We have dam A and sire A. (both cardiac echo normal/clear).
Dam A bred to sire B produced 11 pups now 2 1/2 yrs old and no TVD affecteds so far.
Dam A bred to sire A produced 3 pups now 1 1/2 yrs old, 1 mild murmur, 1 severe TVD (echoed).

Sire A bred to dam B produced 6 pups now 2 1/2 yrs old and no TVD affected so far.
Sire A bred to dam B produced 3 pups now 1yr old and no TVD affected so far.
Sire A bred to dam C produced 11 pups now 6 mos old and no TVD affected so far. Running on two pups.

With so many unknowns with TVD not sure what to do. Is it possible that the litter with dam A and sire A maybe something just went wrong in utero and it was a fluke that it produced TVD ? A bad combo ? Or is one or both definate carriers ? Do I cut both sire and dam from further breedings ? I certainly don't want to produce any more TVD. Do I cull the pups I'm running on from the sire A dam C litter ?
I do plan on submitting blood samples to research.
This is the first time I've run into a TVD situation so I'm spinning. Luckily all pups produced are in pet homes with the exception of one. Gut felling tells me not to breed dam A, sire A, or the pups I'm running on until we get more TVD answers and hopefully a test soon.

Don't breed Sire A to Dam A again, and submit all pedigrees for all litters to Meg Sleeper's research program:

Samples and reports should be sent to:

Meg Sleeper, VMD, DACVIM-Cardiology
Section of Cardiology
MJR-VHUP
3900 Delancey Street
Philadelphia, PA 19104
sleeper@vet.upenn.edu

http://tarrahlabs.com/nlrc.htm

I agree, something is just not liking Sire A and Dam A together. Submit their pedigrees and litter information as the other person said and then hopefully you know something before you think about breeding your pups that you are running on

I definately wouldn't put sire A and dam A together again. But would you risk putting sire A with another bitch ? So far with other girls the pups have been fine, but I also wouldn't want to risk another case of TVD. I just found out about the TVD pups from sire A and dam A breeding a couple weeks ago.

I wouldn't put Sire A to a pedigree that is very similar to Dam A's. It would be interesting to know how close the pedigrees for Dam B and Dam C are to Dam A. Again, the pedigrees could provide some very useful information to the research project. Please help us get closer to identifying the cause...

All were outcrosses for several generations from sire A. There may be a common dog more then 5 generations back.
Dam B no relation to either dam A or dam C.
Dam C has some of the same linage as dam A, I have
also worked with dam A and dam C's lines for at least
10 yrs and no cases of TVD.

This is what a board certified cardiologist explained when asked about exactly the same scenario. His is a hard line approach since there is no way to determine who contributes the TVD gene.

Dam A, Sire A, Dam B: all echoed clear.

Dam A bred to Sire A produced 10 pups - all pups healthy.

Dam B bred to Sire A produced several TVD affected pups.

Both litters should be spayed/neutered.

Dam B and Sire A both should be eliminated from breeding.

Dam A can be bred.

A couple of questions...

Dam A was only bred the two times - to Sire A and Sire B, producing a total of 14 pups. Of those two breedings, only the cross with Sire A produced TVD, correct?

Sire A was bred a total of five times, producing 23 pups, and only the cross to Dam A produced TVD?

Were all puppies of all litters echo'd with color doppler or just auscultated?

Without knowing the pedigrees involved, I would be looking closely at Dam A as a potential producer - just based on the odds at this point. Sire A has produced a total of 23 pups, with 1 affected and 1 murmur. Dam A has produced 14 pups with 1 affected and 1 murmur. A close study of the pedigrees involved could tell you more, though.

As others have said, please submit all information to Meg Sleeper for research. Also, if you post an anonymous email address (just go to hotmail or yahoo and make one up - like tvdquestion@yahoo.com, for instance), I'm sure you would get more meaningful assistance privately.

Removing both Dam A and Sire A from your breeding program seems a little extreme at this point, given the limited information, though I definitely would not breed those two together again - or similar pedigrees. It is highly likely that one (or perhaps both, but not necessarily) are "carriers" for TVD and it is equally highly unlikely that there was a new spontaneous mutation.

One more question - were any of these litters larger in utero than what was live-born? In other words - on the litter with 3 for instance, were there pups that showed up on an u/s that re-absorbed or were there any pups born doa or didn't survive long?

All were just asculated with the exception of the severe TVD pup.
Yes only the litter out of Sire A and Dam A had TVD affected pups. But you did bring up a very good point. With the litter of Sire A to Dam B that had the 3 pups there were also 5 stilborns. Very possible they were TVD affected pups ? If so that would up the percentage of affected produced by sire A.
I am leaning towards believing the sire is the carrier. There is a rumored TVD carrier a few generations back in his lines. Like I mentioned I've been dealing with the dam A lines (both topside and bottom side) for quite a few years and so far there has never been a TVD problem that I have heard of or produced myself.

