I would put the pup's pedigree on the PDB and list the megaesophagus issue. That way people researching pedigrees can be aware.

 

I wouldn't throw the baby out with the bathwater. Like all health issues, it has to be weighed in terms of many other factors. There are also far worse issues that a dog could produce than MegaE. Especially if it is a mild case that the dog outgrows. Severity, frequency of occurrence, and what the dogs have to offer in terms of other temperament and health traits to their pups all need to be taken into consideration.

We had ONE pup in a litter of 9 with MegaE. Jenn's Glory. She outgrew symptoms in puppyhood. No other pups in the litter were affected. Neither sire nor dam was retired due to that one pup. The dam had one more litter with a different sire, 11 pups, no MegaE. So 20 pups total from the dam, only 1 MegaE. The sire has had several other litters to total many dozens of pups, with several different dams, all with no MegaE. Two full sisters and one half sister of the dam have also been bred, producing several other litters between them, with no MegaE in any of those either.

So there would certainly appear to be much more complexity to the inheritence of this disorder than a simple autosomal recessive as some believe. And it's not impossible that as with other similiar disorders, inheritance in one breed isn't the same as in other breeds. Regardless of means of inheritance, people have to keep the total dog in mind as well as overall production record. If every dog is eliminated from breeding if it produces one undesireable trait or pup, even if pretty severe, there won't be many dogs left to breed.

 

They have actually figured out more on the inheritance portion of ME in regards to GSD's. If a dog actively has ME and is bred, it only takes that one parent. If not, then both the sire and dam have to have the gene to pass it to the pups. So if the dogs are still being bred, they continue to pass the gene on and make more carriers.

Why is it different with ME than it is with hip displaysia? If a dog has severe hip displaysia then the dog would not (or at least should not) be bred. Wouldn't that be considered taking dogs out of the gene pool as well?

 

They have actually figured out more on the inheritance portion of ME in regards to GSD's. If a dog actively has ME and is bred, it only takes that one parent. If not, then both the sire and dam have to have the gene to pass it to the pups. So if the dogs are still being bred, they continue to pass the gene on and make more carriers.

They thought they had inheritance of DM figured out in GSDs too, but there sure seems to be a lot of evidence to the contrary coming out, and I think it would be very detrimental to throw out all the dogs who might have 'bad genes' especially when these DNA marker tests are apparently not as cut and dried as some people think.

And if the tests are accurate, then there is the option of utilizing them to prevent producing dogs who are affected without having to eliminate all carriers from breeding and potentially narrow the gene pool severely in doing so.

Every dog has bad genes and will pass them on. Eliminate every dog without perfect genes from the genepool, and there will be no more dogs. Period. Breeders have to gather as much info as possible and use it judiciously to minimize risk, but no matter how much we all may wish things were different, there is no way to eliminate risk.

It's interesting that there are breeding programs out there that overfocused on specific health problems, and did in fact all but completely eliminate those health problems from their lines, only to have new ones pop up in much greater frequency than exists in the general GSD population. It's always balance, and as the saying goes "when you breed something in, you breed something else out" and vice versa.

Why is it different with ME than it is with hip displaysia? If a dog has severe hip displaysia then the dog would not (or at least should not) be bred. Wouldn't that be considered taking dogs out of the gene pool as well?

It isn't. But originally you were talking about a dog who had produced a pup with MegaE. Now you're talking about a dog who HAS severe dysplasia. That IS different.

The affected dog should not be bred. A dog who is related to the affected dog, even if a littermate or parent, IMO should not automatically be thrown out on that alone. Goodness, if we eliminated every dog who produced or had a littermate with HD from breeding, we really wouldn't have anymore GSDs. The same common sense, look at the big picture approach needs to apply to all traits.

And honestly, one area where MegaE is preferable to other health problems is that it is becomes apparent when pups are very young. Usually as soon as they start solid food. So it should never be a surprise to the new owner. The breeder ought to be able to identify it well before pups are going home, determine the severity and then either euthanize or place the pup in a home appropriately based on that information.

 

Is there published data available about the inheritance of mega-E?

As someone who had a dog with it, and who has raised puppies with it.... it can be a heartbreaking disease.

Chris- At what point did you know Glory had Mega-E?

 

Is there published data available about the inheritance of mega-E?

As someone who had a dog with it, and who has raised puppies with it.... it can be a heartbreaking disease.

