No one in this thread posted pictures of landgraf. Again, I have never seen a photo of landgraf that suggests he had dsld, nor have I noted any correlation with landgraf and presentation of dsld. Hypp has been traced to impressive. Dsld is not common in landgraf line horses, as it isnt really common at all, and no studies have been done or evidence presented that suggest that landgraf line horses commonly present with dsld.
the comparison between hypp/impressive with dsld/landgraf is poor.
In case it helps someone, here is a picture of my mare at one day and another at three years, and another the year I first suspected something. You can see how much straighter her hind legs are.
Did you do the biopsy?
Extremely straight legged horses can drop their fetlocks, which looks like DSLD/EPSA, but isnât always EPSA/DSLD.
So sorry, either way. 
How old was she in the first pic - is that her 1 day old pic? I ask, because her hind legs look too straight for her age. It looks more like adult angulation, rather than foal angulation. Foalsâ legs are so long compared to their body, especially the long femur, that they are typically fairly camped out. I know that pic was taken from behind, so does change what we see. But thatâs something I look for when judging foal hind leg confo - they need to be camped out when really young, just like pasterns need to be pretty upright at that age, so that adult growth âfixesâ them.
So for a foal to be âtoo straightâ behind, they will definitely be too straight as an adult.
Just a question, and potentially off topic.
Given the parallel conversation regarding Fragile Foal Syndrome manifesting in homozygous scenarios, has anyone looked at whether those with DSLD are heterozygous for FFS? The collagen breakdown in both sounds similar but DSLD takes longer.
Except doesnât it read like fragile foal syndrome exclusively manifests in wbs? (Which as someone else pointed out on that thread is so odd given that wb isnât a breed so what are we really talking about? I would think particular bloodlines) Yours is an interesting question given dsld is common in tbs and tbs are heavily represented in wb breeding, but something like dsld is so uncommon it seems quite difficult to pin down where it ultimately stems from.
Maybe DSLD is difficult to pin down because it spans breeds. I know of a mother/daughter pair of Arabians that had it, and I know it is well known in Pasos.
ASFAIK, WFSS only happens in WBs⊠which is not a closed gene pool, necessarily â however, that probably boils down to it really only being present in certain families of WBs⊠Thereâs a lot of common ancestry in WBs, same as with TBs.
It doesnât happen in TBs, which are contributors, or Arabs, which are contributors⊠so it sounds like, to me, it is separate â though possibly, your train of thought might not be too farfetched as a theory if it was something that manifested in one (WB) individual that had âEPSA genesâ but was only passed on to WBs, because presently WBs usually only breed with other WBs and obviously would never have the chance to proliferate a closed stud-book like Arabians or TBs (where DSLD has happened, also extremely rarely).
Right. Although as I said earlier in the thread it does tend to manifest more in particular breeds, tbs and pasos, to name two. But it isnât common even in those breed where it more commonly manifests. And since the problems progress at different rates, some horses are never diagnosed, they just get old and retire, and as above other issues can manifest the same symptoms. We certainly have a long way to go to understanding. But while we are working on that please donât breed those horses :lol:
The picture of her as a chestnut baby is marked as one day old in my file, it may be a week or two old and just in with the bunch marked 1 day. By fall of her first year she had already started to show gray hyperpigmentation.
See post 78. :), You are right, the comparison is poor, Impressive did not show signs of the disease but in the picture posted, (albeit a poor quality shot and one cannot draw a conclusion only supposition from a photo) Landgraf does appear to have a low/soft/saggy fetlock. It took years to implicate Impressive and longer to âproveâ, DSLD/ESPA is still being recognized, it will take many years and much research to trace its origins if it is even possible without an easier way to conclusively diagnose. There are still way too many missed diagnoses and misdiagnosis. I have nothing against Landgraf, just noted that of two warmbloods mentioned in this thread he is a common point.
I guess we are seeing different things 
good thing more research is being done, egh?
DSLD/ESPA is proving to be difficult to pin down because it is likely a multi-gene disease, ie not just 1 test of 1 gene to see what status itâs in, like HYPP or WFFS or HERDA or Frame/LWO. Combine that with some thought that it might be something that âflipsâ under certain environmental stresses, and that could make it extremely difficult to pin down.
I honestly donât know if there are a known category of genes that are more easily flipped than others, in the science of epigenetics. Since @mvp has weighed in on the WFFS thread with obvious genetic knowledge, I wonder if she has any insight into that.
Thanks, I just wanted to make sure I was reading âone dayâ as " 1 day old" 
So yes, my thought on that still stands - that she looks like she was conformed more like an adult, instead of a very young foal, so her straight hind end was there from the start. Then because it all straightens as they grow, it became too straight as an adult as well.
A small quibble - is it really âmanifesting moreâ in TBs? I know it is more common in Pasos because of how extremely limited their gene-pool is, and because they breed for a specific type â but the TB gene pool is still enormous when compared to Paso and some other registries.
I only ask because in my professional experience, I have seen it much more in WBs⊠but I work primarily with TBs, and AFAIK, there has been no conclusive study done that isolates TBs as having much more of a predisposition for the disease. I have seen a few comments like this blaming TBs for the disease in WBs - and I have to wonder, because itâs a disease that has been documented in almost every hot-breed from Morgan to Trotter, that it is probably not something from a specific breed and is probably something that has been existing in the horse population for a long, long time - before any of these breeds were established.
