That does seem expensive. I recently paid ~$300 for one session for comparison.
Maybe that estimate also includes ultrasounds or sedation or you have a higher call fee?
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Slight tangent: Ok, I know this is going to be a bit tin foil hatâŠthe research was intense into finding the origins of WFFS for a few reasons, and I think that one of them was so they could try to âblameâ some other non-WB breed/type. Or say that itâs so far back, and look, itâs been around for awhile and these carriers are all fine.
In all honestly, who, outside of maybe the veterinary/medical community (and that requires funding) would want to make a connection if there even is one? Many breeders certainly donât. That has the potential to decrease their stallions (or broodmares) value. It (could be) about the money, to some extent.
That being said, I donât know if anyone has tried to look into this deeply, and maybe there are no connections to be made.
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Absolutely, on some level some wanted to point a finger at someone, but that doesnât do any good. There are some good thoughts on the founder, way way WAY back long dead dead, and not a single soul could have known it was him back then, any more than anyone could have known Impressive had the HYPP mutation or Poco Bueno had the HERDA mutation. It just took generations for 2 carriers to be bred and produce a diseased horse, by which time it wasnât obvious at all who had the original mutation.
And yes, they did find it was a non-WB origin, which is why itâs FFS, not WFFS
Thereâs so much testing done now, someone would have gotten a whiff of there being a health issue connected with a carrier, at least IMHO 
It is $540 for shockwave, $40 for sedation and $90 call fee plus 13% tax. Comes to just over $750 a session. Ultrasound is just under $300, plus $40 sedations and $90 call fee. So total of 3 sessions and then the ultrasound is $2700
Definitely seems more reasonable when broken out like that. I was just quoting the price of the treatment itself.
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You can always pull hair and test him to see if he inherited the FFS gene but there is no research that says being heterozygous for the gene causes problems. The problem is when two carriers breed and the foal gets two copies and that is always fatal at a young age, if the foal is even born alive. As far as figuring out who patient #1 was - it would be interesting to know but I suspect it was some obscure animal so far back in time that FFS slowly made its way into the gene pool before it was at a high enough level to be noticed. The only reason I think it might have been an obscure TB is that FFS has been found in a few TBâs, but these were horses from very obscure pedigrees, not ancestors found in todayâs racehorses. If it had been a popular widely used TB sire it would have shown up in racehorses and it would not have been an obscure disease anymore because now you are talking big bucks. And back in those times before DNA testing there were parentage questions that were never answered so maybe these few affected TBâs actually had a WB ancestor way back 100âs of years ago. Who knows.
I have a mare that is prone to anything causing a sore or wound on her. She just has thin skin. Legs and feet do not have great circulation so I could see something like that not healing perfectly in a healthy horse.
To my knowledge itâs not definitively decided, but Bay Ronald xx or his son Dark Ronald xx are among the leaders. So, early 1900s, but far from obscure stallions. Obscure horses donât tend to make their mark on history, not only because they didnât produce enough, but didnât produce enough good horses who were then line bred (or even in-bred) to create the first diseased horse.
Another thought is that it was Furioso xx who certainly made an enormous contribution to the WB pool, but it still could have been one of the Ronald horses and it happened to be Furiosos who ended up propagating it the most. These just happened to be bigger sporthorse sires, than racehorse sires
Yes I heard the theories about Bay Ronald/ Dark Ronald but these are widely used sires in TB breeding if you go back far enough. Probably more widespread in WBâs but not unknown in racing TBâs. So why has this problem never shown up in race horse breeding? I donât subscribe to some conspiracy theories that race horses with FFS have been hidden by the big TB breeders. The economics of those breeding programs suggest to me that if it reared its ugly head there would have been earth shattering amounts of money involved in getting to the root of it, not a cover-up.
And I think if it was Furioso xx, it would have been a bigger crisis than it is. Hard to find a WB that does not go back to him multiple times. But I agree he is not found in racing pedigrees as far as I know. Last I read the estimate of carriers is about 10 percent of WBâs. But this might not be accurate because this is only 10 percent of those tested, not 10 percent of the population. These figures may not be accurate these days. But I think if it was a mutation of a stallion as widely represented in WBâs as Bay Ronald or especially Furioso xx, the incidence would be much higher and people would have been investigating the problem decades ago. All the mutation needs to do to is infiltrate one stallion that was used for breeding lots of mares and boom! It doesnât have to originate in a widely used stallion. It just has to creep up the genetic ladder until it is an ancestor of a widely used stallion. I would love to know who the originator is but, unlike Impressive, I think it is too far back to really know.
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How many horses line-bred back to either of them? Also, itâs theorized to have a relatively high fetal mortality rate, so a foal was never born, which makes it much harder to know the true history of the progression
But until it gets to a widely used stallion who produces enough offspring that are also bred and eventually line bred, it could take a very long time to really start showing up as the actual disease.
I also donât think weâll ever know who started it because I also think itâs just too far back, unlike Impressive and Poco Bueno. And at this point it doesnât matter.
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âHow many horses line-bred back to either of them?â I know n=1 is not a statistic but I looked back at my mareâs TB grandmother who was bred to race and not for sport. I ASSume she was not very fast because she ended up in a sport horse breeding program. By Stage Door Johnny and out of an Arts and Letters mare. A pedigree that is not as prevalent these days but still a legitimate racing pedigree. Multiple crosses to Bay Ronald (and Dark Ronald) if you followed her pedigree back that far. Through Princequillo, Hyperian, Ribot and other well known TB lines at that time - multiple crosses. So even if these crosses are not as prevalent these days, there are still plenty of horses that trace to these old stallions way back in their pedigree. And have lots of ancestors tracing to Bayardo ( Bay Ronald son) or Dark Ronald. And foals that are born with this horrible affliction I think are not easily dismissed and somebody in the racing world would have thrown $$$ at it to get answers. Too expensive not to get answers.
