without first seeing another horse doing it. If it was only inherited then we should have witnessed a young horse taking it up when the environmental factors were right but we have not.[/QUOTE]

perhaps their common uniting factor is their management… cribbing is a stereotypy, a coping mechanism from some sort of external trauma (either physical or mental) or stressor.

are your foals stalled? did they develop this behavior during/after weaning?

in my experience it is not something a content horse watches another horse do and replicates: it’s something a stressed (for whatever reason) animal does to cope with its stresses. it could be anything from extreme boredom to unhappiness with isolation, stall rest, weaning, etc. i never had a single one of my horses ‘learn’ to crib even when housed next to very active cribbers.

[JB]

The studies have fairly well proven it’s not a learned behavior.

When I boarded, there was a cribber and a stall walker. My TB (yes, a TB) was stalled in various configurations of being beside them, and in eye sight of them both. Years. He did neither. And they were stalled most of the time, it’s how the barn was. Turnout a couple hours a day, worked an hour or so a day (my horse and the cribber) to a couple hours (the stall walker, he was a lesson horse).

That N=1 definitely doesn’t prove this isn’t a learned behavior, but there a lot more Ns than just mine. And there were usually about 15 other horses in that barn, with various ones housed beside and in eye sight of these 2, and nobody else ever developed either of those habits. This was not just a year or 2, this was closer to 20 years.

Not seeing a stereotypie come up when environmental factors are “just right” doesn’t prove it’s not inherited. Every individual has their individual tolerance for stress, both physical and mental. Who are we to determine This Set of Environmental Factors is perfectly acceptable to a given horse and that all should be right in his world? Why do certain horses in a seemingly quiet herd turnout environment develop ulcers, while others getting the same management do not? The playful horse will tolerate a lot more activity in his environment, for example, as he views it as entertaining stimulus, than the quiet, leave me alone horse who doesn’t thrive on that much activity. It’s not up to us to say a very active barn is good for horses, or a very quiet barn is good for horses. They are affected how they are affected.

[The_Blonde_amp_The_Bay]

@Angela Freda

in some cases, environmental influences that lead an animal to exhibit the symptoms [fetlocks drop, skin gets sensitive, etc] that may have otherwise stayed latent/dormant sans environmental influence.

I’m a bad post follower, apologies for the late response! I do agree with your ideas about both the possibility of hereditary influences and environmental, especially nutrition based. I’m curious, did you learn that sensitive skin is a condition of DSLD? Lately my guy can hardly tolerate brushing and this line piqued my interest.

@Angela Freda

That a DVM is researching the genetics of it is great to hear, and news to me.
If anyone has any links to more about that I would love to learn more.

I’ll find my links and post shortly. There basically isn’t enough funding so the research is very slow going, but as far as I know there are three doctors working; Dr Halper, Dr Mero and Dr Kellon. Dr Halper is who I’ve spoken with.

[JB]

Given that DSLD is a disease of connective tissue, it makes sense that some horses might become sensitive to being touched/groomed/saddled/etc.

If the genetics aren’t there, environment (incidents, nutrition, etc) won’t cause DSLD. Injuries can cause SLD - suspensory ligament desmitis - which is not bilateral (unless the injury was, or compensation ends up making it that way) and does not affect other parts of the body. The genetics have to be there, and either that’s enough to cause the condition to present itself, or something external precipitates its surfacing.

[The_Blonde_amp_The_Bay]

@rebecca yount

I think DSLD is related to the horse using itself incorrectly, and it is repetitive strain injury most likely due to a tight and locked back which causes abnormal stresses on the limbs. Therefore, breeds that tend to drop and lock their backs either because they have been selected for a certain type of movement (Saddlebreds, Arabians, gaited horses) or due to being worked incorrectly with respect to use of their backs. Also long pasterns I believe are contributory. Since it therefore may appear more in those particular breeds people tend to believe it is “genetic”. How do you separate conformation and way of moving from genetics??I think what’s genetic/inherited is conformation and body mechanics that leads to DSLD.

This is incorrect. DSLD/ESPA has absolutely nothing to do with the horse using itself incorrectly. The horse may indeed use itself incorrectly because of the DSLD, but it is not caused by a horse not coming through its back. The disease can affect every tissue in the horse’s body, including the nuchal ligament and eyes. In a basic sense; the tissue cannot maintain its function, breaks down, and then cannot repair itself correctly.

In my horse’s case, his suspensory could not perform its job which led to the hocks straightening, which led to the stifles catching, which led to the SI pain, and so on. The entire mechanism of his leg is failing because the supportive tissue cannot function correctly.

[Alternamoose]

Was it confirmed that your horse does have DLSD?