My point being, I havenât found it to be the case at all that it is more common in TBs, so if you have information on that, Iâd love to be able to read it.
Otherwise, I agree with you⊠and also agree, have worked with several Landgraf horses who never showed any sign of DSLD. Not saying itâs not possible but I think JB is right on the money that DSLD/EPSA is definitely a multi-gene disease⊠which is why I think we see it in some family instances, and not at all in some other members of the same family. I also strongly suspect that is why the disease manifests, across the board, in some very different breeds â the Paso and TB could not be more different, and donât share any recent ancestry that I know of - same goes for the Paso and WB â have they had similar recent ancestry contributions?
I think it goes much deeper than breed - my suspicion is that it is probably a specific ancestor that is well beyond tracing on a page, and that the subsequent bottle-necking of some breed gene pools has brought this about.
I think I said several times that in my experience Iâve seen it most in tbs. I also said you still donât see it much. I donât know why it manifests where it does. Good thing we are doing research. I donât think we should breed confirmed cases, because Iâve seen it done, it wasnât good, it was pretty devastating, and thereâs no use in it. I donât think we are bottlenecking a gene pool by taking out real problems. But rest assured, no one is listening to me telling them not to breed their sick or unsound or ill conformed animals.
I know, but to baldly put statements like âit manifests more in TBsâ, are at this time anecdotes and not factual. I didnât see an âin my experience it tends to happen moreâ, I saw âit tends to happen more in XYZâŠâ, which I think you could appreciate the difference since you seem like a pretty intelligent and thoughtful poster.
Iâve seen it almost exclusively in WBs, but I donât think I could say âit manifests more in WBs than in other breedsâ. Itâs rare no matter the breed, and sometimes itâs misdiagnosed (bilateral suspensory desmitis, straight hind ends, etc), or not diagnosed at all â so itâs really hard to get a good number on the true % present in a population
Itâs just that this information could be oft repeated, and considered as fact, when while it has a basis on someoneâs experience (which I believe you when you say youâve dealt with it more in TBs) it isnât fact until confirmed scientifically.
I agree I donât think weâd be bottlenecking or doing any disservice whatsoever culling those that are affected, or carriers â if carrier is a thing with EPSA/DSLD. However, with WBs that would probably take some very prominent WBs out of the genepool that have made wonderful contributions in other areas. So⊠when the nature of the diseaseâs inheritance comes to light, I think itâs going to be very hard to eradicate, and I think weâre going to see it perpetuated because it is unfortunately something that is present in some very popular lines today in WBs.
I work almost exclusively with warmbloods, specifically FEI show jumpers, your experience isnât my experience as I said, several times, Iâve primarily seen it manifest in tbs. I canât say enough to say if it was limited to particular bloodlines. It will be very interesting to see what continued research reveals. I also still totally donât think people should breed diagnosed cases. You can absolutely disagree.
Weâre on the same page about not breeding them. If that is not what you got from my post, then I wasnât clear. I donât think that carriers or affected EPSA/DSLD should be bred at all. I just know people well enough to know that unless there is something grotesquely obviously wrong with the offspring, people are going to be selfish and dumb and breed EPSA/DSLD carriers.
As it is, I am still amazed a certain WB stallion is standing considering he now has multiple documented offspring with DSLD/EPSA. And no transparency or openness whatsoever from the major breeder that stands him.
Case in point in the other thread weâre both part of, with WFSS, which we seem to be on the same page as well.
For the record, since you brought up your professional experience, you probably havenât seen it as much because a horse with DSLD/EPSA is not going to end up in an FEI barn because they rarely can handle the physical rigors of an athletic career. Iâve not seen one in any UL/FEI occupation that Iâve been part of (eventing), but have seen it in plenty of client horses in non-FEI barns. All of them WBs except for one.
Itâs probably also because the disease progresses at different rates and most FEI horses tend to be on the younger side. And you are also Iâm sure absolutely on to something that these cases are much more likely to be culled from the upper levels and sold to unsuspecting amateurs. Although the worst cases I saw, both tbs, the horses were seriously dropped before age 10, so even an amateur could look at them and go yeah, no but thanks. But one had been raised since birth and the other purchases off the track by a professional, so God knows it didnât manifest early enough to save lots of money and heartache.
Indeed, very sad for all involved. I really am glad that there are a few vet schools that are, reportedly, tracking the incidences of EPSA they discover via nuchal ligament biopsy. It would be interesting to see their findings but I imagine we will have to wait several years.
Seems to me that since we know it is established in the PP population, that maybe a look into what their stud-book is doing (presently) might be revealing on how to handle it in our own populations, if they are handling it at all. God knows (most) times it doesnât manifest early enough to hamper a TBâs racing career, though I have wondered before if the diseaseâs manner of affecting connective tissue would somehow limit the soundness or longevity of a horse, TBs included. I do think that the JC has a vested interest in these things, because they recognize the lives theyâre producing en-masse - the cynical part of me thinks that it will be much harder for TBs & WBs, which are high dollar stud-books, to fully eradicate the disease.
It does seem to me that some horses with EPSA do have other soundness issues - is it because of the disease, or is it unrelated?
It would be nice to get answers.
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