And there's the problem...you're making assumptions based on rumor.

We have no way of identifying "carriers" of TVD and won't until we have more research done. Rumors are not facts that you should base a breeding program on. If you suspect a dog of producing a TVD affected pup, call the owner of the suspect dog and ask. Find out both sides of the equation, get information on the dam of the TVD affected pup too.

I remember hearing "rumors" of a well-known dog dying of TVD and rumors were coming from long-time breeders who should have known better than to repeat hearsay. When I got ready to breed my girl to a dog that had this rumored dog in its pedigree, I called and spoke with the owner of the rumored dog. She was honest and very gracious, and provided me with a copy of the autopsy of the dog. He died of something completely unrelated to TVD. She told me that he did produce one puppy with TVD, but out of the hundreds of puppies he produced, that one is the only one I know of. I believe the combination of him and the dam was the problem.

Please don't make breeding decisions based on rumors.

No I'm not baseing my decision on the rumor of a possibly TVD producer in his lines. I'm basing it
on the fact that he produced a litter with definate TVD pups. While I don't know for sure if it came from the sire or dam or both, I'm leaning on the possibility that it may be the sire since I have be using the dams lines for years without any TVD. Either
way I don't plan on breeding the sire or dam anymore just to be on the safe side, I certainly don't want to produce another TVD pup. The rumor of a possibly TVD producer in his lines is an extra kicker but my decision is not solely based on that since it is a rumor and not a for sure fact.

Unfortunately, auscultation alone will not detect all cases of TVD. Statistically, it has been shown to miss about 20% of affected dogs - so you could have more affected get that do not present with murmurs detectable by auscultation. If there is any way possible to do so, get as many of the get echo'd as you can. If you have a teaching vet school nearby, or an established cardiac vet hospital - talk to them about a clinic price or group rate. Many of them will work with you. It is only with echo and color doppler that you will have a true count of TVD affected puppies. However, I know how difficult and expensive it can be to get pet owners to fork over the money for a test for a healthy puppy.

As to the 5 stillborn, there has been some speculation that true homozygous for TVD (TT) is fatal in utero. That is speculation only! But it is an interesting factor when you start looking at litters of suspected and known TVD producers.

Good luck with your research and let us know how it goes.

When thinking of stillborns- would there be any value in having necropsy(s) on pups? I am wondering if they would be able to tell if they had TVD, or the death in utero was cardiac related. just curious.

Just did that, and they only tell if there is regurg, but TVD would not yet show.

I thought TVD was a congenital (present from birth) abnormality of the tricuspid valve flaps (they are "stuck" to the wall of the heart rather than releasing properly so the valve does not close as it should). Wonder why a necropsy of a neonate would not show that. Anyone know?

Mode of inheritance is simply unknown for TVD. It can be spontaneous (birth defect) or it can be genetic. It can be recessive -- or -- could be dominant with incomplete penetration.

Wow...doesn't help us as breeders does it? IMHO -- Old Timer has it right. Keep Dam A and remove all others from the breeding program. If TVD turns out to be dominant with incomplete penetration, this is the only way.

Had there been just one pup in the litter that was affected -- then it could have been spontaneous. Your chances diminish greatly with each subsequent pup from the same litter that is affected.

Its a hard decision to make, but in a few years you'll look back and be thankful you made that decision.

Interesting view point. I've not seen any research that supports that TVD could be a birth defect. Can you give us a link to that? I would like to see it.

That is what all the research that I've read shows, Patty - which would lead me to believe that it could be detected in a necropsy. Regurgitation, however, would be more difficult to detect after the heart quits pumping, I would think.

I would be very interested in reading any research that shows otherwise. Can anyone provide a link?

I'm strongly in agreement with both old timer and you. A good discussion.

I'm not sure I understand your logic. Are you referring to the OP's post or someone else's?

Dam A was the only dam in the OP's post that produced TVD pup. Dam B and Dam C did not produce TVD pups when bred to Sire A. I'm not sure why you would remove the two bitches who didn't produce TVD pups from a breeding program, but keep the one who did produce it (when bred to a certain stud dog).

Please clarify.

To Huh

This is the scenario they were agreeing with:

In the OP's scenario, there were:
Dam A - produced TVD
Dam B - did not produce TVD
Dam C - did not produce TVD
Sire A - produced TVD
Sire B - did not produce TVD

Dam A bred to sire B produced 11 pups now 2 1/2 yrs old and no TVD affecteds so far.

Dam A bred to sire A produced severe TVD

Dam B bred to Sire A produced no TVD affected so far

Dam C bred to Sire A produced no TVD affected so far.
****
Dam A and Sire A have produced TVD.
Dam B & Dam C have not produced TVD
Sire B has not produced TVD

If following the hard line approach, Dam A and Sire A should not be bred again to anyone.

Some heart murmurs involving other valves may be a heart defect that's not hereditary.