[colorfan]

My lovely mare has been positively confirmed as having ESPA/DSLS. I can see how someone might call her skin sensitive, I call her body sore… I can see how someone might think improper riding could be a contributing factor, it may, I stress may, cause the disease to manifest sooner but I seriously wonder the horse was sore, not enough to be ‘off’ but sore enough to be ‘tight’ or not come through, or slow in lead changes, etc (if someone had noticed these kinds of things in their horses).
My mare is a wb/x a mix of Holstein,TB,Arab,Percheron. She always has had fairly straight hind legs but a good angle to her pasterns. She has only been diagnosed for a few months, since the disease is progressive it is hard to say when it first manifested itself.
Her fetlocks seem to be lower some days than others, I have taken pictures to document her progression. I don’t ride her as I believe she is uncomfortable. She has eye wrinkles almost all the time, they go away about an hour after a dose of bute. She rarely offers to do more than a few steps of trot when in the field. I notice she moves differently, not as fluidly as she used to.
She often comes and stands in the saddle-up spot looking at me, I imagine she wonders why she doesn’t get picked anymore.
I hate this disease.

[beowulf]

@colorfan

My lovely mare has been positively confirmed as having ESPA/DSLS. I can see how someone might call her skin sensitive, I call her body sore… I can see how someone might think improper riding could be a contributing factor, it may, I stress may, cause the disease to manifest sooner but I seriously wonder the horse was sore, not enough to be ‘off’ but sore enough to be ‘tight’ or not come through, or slow in lead changes, etc (if someone had noticed these kinds of things in their horses).
My mare is a wb/x a mix of Holstein,TB,Arab,Percheron. She always has had fairly straight hind legs but a good angle to her pasterns. She has only been diagnosed for a few months, since the disease is progressive it is hard to say when it first manifested itself.
Her fetlocks seem to be lower some days than others, I have taken pictures to document her progression. I don’t ride her as I believe she is uncomfortable. She has eye wrinkles almost all the time, they go away about an hour after a dose of bute. She rarely offers to do more than a few steps of trot when in the field. I notice she moves differently, not as fluidly as she used to.
She often comes and stands in the saddle-up spot looking at me, I imagine she wonders why she doesn’t get picked anymore.
I hate this disease.

i am so sorry. ((hugs))

do you mind sharing her pedigree? this is such a devastating disease i think it is SO important to be keeping track of what bloodlines get it.

[JB]

@colorfan I’m so sorry I love that you’re documenting her progress though. I think if you are able to share that at some point, it will help a lot of people. Documenting her demeanor at each phase is great as well.

Have you looked into shoeing options? IIRC many have become more sound and comfortable with wedges behind.

[Mozart]

Has anyone heard of this being an issue in the W line? And are there any reasons, other than DSLD, that an older horse would have significantly dropped fetlocks? (bilateral)

[Lingkra]

Does anyone have any young horse or foal examples (pictures would be great!) of horses that developed DSLD later in life?

[mzm_farm]

Red Unicorn, yes please post pedigree and current pics. Thanks for sharing!

[clint]

@Red unicorn

Here are a couple of my Holsteiner when he was a foal. He’s currently 12 and was diagnosed earlier this year. I have a full record of bloodlines including photos if you guys want to see them. I got the ok from my vet to continue normal riding as well as jumping, but we have a lot of maintenance. He’s on a daily dose of previcox, lives in standing wraps, gets ice and liniment after each ride and if there’s a bad day, surpass. Still loves jumping, but you definitely can tell he’s different by the way he canters and changes leads.

Because so many foals are born with angular limb deformities, especially down in the fetlocks, I wouldn’t take foal pics as an indication of later DSLD. I would love to see current pictures of him.

[Really]

I have one, sadly. He is 3 1/2, full Hanoverian, long pasterns (almost horizontal in the back) sloping croup, straight-ish hind legs. Just had a full workup with the vets and they had never seen a young horse so bad. He is 16.2/16.3h and growing. By an “S” line stallion out of a Weltmeyer mare who competed up to PSG. Neither parent has the problem (as least visually) but both may be carriers. Heartbreaking to say the least. I will most likely have to put him down since the vets think it will only get worse, especially as he gets bigger. Was born with long, sloping pasterns but they never really straightened up to the degree they were supposed to. Vet is pulling nuchal ligament specimen to send to another lab for testing but we did do ultrasound and extensive testing with a team from the vet school. His 1/2 sister by a different stallion is perfect. Could be like Herda in the QH world, one copy = desired trait, 2 copies = undesirable phenotype.

[cyberbay]

I have a Dutch WB/TB cross with this disease. He manifested symptoms when he was about 5 or 6 – a bull-nosed hind hoof. The vet diagnosed the cause of that as a lax suspensory. The remedy was different shoeing (trailers); the vet said, “you don’t need to worry about this for another 10 years.”

