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Old 07-21-2010, 10:23 PM   #1 (permalink)
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Default Responsible Breeders: ARVC DNA Test?

Three questions for the responsible breeders:
  • Are you running the ARVC DNA tests on your breeding stock?
  • Why or why not?
  • Am I limiting myself too much if I only consider breeders that are running the ARVC (and DM) DNA tests?
A little background on this we are currently managing ARVC in our 5 year old. Were not ready or interested in a puppy right at the moment, but the deck is seriously stacked against us that our girl will live to a ripe old age (ARVC isn't the only issue). I want to take my time and start searching now for a good breeder for a future puppy.
Im looking for a responsible breeder in the southern GA/northern FL area and am having a tough time finding one with good lines that is ethical and running all the health checks Im interested in. Basically, Im looking for the recommended health checks with a recent clear holter and DM/ARVC DNA.
The reason I'm interested in the DNA test in addition to holters is because ARVC is an adult onset disease that may not have displayed on a holter yet. Im interested in the total health of the line/puppies; Im just extra sensitive to ARVC because thats what were dealing with.
I understand that research is unfolding and that a negative DNA test does not mean the dog wont develop the disease. I also understand incomplete penetrance and that a heterozygous positive dog wont necessarily develop the disease. Finally, I understand that you can run all the tests in the world and still end up with a sick puppy; I just want to increase our odds as high as possible that well end up with a healthy, happy pup.
Thanks in advance for your thoughts!
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Old 07-21-2010, 10:26 PM   #2 (permalink)
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Jennifer (Newcastle) might be able to point you in the right direction when it comes to finding a breeder. I have noticed that most responsible breeders are running the ARVC as well as DM on their dogs. Keep in mind, that you can have a puppy shipped to you if you cannot find a suitable breeder in your area. Good luck!
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Old 07-22-2010, 06:48 AM   #3 (permalink)
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I, too, am dealing with heart problems in my Laney....She was diagnosed at 2-1/2 yr old!!! Needless to say, I am always on pins & needles. She gets her "bad days", but most are "great days". I lost my previous boxer girl, Nikki, to a bad heart, but she lived to be almost 12yr old. I just want my Laney to live a full, comfortable, loving life. Laney is my 3rd boxer. At this point, I don't feel like I want to go thru the heartbreak again. Lots of luck to you finding a good breeder.
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Old 07-22-2010, 10:31 AM   #4 (permalink)
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Quote:
Am I limiting myself too much if I only consider breeders that are running the ARVC (and DM) DNA tests?
Without a doubt.

I have done the ARVC and DM DNA tests on all my current dogs. I'm undecided on whether I'll do them in the future. If I do, it will be purely for informational purposes - I'm not making breeding decisions based on the test results.

Many breeders I know have decided to forego the ARVC DNA test at this time, since repeated clear holters are far more meaningful. (As well, while the DM test is somewhat more indicative, homozygous positive is still only a possibility; family history is the key factor there, and frankly at this point most breeders are more concerned with heart issues that kill Boxers at 3-5-8 years old than DM which may or may not result in their death at 12+.)

Quote:
a heterozygous positive dog won’t necessarily develop the disease.
A homozygous positive dog won't necessarily develop the disease, either. The only thing the ARVC test really tells you is whether the dog has any copies of a mutation that causes decreased adhesion between cardiac cells. This decreased adhesion may, in some dogs, result in ARVC - but in others it will not, and there's no way (at this point in time) to know which dogs are which.

The ARVC research was recently (finally!) published - in a human genetics journal, so the peer review was on the methodology of finding the genetic marker moreso than on the cardiac/veterinary aspect. (I'm not sure if it will be published in a veterinary/cardiology journal at some point or not.) Here are some highlights from the published article:

Quote:
As part of an ongoing study of the heritability of canine ARVC, 300 pet boxer dogs over 1 year of age were prospectively recruited for participation. All dogs were evaluated with physical examination, electrocardiogram, echocardiogram, and a 24-h ambulatory electrocardiogram using a three-channel transthoracic system. Pedigrees were collected when available.