I just donât think it statistically possible for a stallion that prevalent in race breeding to be the original mutation. Maybe not as prevalent these days but still significant if you go back to the early 1900âs in their pedigrees.
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Itâs been proven that Dark Ronald is not the source of WFFS. Westfalen was the one that originally posted that claim, and they dirty-deleted it when it was proven false by a DNA test. Current speculation is that it may originate from an 1800s Hanoverian stallion. Itâs probably much older.
https://onlinelibrary.wiley.com/doi/full/10.1111/age.12972?campaign=wolearlyview
OP, did your boy bandage bow when the reaction to the wrap happened?
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FFS (no longer called WFFS) has been identified in Warmbloods, Thoroughbreds and Haflingers, Knabstruppers and American Sport Ponies. Either the source of the mutation goes farther back than the Hanoverian stallion that some research has suggested might be the source, or there are multiple sources of the mutation cropping up in different populations.
You could always get him tested and see if he is a carrier but I think it is unlikely to be caused by FFS. It looks like an old bandage bow to me. I had a horse that came to me with a leg that looked like that and he jumped up to 1.50m with no issues with it. If it doesnât bother him, I wouldnât worry and would leave it be.
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I donât know about that. Look at the death threats that kept the information about the lines carrying the C6-C7 malformation from being released.
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Didnât Sharon May-Davis say that she found that it ran in some TB lines and received threats when she was going to publish the info?
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Yes, she did receive threats. What I was pointing out is that the incentive or ability to âcover upâ is quite different from one to another. If a stallion or mare line does not produce the expected number of live foals by a full quarter- that would be well known immediately even if itâs not publicized. Those rumors fly pretty quickly after the first breeding season. I heard Cigar was infertile within months, long before it was public and Iâm not embedded in racing circles. Its not something you could easily cover up. And even if you could a 25% abortion/ death rate would show up on the insurance side.
Breeding horses that underperform or break down years later on after getting high prices at the sales? At which point itâs hard to pinpoint why they did poorly? And at a much lower percentage? That potentially could be covered up for a long time. People tried to pretend HYPP wasnât a thing for years to save their incomes but not HERDA, that wasnât possible because they died so young.
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It is hard to get a good picture of his leg, but it is not a bandage bow. The bump is actually on the side of his leg right where the small incision was. This is why my vet first thought he had an allergic reaction to the sutures as it was odd to her to have such a hard lump on the site. She did ultrasound it and you can see where the check ligament was cut and it appears to be ok above and below the bump. But right on the bump the tissue is damaged and âangryâ looking (vets words). Thatâs when she mentioned that he might have a collagen deficiency as he healed so poorly at the incision site (plus with all of his other healing issues he has had pretty much his whole life - he was also a dummy foal saved by the madagan foal squeeze, had a crooked leg braced after foaling, had a belly button infection 3 months after birth, issues with gelding, a small cut on a hind leg that was literally nothing that blew up and has scared with a big lump 2 years later, etc, etc.), but all else appears to be just fine. The it got me thinking about his sire being a carrier for FFS and how resulting foals are collagen deficient. He has always been on a glucosamine/chondroitin supplement (as per his surgeon) and now I have just added 2 scoops (20g) of collagen to his diet just in case. Neither cost much so it shouldnât do any harm anyway.
She did say motion is lotion and to for sure get him started but to do it slowly. He is on long turnout (about 14-18hr day now and goes to 24hr turnout next week) which he has been for his whole life. I am going to send him to the trainers this weekend to get him slowly backed, no rush - he will be on 24hr turnout as their option was either 24hr or about 8hr/day for indoor so I opted for the 24hr for him.
I wonât be jumping him at all this year I just want him to get the idea of having a job and then will let him sit for the winter (as in still lots of turnout, just not riding work). I do believe he still has an inch or two to grow as well. Fingers crossed all goes well.!
This is him yesterday (the other photos above were when he was a 2 year old). His mane was past his neck last week but I was able to pull it while he was sedated for his teeth.
IMG_8661|666x500
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Thanks! And how interesting that itâs suspected well back into the 1800s
But heâd have to consistently breed to FFS carrier mares (very tiny chance), and both would have to pass their FFS on a consistent basis, and the statistics of either, let alone both, are just about 0
but itâs the resulting homozygous foals who are collagen deficient, and they donât live
He really is such a lovely horse! He may just be one of those more sensitive ones who exaggerate even small insults to his body 
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This has been such an interesting and informative thread! So glad, OP, that youâve kept updating. Was curious if you have ever had the foot re-e-xrayed? Would love to see an update on that, if yes.
I have not re-xrayed his foot yet but it would be very interesting to do for sure! Once I get caught up on vet bills, I will get it re done at some point for sure. Iâm just so happy that his foot looks normal so it hasnât been too high on my priority list, but I would love to compare them to his original xray done at 14 months.
He is out for training now and is w/t/c and seems to be doing really well. I will bring him home at the end of next month and canât wait! I just went to see him go yesterday and he looks amazing.
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Iâm glad to hear he is doing so well! The change with the foot is absolutely amazing. I appreciate the vet bills, for sure.
Iâve certainly learnt a lot from this thread. Very glad youâve posted all that you have, along with the pictures.
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