The shoeing relieved the bullnose profile, although the fetlock on that leg was more up/down than that of the other hind leg, and I was able to use this horse under saddle for those 10 years, just as the vet said I would be able to do. In that 10th year, kaboom, the symptoms re-flared: soreness, even more dropped fetlock, etc. Periodic ultrasounds revealed a “swiss cheese” suspensory in that leg, His symptoms are mostly in that single hind leg. I asked the vet (a different one at this point) how to differentiate between a routine suspensory injury and ESPA, and he said a suspensory injury would usually have just a single tear, while ESPA has multiple ‘disintegrations’ (my word).

He was fully retired two years later. He is wandering carefully a nice field with a good friend, and has a stall at night. He is now age 23. I visit him 3-4x/month. He, for sure, has fallen in the stall, probably trying to rise from sleep, and he has permanent wounds just below the knee on a front leg from having to work so hard to get up. I think the pain of the ESPA leg is why he has struggles with the up/down.

I did the Dr. Kellon protocol with the herbs for the first few years after the diagnosis, and then retired that program so that I could put him instead on NSAIDs. He is on 114 mg. of Previcox and we stack with bute on the days he looks more uncomfortable. But he does all right, and has a bright eye.

He also has had navicular syndrome, starting about his 8th year, and a lousy stifle since his earliest days. The navicular resolved nicely finally by going barefoot; the stifle did great on joint injections until they had zero effect. That leg is badly bothered and it is a malevolent companion to the ESPA leg. Whether these two conditions are a result of the ESPA, not sure.

It’s my understanding that this disease is systemic, affecting the Type 1 collagen, of which the suspensory is made. There are other symptoms, too, such as mild colics and loose skin. My horse did seem to have mild colics, usually in the very early autumn (August) – I also think that his symptoms would flare a bit this time of year, too – but no loose skin. He is not particularly post-legged behind.

As well, as I understand it, there is nearly no $ for any study, and there is a request for cadavers (if that is the correct word) of horses that suffered this disease by UGA??

I personally suspect ESPA when I hear of young-ish horses (mid-teens) dying of a heart condition, such as a burst aorta. The aorta is made of Type 1 Collagen.

I hope this helps. It’s long and drawn out, but we have all managed our horses pretty successfully.

[colorfan]

Sorry I haven’t gotten back to this thread before now. Red Unicorn, interesting that Landgraf 1 appears to have dropped fetlocks also, he is in my mare’s pedigree.
No amount of wrapping removes the swelling around my mare’s fetlocks, sometimes I think wrapping helps reduce how far up her cannons the swelling goes.

I feel the winter, (perpetual cold wraps) has helped reduce the puffiness but at my last measurement her fetlocks have not changed.
Interesting note about the bullnose on the hinds, I had noticed that the summer before her diagnosis, tried a shorter trim cycle, tweaking her trim…wondered about it

I looked for copies of her u/s, can’t seem to find them.

[ladyj79]

I have never seen a photograph of Landgraf that led me to think he had dsld.

[clint]

@ladyj79

I have never seen a photograph of Landgraf that led me to think he had dsld.

I had a Landgraf granddaughter who had no fetlock issues at all.

[ladyj79]

@clint

I had a Landgraf granddaughter who had no fetlock issues at all.

Landgraf is ubiquitous in the pedigrees of Holstein and other registries. Like there are lots and lots of Landgrafs, and I’ve not noticed anything like a bunch of landgraf dsld cases. And again, I’ve never seen a photo of landgraf that looked at all like a presentation of dsld.

[colorfan]

Someone in this thread posted several pictures of their horse and Landgraf 1. Not a great pic but he does appear to have low fetlocks.
There are many many Impressive babies out there, not all of them have HYPP but there is no doubt it came from him. I am not accusing Landgraf, he is just a point in common.
As far as my mare goes the only part I know for sure is the WB. The WB is Lynx(1987) and Allie Nicks.

So many unconfirmed diagnosis make this a difficult disease to track. I suspect many of the older horses may not have ‘inherited’ ESPA.
Confirmed cases are found in more and more breeds.
It seems to progress quickly in some horses and slowly in others. Whether this is due to actual differences in the disease or misdiagnosis is unclear.

When I first suspected something there was a noticeable difference between the two hind legs. They now look fairly similar.

This winter has been hard. I am finally coming to terms with this truly is the end of our riding career together.It has been really hard to let go, I have learned so much with her, she knows more than I which she proved at the last clinic we went to together. The clinician rode her and did quite a bit more with her than I could. Such a good girl. Training goals we will never get to now.
I don’t know how much longer we will have together but for now she still makes my day with her good morning nicker.

I have found a little bit more heel seems to make her more comfortable.