Diagnostic criteria for canine ARVC included the presence of [greater than or equal to] 500 VPCs of right ventricular origin/24 h (normal dogs have an average of 2/24 h) and, when present, syncope.... Dogs with echocardiographic abnormalities suggestive of congenital heart disease or dilated cardiomyopathy were excluded. Using these criteria, 65 boxer dogs were diagnosed as ARVC-affected. This included 30 males (18 castrated, 12 intact) and 35 females (16 spayed, 19 intact) with an average age of 7 years. Criteria for accepting a boxer dog as a control required a minimum age of 6 years, and a normal cardiovascular physical examination with [less than] 100 VPCs/24 h. One hundred canine DNA samples were also obtained from the laboratory bank of canine DNA collected from 11 different breeds of dogs as controls.

Genome-wide analysis (GWA) was performed with ... DNA from 46 boxer ARVC cases and 43 boxer controls. Only affected and control dogs with pedigrees were used for the GWA and participating dogs were specifically selected so that no dogs were related within a three generational pedigree.
....

Subsequently, sequences from 61 cases (42/46 samples from GWA that had sufficient amount of remaining DNA), 38 controls (38/43 from GWA) and 100 non-boxer (11 different breeds) dog controls were genotyped for the 8-bp deletion at the 30 UTR region of Striatin.
....

Dogs that were homozygous for the deletion ... had more severe disease based on VPCs number than heterozygous dogs. Homozygous dogs recorded 1,091-32,000 VPCs/24 h (median of 5,102) and heterozygous ARVC dogs 109-19,000 VPCs/24 h (median of 2,515).
....

Four dogs originally diagnosed with ARVC did not have the deletion.... [I]t is possible that the dogs were incorrectly phenotyped as affected and actually had other disease processes that mimic ARVC. An additional possibility is that, as in human beings, ARVC may be a disease of significant genetic heterogeneity in the dog. In human beings, more than 100 pathogenic variants have been identified in 8 genes at this time. It is possible that the canine form of ARVC may be associated with more than one genetic mutation and likely more than one gene. Although it is true that the boxer dog is a pure breed dog with a fairly closed gene pool, it has an estimated heterozygosity of approximately 47%. The development of more than one novel mutation is possible, especially given the significant genetic heterogeneity of the disease in human beings. ARVC in these four dogs (7% of the ARVC cases) may be due to a different, yet to be identified, genetic variant. In human beings, approximately 60% of ARVC cases do not have a mutation in a known disease causing gene.

Likewise, 11 of the 35 dogs classified as controls were found to be heterozygous for the deletion. In this study, we classified dogs as unaffected controls if they were at least 6 years of age and had less than 100 VPCs/24 h. Boxer ARVC is an adult onset disease with a variable age of onset. The diagnosis of canine ARVC has been reported in dogs as young as 1 year of age and as old as 13 years of age with a median age of onset of 6 years of age. It is possible that dogs with the deletion who were not yet demonstrating the ARVC phenotype will express the disease at an older age. The variant described in this study had an approximately 72% penetrance. In human beings, ARVC is a disease with age-related, relatively low penetrance and variable expressivity. In some kindreds with the autosomal dominant form of ARVC, the penetrance may be as low as 20-30%. Many individuals with a known genetic mutation will never develop clinically significant disease and even within the same family, some individuals will have a more benign disease course than others. Degree of penetrance may be somewhat dependent on the specific causative gene....

The incomplete penetrance and variability of expressivity in ARVC likely suggests the role of environmental factors and genetic modifiers in the presentation of this disease and supports further investigation of the second strongly associated region at 35-38.5 Mb.
The abstract is here: SpringerLink - Journal Article
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Old 07-22-2010, 11:13 AM   #5 (permalink)
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Laney's Mom - I'm so sorry to hear about your little girl's heart issues. I hope that she continues to have many more great days
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Old 07-22-2010, 02:19 PM   #6 (permalink)
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Quote:
Originally Posted by RoyalBoxVA View Post
Laney's Mom - I'm so sorry to hear about your little girl's heart issues. I hope that she continues to have many more great days

Thank you, RoyalBox. She takes meds every day....so far so good. She was diagnosed last August. I just kinda take it easy with her. I appreciate your concern.
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Old 07-22-2010, 08:43 PM   #7 (permalink)
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Newcastle - Thank you very much for this information. I appreciate how much detail you included and your thoughts on it. Sounds like I need to come up with a different plan.

Laneysmom – I would love to compare notes if you don’t mind. There may be something that you’re doing for Laney that we weren’t advised of and vice versa. I’ll start a new thread.
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