Spinoff from DSLD/ESPA thread: breeders sharing health issues openly?

[halt]

@BeeHoney

IME, stallion owners are VERY cagey about sharing about problems in offspring.

First of all, there are a lot of problems that aren’t necessarily genetic. OCD can be genetic, but seems to also be linked to larger, better performing equine athletes, and there also can be a nutritional/environmental component. I Xray all of my yearlings late in the fall of the yearling year and we periodically find OCDs and when I have mentioned it to stallion owners they invariably say something horrified/defensive along the lines of “We’ve never heard of one of stallion X’s offspring having an OCD before.” Seriously? Or maybe no one else is Xraying? No one else is reporting back? I’m not blaming them, I breed larger horses so OCDs are occasionally going to happen, I’m just reporting back.

Aside from the OCD issue, I would say that many American breeders are not selective enough about their mares. FWIW, when I first started breeding 20 or more years ago I was not selective enough about my mares. Myself and a lot of other people have improved greatly on this count, but there are still many small breeders who are breeding horses that shouldn’t be bred. People think that breeding to a good stallion will dilute their mare’s faults, but in many cases flaws can appear or be amplified in offspring through no fault of the stallion. There are also still a great many backyard breeders, some of whom lack expertise in correctly managing the health and nutrition of breeding stock. I can understand why a SO would not want to accept that their stallion was at fault for a problem if there was some question about the quality or management of the mare. Additionally, some defects are just due to chance or bad luck.

There’s also the cost factor. What does it cost to own and raise a nice purebred stud dog? Now compare that to what it costs to purchase or raise/develop/get approved/get a show record for/market a breeding stallion. Let’s be frank–it costs a fortune. By the time a stallion is standing at stud and has a few offspring on the ground, there’s been a ton of $$ invested. I can understand the lack of interest a SO might have regarding testing their stallion for genetic flaws. I don’t see stallion owners being enthusiastic about testing for DSLD. To make it work, the test would have to be relatively inexpensive and something that could be done at an early age before too much $$ had been invested. Even then–what breeder wants to find out that their nice young horse has a flaw and is thus unsellable?

In 25 years of breeding, I have not seen much in the way of increasing investigation of / transparency about genetic flaws. When I choose a stallion, I do the same thing I did 25 years ago–reach out to people with offspring, talk to trainers or grooms or other connections about the horse, see the horse in person (if possible) or get current pictures/video, ask the farm vet if I feel comfortable (who certainly wouldn’t say anything bad, but if they are enthusiastic or have bred one of their own mares that’s a good sign).

FWIW, the same issues regarding lack of transparency about possible genetic flaws are present in the TB industry–probably even worse there. There’s just no motivation for disclosing anything that might cost the SOs business. I know of one TB stallion that has had spine surgery at a relatively young age and it is not disclosed to mare owners. The only reason I know is through the grapevine. Who knows if the problem is genetic or not? But personally I would avoid a stallion that had such a serious health issue at a young age.

The difference is OCD doesn’t really kill a horse, but EPSA/DSLD does.

It’s funny you blame american breeders - some of the worst offenders come from European celles…

[Donella]

Our guy is in the early stages of the disease ( at 11 yrs old) and the biopsy showed the kind of tissue damage that is consistent with the disease. Our guy doesn’t have soft pasterns at all and is sickle hocked ( not post legged). We suspected DSLD because he had mild lameness in almost every joint in his hind legs for the last two years. At first it was the stifle. When a joint injection didn’t work, we tried IRAP. That worked for about six months. Then he flexed off in the hocks. Then the fetlocks. Then the stifle again. Eventually, we blocked out the suspensories. Both my vets are quite familiar with DSLD and wondered… What else would explain this kind of lameness pattern on a horse that does 2nd level work 4 days a week? So an ultrasound of the suspensories showed a very obvious " moth-eaten" appearance and some of the other soft tissues around that area looked suspect. The biopsy confirmed it. There is a very distinct tissue pattern that is seen in horses with DSLD. But honestly, nobody would EVER look at our stallion and think even for a second he has this disease. No idea though if this biopsy would be an effective diagnostic tool in a 2 yr old that is not asymptomatic. Fwiw, we did the biopsy when he was put under for castration. I can’t remember the cost as it is my mom’s horse but I will ask. It was a hassle to get it across the border too. It was sent back as Georgia didn’t fill out the correct paperwork and my vet ended up driving it across the border. There is nowhere in Canada where you can get the biopsy done.