Chris- At what point did you know Glory had Mega-E?

http://www.akcchf.org/news-events/library/articles/germanshepherdupdate0909.pdf

Megaesophagus - Clemson Canine Genetics

 

I don't know alot about mega e on how it's passed. But I see in your first post you said that "BOTH" had to have the gene to pass it on? If this is so, who's to say if bred to a different sire/dam that it would ever happen again??

Is there a 'test' to see if a dog is a meg e carrier? I mean how do they "know" for sure that both dogs are mega e carriers?

 

I don't know alot about mega e on how it's passed. But I see in your first post you said that "BOTH" had to have the gene to pass it on? If this is so, who's to say if bred to a different sire/dam that it would ever happen again??

Is there a 'test' to see if a dog is a meg e carrier? I mean how do they "know" for sure that both dogs are mega e carriers?

There is no test yet. Clemson university is currently working on it, but they are still in the early stages.

If there was a test, it would be easy. Carriers breed to clear, no breeding of affected. Too bad it isn't that easy.

 

DM tests are not as accurate as once thought, either.

 

That is true. However, it is better than absolutely nothing.

 

If I was a breeder, and I had a dog that had produced a Mega-E pup, but was an outstanding dog in every other aspect, I don't know if I would retire him from breeding. But I would certainly be honest and open about the Mega-E issue, and I would hope anyone else in the same situation would be honest and open about it. Otherwise you could be breeding carrier to carrier and never know it! If the guy with the stud dog is lying to people or conveniently failing to mention that his stud has produced Mega-E, I would save him the time and trouble and just make it a matter of public record. I think you can enter it into the PDB database.

 

If I was a breeder, and I had a dog that had produced a Mega-E pup, but was an outstanding dog in every other aspect, I don't know if I would retire him from breeding. But I would certainly be honest and open about the Mega-E issue, and I would hope anyone else in the same situation would be honest and open about it.

I would certainly hope any 'reputable' breeder would provide that information as well. If not, I see a very fine line between that type of breeder and a byb, where profit comes first.

 

Yes, the litter I raised it was obvious from day 1 that something was wrong. They were severely affected. I picked them up, took them to the vet who told me impossible that it was mega-e this young. By 3 weeks we did confirm, but a total of 7 out of 9 puppies died. The two females lived.

 

I read the articles and don't find where they are saying that they understand the inheritance pattern. The Clemson site says that they think they've identified the chromosome it is carried on, but not much more than that except that they believe it to be "complicated" in GSDs. Which would indicate not a simple recessive or dominant but rather a polygenic disorder like HD and most others. MegaE has been proven to have simple inheritance patterns in some other breeds, recessive in some and dominant in others (so clearly it isn't always the same across breeds), but not in GSDs. But I don't see where they are saying that they know enough about it in GSDs to be assuming anything about carrier status of other related dogs, nor where the statement that if a dog is affected it only takes that one dog to produce a MegaE pup but if not affected it takes 2. That seems contridictory, as the first statement indicates a dominant inheritance pattern, which clearly isn't the case in GSDs, and the second indicates a recessive inheritance. Can't be both unless it is not only polygenic, but also multifactorial.

 

I also don't believe it is as simple as dominant and recessive genes. I had a pup that had MegaE and out of 10 pups he was the only one that had it. If both the mother and father were carriers in theory 2.5 dogs would've had the disease. I know many of us understand alleles and the punnet square theory, but I don't think all genetics work that easily. If this gene was so simple, that liter would've proved it to be so. I'm not sure how gagsd ended up with so many of the pups with the disease but something else must've been at work there, and not being a geneticist I can't really tell you what it was. The breeders decided to retire my pup's mother (we got another dog from that liter) and our first pup lived to be 1.5 years old and then passed away from complications having to do with the disease. The sire has had 4 liters, and only that one pup has had the disease. 3 liters were with another dam so it makes sense why they didn't have any signs, but in theory they should all be carriers. So imagine the spread of the disease if it was truly that genetically simple.

 

Chris, I can't do the quotes like you did so I will try to answer here.

The HD comment was nothing more than an example, not a change of topic. It was meant as one is cut out so why not the other.

My biggest thing is when is enough enough, if that makes sense. It's kinda of like trying to mask the gene through breeding instead of trying to get rid of it. I know I have alot to learn with genetics and pairings for breeding, as well as multiple other things. I am just really trying to get a good grasp on this defect.

