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Dcm 2

12K views 30 replies 12 participants last post by  windamyr 
#1 ·
I just received the report back from NC vet College after submitting cheek swabs on my 2 yr old boy. His DCM 1 was negative...DCM2 was heterozygous positive. So, he has one normal gene and one affected.
I lost my first Dobe at age 7 from DCM- and his DCM was negative. They only had the first gene test available in 2008. So, I was really unhappy to read this current report.
I do understand that this does not mean he will get ill. The report stated that having the one affected gene does not necessarilly predispose the dog to DCM. Yeah, yeah.... but its worrisome.
Anyone who has gone through the horrors of DCM with a cherished companion knows what I mean.
I am trying to remind myself that this is not conclusive: how many other genes are involved that no one knows about yet? My boy is super healthy and full of energy....he WILL have a long, fantastic life!
Has anyone else received a less-than-wonderful report back?
My breeder said that probably a majority of our dogs fall into this half/half category. Maybe so. but this is MY dog.

Somebody- please- make me feel better!
 
#2 ·
Honestly, I wouldn't even stress about it at all. There's not much data out there to indicate what these results really indicate in terms of actual risk of developing this disease. My backyard bred bitch came back negative for both genes. It still doesn't mean that she's not at risk for DCM and we will still check her via holter and echo regularly. I'm still waiting on results for some of my others.
 
#4 ·
I requested the swabs by email and they came in the mail within a few days. I sent them back and I got the results for 2 of my dogs within a week, the other 2 are still pending.

I am particularly interested in my male's result since he has DCM. He's been doing well with medications and his 8th birthday is today. It's important to keep screening your dogs regularly because treatment can help prolong life with excellent quality of life.

I am hopeful that someday we will have more tools available to make predictive decisions towards breeding and the health of our dogs.
 
#14 ·
Yes, it is helpful. Also, if your dog ends up getting DCM you should let them know. Holters and echos are still very much needed to catch it. They know these 2 genes are in the makeup of some forms of DCM but there are more genes out there so this test is no guarantee. I know the PDK4 gene has not shown to have impact on Euro. dobes I don't know about the DCM 2 gene. Any euro breeder not holtering and echo. and saying their lines are free from Cardio are either crooked, ignorant on the subject, or both.
 
#15 ·
Okay will do, is there somewhere a adress or something that i can buy or atain a test for my Vet i will be doing Holter in 5 months on all 3 of them again so it would be perfeckt. Do we on the Board have a DCM List somewhere i could contribute a lot of names from Euro Dobes with date of death and date of birth some with parantage.
 
#24 ·
Trying to eqate the DCM tests (DCM 1 and DCM2) to something as simple as color genetics just doesn't really work.

For one thing if you look at information on the human form of DCM (and there is one which is very similar to the Doberman form, you'll find that there are multiple genes which affect what happens with human cardio (of the DCM type)--last information I read was that they had isolated something like 22 or 23 genes which relate to DCM in people.

So far we only have identified two gene sets that relate to DCM in canines. We are stll in the baby step phase of identifying what happens genetically when you are talking about the genetics of stuff that is caused by multiple sets of genes.

If you think about a very simple genetic cause--coat color for instance--it becomes very obvious that even there, it is more complex than it may appear superficially.

Basic coat color in Dobes is the result of two genes--one supplied by the dam and one supplied by the sire of puppies. A black doberman carrying only the dominant genes BB bred to a mate who was red (bb) will produce puppies that are all genetically Bb--this means they are all visually black puppies (phenotype) but genetically they carry the red gene. Then in Dobes there is a dilution gene--DD--that gene would produce a dog who was visually whatever the red/black gene dictated. If, however a dog carried the recessive dd gene the dog would visually be either blue or fawn. And additionally there is now a test for the albino gene which if present in the recessive form would produce a Doberman who was "white" (actually more like varying shades of very light cream with blue eyes).

Doberman color genetics are some of the most simple genetics that exist--in other breeds color heredity is much more complex for a variety of reasons but even for a Dobe as you see the simple visual color can be caused by a number of different genetic combinations. This is not exactly a one explanation fits all cases.

Cardio (Doberman DCM type) with only two identified gene pairs to look at has only hit the high point of that particular iceberg. And Dr Meurs has said this over and over.

Is it worth having your dogs tested--I think so--it all provides more baby steps and more information for the people who are engaged in determining what the causes of DCM in our dogs are and what they mean for life span and general health.

I also test my dogs via ultrasound and holter--yearly starting at two years and every six months from 6 on. The first Dobe I had developed DCM at some point and was diagnoed only when he was well into CHF--there weren't any good tests--no ultrasounds, no holters and about the only medication that was used was lasix on a dog already in advanced congestive heart failure--that dog made it to almost 10 and that was with less than three months after his diagnosis. We've made huge strides in treatment and diagnosis since then (1968) and the best bet still, is early diagnosis and treatment.

There aren't now and won't be for the immediate future any absolute answers--we've got a long way to go...
 
#26 ·
I just mailed Indy's DCM-2 swabs. He is PDK4 negative, most recent ProBNP was excellent and normal echo in March. His holter in February showed 110 SVT's but the Cardiologist said to holter and echo again in a year; no meds at this time. He is also hypothyroid.

I'm going to holter again next month though just for peace of mind. He will be 8 on July 4th.
 
#30 ·
It's important to not read too much into these studies.

I have to say, I'm less impressed with both the researcher and the research after seeing some of the things Muers is claiming from the video of a presentation she gave recently. I won't go so far as to say she's a quack, but she is claiming that the PDK4 mitochondrial mutation is directly responsible for DCM, that the observable (phenotype) defect in cardiac muscle composition is due to this. That's an unsubstantiated stretch, it has not been demonstrated, to the best of my knowledge, even in relatively well-researched human medicine.

Muers has made a very strong statement, repeatedly, that homozygous positive dogs should not be bred. I think that is an irresponsible statement because the correlation just isn't that strong, the test is simply not that meaningful. It'd be nice to see data from the years the test has been available to see how well the larger dataset upholds the original research. The European study that found no correlation was far from conclusive, it had a relatively small sample size, but it does raise doubts that should be confirmed or debunked through analyzing data.

I, too, would like to hear the actual claim on DCM2, what splice site it associates with, and how significant it is from a statistical standpoint. It makes very little sense to me that they are offering it commercially without publishing any peer-reviewed research findings or even bothering to explain what they think they've found in any level of detail.

Don't get me wrong, I think it's great that a researcher is putting time into the Doberman specifically, but overstating results does nobody any favors.
 
#31 ·
I'd really like to see the study out of Canada from Guelph, they were working on some treatment protocol last I heard that was showing promise. But that was the last I heard so if anyone has any updated info, I'd love to see it!

With as many genes as are likely involved in DCM, I'm going to guess there probably are some genes of major influence, with many lesser contributory genes involved. With JUST the major gene, the dog may never develop the problem, but with the major(s) and a compliment of contributors, it tips things over into clinical disease. Just me theorizing on that one!
 
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