Also something that I thought was interesting: when our guy arrived from Spain into LAX he had a swollen sheath. The vet in LA thought he had an infection and put him on antibiotics. It never resolved. Then my vet thought maybe he was metabolic and his blood did show that he was borderline, but even with pergolide, it never changed. I recently read that this is a common symptom in horses with DSLD. He also has a lot of sinking in his back. Not the whole back, but just exactly where the saddle sits. It’s not a fit issue. It’s like a strange tissue response to the saddle. I will see if I can get a picture and post it. It’s really bizarre actually.

[Marla_100]

My understanding is that because this is a disease that manifests in defective tissue throughout the body, including
in the organs, the actual breakdown in tissue is happening long before external symptoms appear. Yes, they’re
now questioning if it isn’t somehow connected to IR and to the fatal condition of Aortic Rupture seen more and more
in eventing horses.

[JB]

@Donella

So an ultrasound of the suspensories showed a very obvious " moth-eaten" appearance and some of the other soft tissues around that area looked suspect.

Also something that I thought was interesting: when our guy arrived from Spain into LAX he had a swollen sheath. The vet in LA thought he had an infection and put him on antibiotics.

He also has a lot of sinking in his back. Not the whole back, but just exactly where the saddle sits. It’s not a fit issue. It’s like a strange tissue response to the saddle. I will see if I can get a picture and post it. It’s really bizarre actually.

All this triggered a thought. What abx was he put on, do you know?

There is some evidence about the fluoroquinolones class of antibiotics and their damage to tendons (potentially ligaments?), as well as potential nerve damage.

The bigger thought (mine, not necessarily a community) is around the possibility of something like this being a catalyst for the disease to manifest. Or, a bigger stretch, BE the “disease”, or at least mimic it.

[keysfins]

@JB

All this triggered a thought. What abx was he put on, do you know?

There is some evidence about the fluoroquinolones class of antibiotics and their damage to tendons (potentially ligaments?), as well as potential nerve damage.

The bigger thought (mine, not necessarily a community) is around the possibility of something like this being a catalyst for the disease to manifest. Or, a bigger stretch, BE the “disease”, or at least mimic it.

Interesting, I’m following your thinking on that. Hmmmm.

[mvp]

@IPEsq

I suspect that this is true. Only on a young horse that is already becoming symptomatic somewhere would the biopsy be useful. Making a genetic correlation (if there is one to be made) will take a lot of samples from diagnosed horses and a lot of time most likely. Considering that the disease tends to manifest later in life, this makes the breeding issue all the more complicated without an easy test and something like a clear genetic correlation, with the marker being available to be found before the biopsy can confirm.

FWIW, I don’t think DSDL starts to manifest later in life. Rather, I think the macroscopic signs of it-- notably the dropped pasterns-- show up later. To me, DSDL in the suspensory apparatus is like fraying a rope. By the time you see those pasterns looking strangely horizontal-y, you merely have frayed enough of the rope to produce mechanical failure. But the rope was fraying before you saw that failure.

I have known another horse and his son who have other skin problems and a hernia. I’m not sure these are all related, but it would be interesting to figure out the physiological process for each oft these things affecting soft tissues and asking if they had a common phenotypic- or genetic basis. In other words, if you intelligently cast the net wider in order to include other phenotypic symptoms, you could see the disease appearing in younger horses.

[mvp]

@IPEsq

I think this is becoming one of those things that is probably more prevalent than we think because we now are starting to understand what we are looking at. And recognize it’s a disease that affects the entire body. I mean, 20 years ago, no one thought about gastric ulcers. Until someone realized that’s a thing in horses and then we started to find out it’s a really common thing. It’s not like horses 25 years ago wouldn’t have had ulcers.

I don’t know if “no one thought about ulcers” back then, But I can tell you that part of what “made ulcers A Thing” is that endoscopy got cheap and feasible.

[Donella]

JB he was put on Excenel so a Cephalosporin.