 

Also, for those of you that pm'd a specific breeder on here thinking I meant them, it IS NOT that breeder. I have already informed them of that.

 

If it were PROVEN to be autosomal recessive, then yes, the stud owner and bitch owner ought to disclose. However it has not been, to my knowledge.

If a dog has been bred several times with zero incidents, then one affected pup pops up.... I personally would not rule out breeding the parents again. Although probably not to each other.

 

I emailed Dr Clark and I hope to hear something back within the next day or 2. I will gladly update when I hear back.

 

Mega E can be a surprise. I have seen two dogs diagnosed with it later. One had been bred before diagnosis. There are variable expressions of the disease. It did become a real problem as to aspiration pneumonia. One girl has a large one and is in her 9th year with not too much trouble managing daily life.

I have seen carriers bred extensively. I am not sure of its incidence in the breed. Would not want to breed an affected dog or put two known carriers together. Can we eliminate all detrimental genes and not loose other valuable ones? I have noted that the geneticists are not quick to say do not breed carriers of several things in an effort to maintain other valuable genetics otherwise in the dogs.

 

Mega E can be a surprise. I have seen two dogs diagnosed with it later. One had been bred before diagnosis. There are variable expressions of the disease. It did become a real problem as to aspiration pneumonia. One girl has a large one and is in her 9th year with not too much trouble managing daily life.

I have seen carriers bred extensively. I am not sure of its incidence in the breed. Would not want to breed an affected dog or put two known carriers together. Can we eliminate all detrimental genes and not loose other valuable ones? I have noted that the geneticists are not quick to say do not breed carriers of several things in an effort to maintain other valuable genetics otherwise in the dogs.

If the dogs showed up with it later it is considered secondary and not genetic. The genetic form is the primary idiopathic MEand shows up in puppies, normally at the time of transition to food or cy up to 8-12 weeks.

If there were tests out there and we could know who the carriers were, it would be much different.

 

Definitely genetic in the dogs I know. It just was not noted or detected early on. There is variable expression. I know the lines and the carrier sire they have in common. They were born with disorder. So, later detection does not necessarily determine that it is not genetic. But, yes, there are other causes of problems with esophageal function.

 

I would hope that anyone wanting to use this(or any) stud would do their research first....see what he's been producing before making the decision to use him. That is what responsible breeders do.

 

I would hope that anyone wanting to use this(or any) stud would do their research first....see what he's been producing before making the decision to use him. That is what responsible breeders do.

I agree with this 100%. The stud has only sired 2 litters so far. Out of the 2, 1 litter was affected. The stud has 2 more breedings this week.

If the stud owner doesn't admit it, how will the potential bitch owners find out?

 

When I did my research on the disease (after the pup we got had it), I'm really not sure how it is passed. In some of my research it seems to be more of a mutation in utero rather than a true genetic disease. Out of 10 pups, one didn't get the nutrients or just got a bad cell that ended up not developing the esophagus while the pup was in the uterus. In theory any dog that has ever had megaE in its family history has a chance to be a carrier. Not sure if you can really track this down without seeing the dog produce a megaE puppy. In the case of a breeder/stud owner not disclosing that this has happened, is in my opinion ethically incorrect, but like the others have said, in my opinion it probably shouldn't rule out that dog as a stud.

 

I have never heard this theory but it has been shown that it causes changes to chromosome 12, so I would think this theory is not correct. The only in utero one that I am aware of is mega e secondary to PRAA.

 

Maggie,

I like what you wrote. I also do not think that mega is becoming more common, just that it is being reported more because culling litters is happening less and less.

I just hate the fact that so much has been hidden in the lines because now it is coming back to bite us in the butt.

 

I guess after what I went through with my pup, he didn't have a mild case. So a mild case in my opinion isn't that big of a deal. If the dog can still live its full life, without that many issues eating food and still be a full size dog, I don't really think its that large of a problem. The dog we had, would regurgitate food unless he was kept upright and even then sometimes would. We gave him back to the breeder because we couldn't be there for him as much as the breeder and the dog lived to be 1.5 years old. But then the disease caused other failures in his body.

But I do understand what you mean by 100% of the liter being affected...its wrong even if it is a minor case that doesn't affect the dog's quality of life. I hope that breeder can truly figure out what is going on with the disease and try to get it out of their lines, and then explain to the rest of the world what is the cause of it.