Of course there are other types of heart issues. We were discussing TVD this time.

I think we have to say that the other litters have not produced TVD YET. I would want to follow both litters with echoes maybe every other year. Recently a Cardiologist told me he personally feels a dog or bitch should not be considered TVD clear until 5 with clean echoes.

All of this discussion of which one should be culled is unfortunately not founded in knowledge. At best you are guessing, at worst culling the wrong one.

WE DON'T KNOW THE MODE OF INHERITANCE. Any decisions made are pure speculation.

That is not correct. The "hard-line" approach of culling breeding stock who have produced serious genetic issues is the practice in the livestock industry on the recommendation of breeders and genetic experts. Poultry, swine and cattle also have occurrences of autosomal dominant with incomplete penetrance diseases which can be catastrophic to those industries. Since there is no definitive test to diagnose these issues (such as the Labrador situation with TVD) the practice is to remove the breeding stock who produced the issues as well as their progeny from any breeding pool. If you have a sire and dam who have produced TVD and you do a relative-risk assessment, you have to be honest and objective about the results. From a gene load standpoint, using relative-risk assessment, you can apply a risk-benefit analysis to the breeding stock in question who have been responsible for producing a TVD offspring. At the present time, and until we have a reliable genetic test to determine the carriers of the TVD gene, this is our only tool to gain control over "genetic" disease by a careful scrutiny and analysis of the dogs involved for various important inherited characteristics.

I suggest you read Dr. George Padgett's excellent book on canine genetics, "Control of Canine Genetic Diseases" which is a benchmark reference manual for the serious breeder.

Here is just one example of the hard-line approach to removing "suspect" breeding stock in the beef industry. Since the article is referencing a disease which is autosomal dominant with incomplete penetrance, just apply the same principals to a Labrador breeding situation.

Bovine familial convulsions and ataxia
published in the Canadian Veterinary Journal, Oct. 2004
excerpt:
"BFCA is an inherited disease associated with an autosomal dominant gene with incomplete penetrance. Since not all of the animals affected by mutation will show clinical signs of BFCA, it is important to diagnose this disorder and eliminate the source from the genetic pool of a herd as soon as possible to ensure that this genetic defect is eliminated from the breeding herd. Most of the reported outbreaks appear to be associated with a carrier bull; therefore, culling of the carrier bull and its progeny appears to be the most effective control strategy.

In conclusion, the BFCA genetic mutation is present in Aberdeen Angus cross cattle in Canada and most likely in the United States, since the bull associated with the recent Canadian outbreak was sired by a bull from the USA. Accordingly, it is important that clinicians recognize and pathologists diagnose this disorder accurately at early stages of an outbreak in a herd.

Elimination of carriers of this genetic mutation from the breeding stocks as soon as possible will prevent spreading of the genetic defect in Aberdeen Angus cattle in North America."

First, thanks for your post and reading recommendation.

Second, if a newbie is looking for a pup and is not as familiar with potentially troubled lines (involving TVD)- are there specific questions you would suggest the newbie ask the breeder regarding TVD in their lines?( I understand the need to ensure that sire and dam have ECHO)

TIA

further info:

Dam B was also bred to Sire C and had a litter of 12 pups who are currently 3 1/2 yrs old and no TVD. Sire C is litter brother to Dam A. Sire C has also produced other litters with no TVD.

Since those pups were not echo'd, it would be incorrect to say that none of them were TVD affected. All you can really say is that they had no detectable murmurs. Auscultation alone is not a reliable test for TVD, particularly in our deep-chested breed. Murmurs can be hidden and undetectable during auscultation and valve deformaties cannot be determined at all except through echo. Color doppler reveals any regurgitation.

"Second, if a newbie is looking for a pup and is not as familiar with potentially troubled lines (involving TVD)- are there specific questions you would suggest the newbie ask the breeder regarding TVD in their lines?( I understand the need to ensure that sire and dam have ECHO)"

To learn more about TVD in various lines, why not start by talking to the owners of TVD dogs? An email address in your post might help people who are willing to discuss it contact you privately.

To supplement old timers information, here is a quite current publication that just came out by By Lori Seimens, D.V.M., DACVIM. Please read it for the most current information and suggestions by her in The Retriever News.

http://www.theretrievernews.com/Library/Articles/Veterinary/TricuspidDysplasia?FB_Values

It's a good article, but not sure how recent, I thought that the GDC was no longer operating a database?

It is a very good article, however not the most recent. Although I couldn't find the source information, I believe it was written about 4 or 5 years ago - maybe longer. Dr. Lori Siemens is no longer involved in TVD research, as far as I can find out.

Still...a good article

Some were ausculated and a coupled echoed out of Dam A's other litters, none showed signs of TVD. You wonder how many TVD pups may have been produced that we never know about. Unless we were to echo every pup born that we produce we will never know for sure if we produced undetected TVD pups.

Sad, but true.