 

I guess after what I went through with my pup, he didn't have a mild case. So a mild case in my opinion isn't that big of a deal. If the dog can still live its full life, without that many issues eating food and still be a full size dog, I don't really think its that large of a problem.

I think the problem would be if the breeder didn't disclose the possibility. If the breeder knew the possiblity, it would certainly matter to me even if it were a mild case.

If I went to a 'reputable' breeder with the hopes of purchasing the next best dog in the show ring (what ever venue) and possibly one day becoming a breeder myself, and the breeder knowingly sold me a puppy that could possibly NEVER become what I envisioned that, to me, is worse than a byb. Much worse.

 

Unfortunately, the vast majority don't disclose it and continue to hide it.

I think this is a sad but true statement. I am on my second GSD with major health issues and have decided not to get another dog in the future. These so called breeders don't have a clue (or maybe they do and just don't care) how heartbreaking and stressful it is to deal with some of these issues, not to mention very expensive.

It really saddens me to think about what happens to the puppies that end up in homes that are not willing or financially able to care for them

 

Whats Happening

Another breeder's experience with Mega-E, apparently carried by her stud dog, who is out of a VERY popular sire of DDR pups. Note that the females tested were negative, and only the stud showed to be a carrier and she had several affected pups in 2 litters.

 

Whats Happening

Another breeder's experience with Mega-E, apparently carried by her stud dog, who is out of a VERY popular sire of DDR pups. Note that the females tested were negative, and only the stud showed to be a carrier and she had several affected pups in 2 litters.

I actually got this info from that breeder the other day. It isn't 100% correct though. The only test Clemson can do is test the dog to see if they actually have it, not just as a carrier. A dog can have ME but show signs that are so minimal it would easily go un-noticed. In this case, it is entirely possible to pass the gene by only the one parent because the gene is then dominant. If neither parent tests positive for this test, it does not mean they are not a carrier, just that they do not actively have it. In this case, it is recessive and takes both parents to carry it.

I already posed the question to Clemson.

 

Is there a location where breeders (stud or bitch) can gather (health related) information from?

IDK if this registry is still active, haven't been on there in a long time: German Shepherd Dog Breed Betterment Registry

 

IDK if this registry is still active, haven't been on there in a long time: German Shepherd Dog Breed Betterment Registry

I have never seen this before.

 

I have never seen this before.

It's been around for many years and I had forgotten about it. If you search for it on pedigreedatabase you will get a lot of posts by Marjorie on the subject

 

I haven't read all the links so sorry if this is already posted:
Canine Megaesophagus, Aspiration Pneumonia & Myasthenia Gravis - Current Studies

Studies! I always sign my dogs up if I can help; so far the ones they've done were the IgA one at A/M and Anna did some DNA thing at Cornell. Not sure if Ava did as well. So please spread the word about those for any Mega-E dogs.

Canine Megaesophagus, Aspiration Pneumonia & Myasthenia Gravis - Resources has links, including to the Yahoo group for Mega-e dogs.

There is also this: Persistent Right Aortic Arch (PRAA) in Dogs that seems similar.

I hope they are able to get some good info from those studies.

 

I haven't read all the links so sorry if this is already posted:
Canine Megaesophagus, Aspiration Pneumonia & Myasthenia Gravis - Current Studies

Studies! I always sign my dogs up if I can help; so far the ones they've done were the IgA one at A/M and Anna did some DNA thing at Cornell. Not sure if Ava did as well. So please spread the word about those for any Mega-E dogs.

Canine Megaesophagus, Aspiration Pneumonia & Myasthenia Gravis - Resources has links, including to the Yahoo group for Mega-e dogs.

There is also this: Persistent Right Aortic Arch (PRAA) in Dogs that seems similar.

I hope they are able to get some good info from those studies.

Dr Clark is leading the studies for mega e. She is the same one that was leading the studies for EPI when she was at Texas A&M. She is awesome. I am hoping she shoots me an email back soon. I have heard from the lab but I like how she explains stuff.

PRAA is one of the mega e causes in pups. The mega e that is caused by PRAA is considered secondary or aquired. Last I heard on PRAA is that it is not genetic. I know several people that argue this though. They have seen it run in specific lines.

I'm like you Jean. I can't tell you how many times I sent Zappa's blood and DNA places just to do testing. He had so many issues it just felt like the right thing to do. Heck, I even sent Leyna's DNA several places just so I can see her genetic make-up. She is healthy, but it's interesting!